general characteristics Inflammation

Inflammation - Protective-adaptive reaction of a holistic organism on the action of a pathogenic stimulus, manifested by the development of tissue damage or blood circulation organ and an increase in vascular permeability in combination with dystrophy of tissues and cell proliferation. Inflammation is a typical pathological process aimed at eliminating the pathogenic stimulus and restoring damaged tissues.

Famous Russian scientist I.I. Mechnikov at the end of the XIXVEK first showed that inflammation is inherent not only to man, but also lower animals, even one-cell, although in primitive form. At higher animals and humans, the protective role of inflammation is manifested:

a) in localization and elimination of inflammatory hearth from healthy tissues;

b) fixation in place, in the focus of inflammation of the pathogenic factor and its destruction; c) removal of decay products and restoration of tissue integrity; d) work out in the process of inflammation of immunity.

However, I.I. Mechnikov believed that this protective reaction of the body is relative and imperfect, as inflammation is the basis of many diseases, often ending with the death of the patient. Therefore, it is necessary to know the patterns of developing inflammation in order to actively interfere with its course and eliminate the threat of death from this process.

To refer to the inflammation of any organ or tissue to the root of their Latin name, the end of "IT" is added: for example, the inflammation of the kidneys - jade, liver - hepatitis, urinary bubble - cystitis, pleura - pleurisy and. etc. Along with this, the old names of the inflammation of some organs are preserved in medicine: pneumonia is the inflammation of the lungs, Panariums - the inflammation of the nail file of the finger, angina - the inflammation of the oz and some others.

2 causes and conditions of inflammation

The emergence, course and outcome of inflammation in many ways depend on the reactivity of the body, which is determined by age, gender, constitutional features, the state of physiological systems, primarily immune, endocrine and nervous, the presence of concomitant diseases. Important importance in the development and outcome of inflammation has its localization. For example, the brain abscess of the brain is extremely dangerous for life, diphtheria inflammation.

In terms of severity of local and general changes, inflammation is divided into a normal, when the response of the body corresponds to the strength and nature of the stimulus; The hypergic, in which the response of the body for irritation is much more intense than the effect of the stimulus, and the hypergic, when inflammatory changes are defined weakly or not at all expressed. Inflammation may be limited, but may apply to a whole organ or even a system, for example, connective tissue system.

3 stages and inflammation mechanisms

Characteristic of inflammation, distinguishing it from all other pathological processes, is the presence of three consecutive stages of development:

1) alteration,

2) exudations and 3) cell proliferation. These three stages are necessarily present in the zone of any inflammation.

Alteration - Tissue damage - is a starting mechanism for the development of the inflammatory process. It leads to the release of a special class of biologically active substances called inflammation mediators. In general, all changes arising in the focus of inflammation under the influence of these substances are aimed at the development of the second stage of the inflammatory process - exudation. Inflammation mediators change the metabolism, physicochemical properties and fabric functions, rheological properties of blood and function forming elements. Inflammatory mediators include biogenic amines - histamine and serotonin. Histamine is highlighted by Labrocytes in response to tissue damage. It causes pain, the expansion of the microShower and an increase in their permeability, activates phagocytosis, enhances the release of other mediators. Serotonin is released from blood platelets and changes the microcirculation in the focus of inflammation. The lymphocytes are distinguished by mediators, called lymphocins, which are activated by the most important cells of the immune system - T-lymphocytes.

Blood Plasma Polypeptides - Kinin, including Callipers and Bradykin, cause pain, the expansion of the microShospots and an increase in the permeability of their walls, activate phagocytosis.

Inflammatory mediators include some prostaglandins that cause the same effects as kinins, while regulating the intensity of the inflammatory response.

inflammation protective pathogenic

Rearrangement of metabolism in the alteration zone leads to a change physico-chemical properties Tissues and the development of acidosis in them. Acidosis contributes to increasing the permeability of the vessels and membranes of lysosomes, the decay of proteins and dissociation of salts, thereby causing an increase in oncotic and osmotic pressure in damaged tissues. This in turn increases the yield of fluid from the vessels, determining the development of exudation, inflammatory edema and tissue infiltration in the inflammation zone.

Exudation - Output, or sinking, from blood vessels in a liquid type of blood with substances in it, as well as blood cells. Excomuitation occurs very quickly after the alteration and is ensured primarily by the reaction of the microcirculatory bed in the focus of inflammation. The first reaction of microcirculation vessels and regional blood circulation in response to the effect of inflammation mediators, mainly histamine, are spasm arterioles and a decrease in the inflow of arterial blood. As a result, tissue ischemia occurs in the inflammation zone associated with the increase in sympathetic effects. This reaction of vessels is short-lived. Slowing the speed of blood flow and a decrease in the volume of flowing blood leads to a violation of metabolism in tissues and acidosis. Spasm arterioles is replaced by their expansion, increasing blood flow rate, volume of flowing blood and an increase in hydrodynamic pressure, i.e. The appearance of arterial hyperemia. The mechanism of its development is very complex and is associated with the weakening of the sympathetic and increasing parasympathetic effects, as well as with the action of inflammation mediators. Arterial hyperemia helps to increase the metabolism in the focus of inflammation, increases the influx of leukocyte and antibodies to it, contributes to the activation of the lymphatic system, which takes the decomposition of tissue decay. The hyperemia of vessels causes an increase in temperature and redness of the inflammation site.

Arterial hyperemia as inflammation is developing is replaced by venous hyperemia. Blood pressure in venules and postcases increases, the rate of blood flow slows down, the volume of the flowing blood decreases, the venules become convulsions, pecculent blood movements appear in them. In the development of venous hyperemia, the loss of tone of the walls of Volen is matters due to disruption of metabolism and acidisosis of tissues in the focus of inflammation, vesa thrombination, compresses them with educt fluid. Slowing the speed of blood flow in venous hyperemia contributes to the movement of leukocytes from the center of blood flow to its periphery and sticking them to the walls of the vessels. This phenomenon is called edge standing leukocytes, it precedes them to exit vessels and transition to the tissue. Venous hyperemia ends with blood stops, i.e. The emergence of the state, which manifests itself first in Venulah, and later becomes true, capillary. Lymphatic vessels are overwhelmed with lymph, lymphotok slows down, and then stops, since thrombosis of lymphatic vessels occurs. Thus, the focus of inflammation is isolated from intact fabrics. At the same time, blood to it continues to flow, and its outflows and lymphs are dramatically reduced, which prevents the spread of damaging agents, including toxins, by the body.

Excomuitation begins during the period of hyperemia and reaches a maximum in venous hyperemia. The reinforced yield of the liquid part of the blood and substances dissolved in it from vessels into the tissue is due to several factors. The leading importance in the development of the exudation has an increase in the permeability of the walls of the microShosuds under the influence of inflammation mediators, metabolites (lactic acid, ATP decay products), lysosomal enzymes, disorders of the balance of ions to and sa, hypoxia and acidosis. The fluid yield is also due to the increase in the hydrostatic pressure in microsudes, hyperoncia and tissue hyperosmia. Morphologically increased vascular permeability manifests itself in strengthening pinocytosis in the endothelium of vessels, swelling of basal membranes. As the vascular permeability increases from the capillaries to the hearth of inflammation, the shaped elements of blood begin to go out.

The fluid accumulating in the focus of inflammation is called exudate. According to the composition, the exudate is significantly different from the transudate - the accumulation of fluid during edema. In excessive, the protein content is significantly higher (3-5%), and the exudate contains not only albumin, as a transudate, but also proteins with high molecular weight - globuline and fibrinogen. In the exudate, in contrast to the transudate, there are always uniform elements of blood - leukocytes (neutrophils, lymphocytes, monocytes), and often red blood cells, which, accumulating in the focus of inflammation, form inflammatory infiltrate. Exudition, i.e. The current of the vessels from the vessels into the fabric towards the center of the focus of inflammation, prevents the spread of the pathogenic stimulus, the products of the liveliness of the microbes and the decay products of their own tissues, contributes to the inflammation of the leukocytes and other formed elements of blood, antibodies and biologically active substances into the focus. The exudate contains active enzymes, which are released from the dead leukocytes and lysosomes of cells. Their action is directed to the destruction of the microbes, the melting of the remained cells and tissues. In the exudate there are active proteins and polypeptides, stimulating cell proliferation and tissue restoration at the final stage of inflammation. At the same time, the exudate can squeeze the nervous trunks and cause pain, disrupt the function of organs and cause pathological changes to them.

INFLAMMATION - Complex, complex local vascular tissue (mesenchymal) defendant response of a holistic organism on the action of the pathogenic stimulus. This reaction is manifested by the development of the tissue damage or the circulatory change body mainly in the microcirculatory line, an increase in the permeability of the vessels in combination with the tissue dystrophy and cell proliferation.

General pathology

Brief historical information and theories

The question of the meaning and essence of V. was always a great place in medicine. Even Hippocrates believed that V. He has a neutralizing importance for the body that harmful beginnings are destroyed in the purulent focus and therefore the formation of pus is useful, healingly, unless the definite limit of the intensity of the inflammatory process is not exceeded. Hippocratic views on nature V. dominated the 18th century, supplemented by the description of the "cardinal signs" of inflammation.

A. Celsis described four main wedges, a sign of C.: Red ( rubor), swelling ( tumor), pain ( dolor), temperature increase ( calor). Fifth sign - impaired function ( functio Laesa.) described K. Galen; He spoke about inflammation as a local fever and pointed out the variety of ethiol, factors, which can cause it.

The first idea close to the modern idea of \u200b\u200bV. was formulated by the English. Surgeon J. Gunter, K-ry identified V. as the body's reaction to any damage. Gunter considered V. The protective process, always arising at the place of damage, with the help of K-Rogo restores normal function damaged tissue or organ.

The doctrine of V. began to develop after improving the light microscope (mid-19th century), as well as in the first half of the 20th century. In connection with the development of biochem., Biofiz and histochim. methods and methods of electronically microscopic examination of tissues. R. Virhov (1859) drew attention to the damage to the parenchyma of the organs (dystrophic changes of cells) with V. and created the so-called. Nutritive ("Nutrient") Theory of B. This theory has lost importance due to the studies of Samuel (S. Samuel, 1873) and Y. Condheim (1887), the reaction of small vessels (vascular theory in the pathogenesis. .).

A. S. Shklyansky (1869) applied an experimental method for studying blood flow at V. and gave Piz. Explanation of the phenomenon of "Regional standing of leukocytes". A. G. Mamurovsky (1886) noted thrombosis and blockade of Lymph, Vessels in the hearth V.

Especially a great contribution to the development of the problem V. I. I. Mesnikov, which in 1892 formulated the biological theory V., developed the teaching of phagocytosis (see), laid the beginning of a comparative pathology of V. and the theory of cellular and humoral immunity ( cm.). The process of absorption by phagocytes of foreign particles, including the bacteria, was recognized by I. I. Meschnikov the main, the central process characterizing V. in his lectures on the comparative pathology of inflammation I. I. Mechnikov wrote about the process of intracellular digestion carried out in the cytoplasm of phagocytes .

The development of the idea I. I. Mechnikov on the meaning of phagocytosis to protect the body from the pathogenic factor and the formation of immunity was obtained in the works of H. N. Anichkova, A. D. Ado, Kona (E. J. Cohn, 1892 - 1953) and many other scientists . With the discovery in 1955, the cytoplasmic organelle-lysos (see) - the teachings of I. I. Mechnikov about the citzes as the carriers of the digestive function of the cell received further confirmation.

V. V. Voronin in 1897 established the value of the state of interstricular tissue and tone of the vessels with V. Decaying the phagocytosis process, the main mechanisms underlying B., he considered the processes occurring in the interstitial substance of the connective tissue, and gave different Mesnician interpretation of the phenomenon of emigration, wandering of cells and phagocytosis. Voronin's theory did not reveal the biol, the essence of inflammation. V. V. Podweysotsky in the "Fundamentals of General and Experimental Pathology" (1899) wrote that under V. There is a discrepancy between endothelial cells, as a result of which the holes are formed between them, through the binary leukocytes penetrate the vessel into perivascular space.

In 1923, Shada (H. Schade) put forward fiz.-chemical. Theory at.: In his opinion, the basis of B. is tissue acidosis, to-ry and determines the entire set of changes. Ricker (G. Ricker, 1924) considered Phenomena V. as a manifestation of vascular-nervous disorders (Nerivascular theory V.).

Of great importance for the clarification of histogenesis V., the role of cellular forms involved in the inflammatory response had the work of A. A. Maximov (1916, 1927), A. A. Zavarzina (1950) and other scientists who created experimental models V. and studied transformation cellular forms in the hearth V.

Comparative pathology

The classic description of the comparative pathology V. Del I. I. Meschnikov, showing that V. is always an active response of the body, for whatever the evolutionary development stage it is. I. I. Mechnikov traced at different stages of phylogenesis, the development of all phases of the inflammatory response - alteration, exudation and proliferation, described the phagocytosis in detail; In high-organized animals, a large role in phagocytosis took the neuroregulatory mechanisms. The body, indicates I. I. Meschnikov, is protected by means, it has a swarm. Even the simplest single-cell organisms do not belong passively to harmful stimuli, and struggling with them by phagocytosis and digesting the cytoplasm. However, in the simplest single-cell organisms, when exposed to the pathogenic factor, there are an alteration phenomena, similar to some dystrophic processes in multicellular organisms. In multicellular organisms, the reaction to damage is complicated due to the proliferation of cells and the formed vascular system; The body can already "send" a significant number of phagocytes to the place of damage. At the later stages of philogenesis in organisms, cell emigration arises. With the formation of endocrine and nervous systems, neurohumoral regulation factors of the inflammatory response appear.

In highly organized animals, other protective and adaptive processes are joined to phagocytosis: blockade of venous and lymph, vessels, discharge from the focus of V., exudation of the serous fluid, druentizing toxic products, the formation of antibodies by proliferating plasma cells, neutralizing the pathogenic factor.

Data on phases V., obtained in the study of an inflammatory response in phylogenesis, show its complication as the evolution of organisms; Phase V. to a certain extent repeated in the prenatal period of a person. Yu. V. Gulkevich (1973) showed that the embryo has a significantly lower reactivity compared to an adult organism and in the earliest stages of development, the embryo responds to a harmful effect only by death, but already in the early stages of development, cell proliferation may also be observed. Excomuitation with the presence of leukocytes was found in the fruit part of the placenta and the fetal sheath for 10-12 weeks. and is the latest ontogenetic component of the inflammatory reaction. Phagocytosis in the human embryo is carried out in ch. arr. Connecting tissue macrophages, and later segmented granulocytes.

The development of an inflammatory response in human ontogenesis is closely related to the formation of immunol, reactivity, which is morphologically expressed by the appearance of a large number of plasma cells producing immunoglobulins, the number of reasons increases significantly when the inflammatory focus embryo occurs. Studies show that the inflammatory response with the presence of all signs of V. is established at the 4-5th month of the human intrauterine life. In the postnatal period, under V., the impact on the organism of antigenic irritants of the environment and immunol, the processes are more complicated by the clinical morphol. Profile V.

Etiology and pathogenetic mechanisms

The inflammatory reaction consists of several interrelated phases: a) alteration of tissues and their cell components; b) release of physiologically active substances (so called. V. mediators), which is the launching mechanisms V. and entails the reaction of microcirculation vessels; c) increase the permeability of the walls of the capillaries and Vullet; d) the reaction of the blood system for damage, including changes in the rheological properties of blood (see blood, rheology); e) proliferation - reparative stage V.

For practical purposes, it is advisable to conditionally separate the three main interrelated components of V., having a bright clinical morfol. Expression: Alteration with mediators, vascular reaction with exudation and proliferation. The classification of the main morphol, forms V. based on the predominance of one or another of these components.

Alteration (tissue and cell damage) It can be considered as a result of the direct action of the pathogenic factor and exchange disorders arising in damaged tissue. This is the first phase in.; It characterizes the initial processes and morphologically manifests itself from the barely noticeable structural and functional disorders to complete destruction and death (necrobiosis, necrosis) of tissues and cells (see alteration). Alteractive changes in V. are particularly pronounced in highly differentiated tissues performing complex functions, for example, in neurons; In the tissues performing ch. arr. Support function and components of the organ, for example, in connective tissue, alteractive changes are often detected with difficulty. In parenchymathous organs, the alteration is manifested by various types of protein dystrophy (see) and fatty dystrophy (see), a technoon and fibrinoid swelling can occur to fibrinoid necrosis (see fibrinoid transformation).

In c. n. from. The alteration is expressed by the change in ganglion cells (neurocytes) in the form of lysis of basophilic (tigroid) substance, replacing the nuclei to the periphery and picnosis (see), swelling or kneading cells. In the mucous membranes, the alteration is expressed by damage to the epithelium, desquamation (see) with the exposion of the basal membrane; The mucous glands strongly distinguish the mucus, the increasing epithelium is mixed, the lumens of the glands expand (see mucosa dystrophy).

Ultrastructural changes in B. occur both in the components of the cytoplasm and in the core of the cell and its membrane. Mitochondria increase in size, swell; Some mitochondria, on the contrary, wrinkled, cristes are destroyed; The shape and the magnitude of the endoplasmic reticulum tanks are changed (see), vesicles appear, concentric structures, etc. Also vary and ribosomes (see). In the core of the cell, damage is manifested by the edge of the chromatin, the kernel membranes.

In many cases, the alteration is developing through the so-called. Lizosomal effect: when the membranes of lesos is destroyed (see), a variety of, especially hydrolytic, enzymes that play a significant role in damage to the cell structures are released.

Mediators inflammation - A number of physiologically active substances considered as starting mechanisms V., under the influence of boring, the main link V.- The reaction of the vessels of the microcirculatory channel and flowing blood with a violation of the rheological properties of blood, is the initial phase of the inflammatory reaction. V. Mediators contribute to an increase in the permeability of the vessels of the microcirculatory system, especially the venular separation, followed by exudition of plasma proteins, emigration of all types of leukocytes, as well as red blood cells through the walls of these vessels. These physiologically active substances play an important role in the manifestations of V., and some researchers call them "internal engines" V.

Spector and Willobi (W. G. Spector, D. A. Willoughby, 1968) give 25 titles of physiologically active substances (chemical mediators) of different spectrum of action appearing after fabric damage. Especially a lot of work on mediators V. appeared after the discovery of histamine and leukataxin. Although Leutukaxin in subsequent test work turned out to be a substance of heterogeneous nature, studying it served as an incentive for further research of endogenous chemical. V. Mediators, the most important of the to-rye, it is customary to consider histamine, serotonin, plasma kinines, RNA and DNA decay products, hyaluronidase, prostaglandins, etc.

One of the main sources of Chem. V. Mediators are fat cells (see), Gistamine, serotonin, heparin, etc. Cytochroma oxidase, acid and alkaline phosphatase, enzymes for the synthesis of nucleotides, proteases, exerates, leucine amineptidases, plasmin are found in the cytoplasm of the fat cells.

Spector and Willobi most convincingly showed a particularly important role of histamine (see) in the launch mechanisms of V. Histamine - this is the first vasoactive substance that appears immediately after tissue damage; It is with him that the starting stages of vasodilation, an increase in vascular permeability and exudation are connected; Histamine has a predominant effect on Venory. Serotonin also has (see).

Among the mediators B. It is necessary to note the globulin permeability factor (PF / DIL.), Open in the plasma of the blood of the guinea pig Miles (A. A. Miles) from Sot. (1953, 1955) and T. S. Easterina (1953, 1955) in aseptic inflammatory exudate, rabbit serum, dogs and a person; This factor contributes to the liberation of Bradikinin with the help of Kallikrein. The SPECTOR believes that the globulin permeability factor has a close relationship with the blood coagulation mechanism, and in particular with the Hageman factor (see the chopping system). According to Miles, the chageman factor activates the PF / DIL globulin precursor.

Some nucleosides take part in the inflammatory response; adenosine may cause an increase in the permeability of the walls of microspides and local accumulation of leukocytes; Some nucleosides are liberators (released) histamine.

Vascular reaction with exudation Plays a very large role in the mechanisms of V. A number of authors claims that the entire "inflammation appearance", all its features, the entire gamma of tissue changes is determined by the vascular reaction, the permeability of the microcirculatory vessels, the severity of its damage.

In the earliest phases of V. marked the activation of the functions of the endothelium of capillaries. In the cytoplasm of the endothelium, the number of microwaves increases, the cytographic groups appear, the polyribosomes are formed, mitochondria swell, the cavities of the endoplasmic reticulum are expanding. Endothelial cells somewhat change their configuration, swell, their membranes become loose (see permeability).

The mechanisms of passing the substances of various molecular weight and blood cells through the endothelial dilution and the basal membrane of the capillaries and the Vevel remained unclear for a long time. With the use of electron microscopy methods, it has been established that endothelial cells in capillaries with continuous endothelium, closely adjacent to each other, only in separate places are connected with each other with the help of despair (dense compounds). The cell on the basal membrane is reinforced and is fastened with adjacent cells of the colloidal weight of the type of calcium proteinate in combination with mucopolysaccharides. In the pathol, the cell body conditions can be reduced, change its shape and move. The complex of endothelial cells, lining the inner surface of the microcirculation vessels, is a movable system, when operating to-point, gaps may occur between endothelial cells, and even channels in the body of cells. Monendothelial gaps should be attributed to the so-called. Small pores, and the channels in the body of the endothelial cell (microwave transport) - to the so-called. Big persecution, through to-ry and transcapillary transport. Dynamic electronic microscopic observations

A. M. Chernukha from Sot. It was shown that, for example, at pneumonia, the microwavesuculation of the endothelium of capillaries and the formation of larger endothelial microposters is significantly enhanced, which indicates an increase in tissue exchange.

In the focus of B. There are pronounced disorders of blood flow and lymphorty. After the tissue is damaged by the earliest change in an acute inflammatory response, it is quickly passing (from 10-20 seconds to a few minutes) the reduction of arterioles. Most researchers do not give much significance to this phenomenon, but Spector and Willobi consider it a protective reaction caused by catecholamines. Soon the two phases of extending vessels are developing. The first phase (immediate vasodulation), accompanied by an increase in permeability with respect to blood proteins, reaches a maximum on average after 10 minutes; The second phase, much longer, is measured by several hours. Due to the second phase of the extension of the vessels, infiltration of leukocyte tissues occurs, inflammatory hyperemia (see), the rheological properties of blood change, there are stranges, local hemorrhages, thrombosis of small vessels; In the focus of V. Increases metabolism, which is expressed by an increase in concentration hydrogen ions, acidosis, hyperosmia. Limph, microsudes develop lymphostasis and lymphhotromboosis.

The shifts of the rheological properties of blood begin with changes in blood flow rate, axial current disorders, bringing out white blood cells from it and arrange them along the walls of post-cylinder veul (so-called, edible standing leukocytes); Frame platelet aggregates and erythrocytes, stas and thrombosis Volet and capillaries are formed. Thrombosis arises in connection with the activation of the chageman factor, an important component Cutting blood system. Then there is an exudation (see), i.e., extinguishing from vessels in the tissue of components of blood - water, proteins, salts and blood cells. In the focus, V. detect the methods of metabolic products, toxins released from the blood current, i.e. Focus V. Performs a drainage eliminitive function as it were. Excessive or introduced directly to the center of V. Substances (eg, paints) are derived slightly due to thrombing of venous and lymph, vessels in inflamed tissues.

Exudition of proteins occurs in the sequence, K-paradium explains the magnitude of molecules (the smallest albumin molecule, the largest - fibrinogen): with a small degree of incidence of permeability, albumines are allocated, as permeability increases - globulines and fibrinogen. Exudition of protein molecules occurs. arr. Through the channels in the body of the endothelial cell (large pores) and to a lesser extent through the slots between the endothelial cells (small pores).

Extinguity from the blood current through the wall of the veins and capillaries of cell elements of blood, ch. arr. leukocytes (segmented granulocytes and monocytes) preceded the boundary standing leukocytes, gluing them to the wall of the vessel. A. S. Shklyansky (1869) showed that the disclosure of leukocytes from axial current is in full compliance with Phys. The law of behavior of particles suspended in the current fluid when slowing the speed of its movement. After gluing to endothelial cells, segmented granulocytes form pseudopodia, penetrating through the vessel wall, the contents of the cell overflowing to the leg stretched out of the vessel, and the leukocyte is out of the vessel. In the occasional tissue segmented granulocytes continue to move and mix for exudate.

The process of emigration of leukocytes is called leukeodiapedesis. It has been established that the emigration of segmented granulocytes and mononuclear cells is somewhat different. Thus, segmented granulocytes (neutrophils, eosinophils and basophils) are emigrated between endothelial cells (inter-endothelial), and agranulocytes (large and small lymphocytes and monocytes) - through the cytoplasm of the endothelial cell (trans-endathelial).

Fig. 1. The interleadothelial emigration of leukocytes through the wall of the vessel with inflammation: A - segmented granulocytes (1) penetrated into the space under the endothelial cell and are located between the endothelium (2) and the basal membrane (3). Endothelial cells (4), collagen fibers (5), granulocyte kernels (6) are visible; x 20 000; B.Tva segmented granulocyte (1) are in perivascular connective tissue (basal membrane recovered in a dense gel). Endothelium (2) is not changed, sequins (4) of its cells and collagen fibers of perivascular connective tissue (5) are visible; vessel clearance (7); x 12 000.

Monendothelial emigration occurs as follows. In the very initial phase, the V. Segmentore granulocyte is glued to the endothelial cell and between it and leukocyte as far as the threads are stretched. Then the endothelial cell is reduced and the pseudopodia is rushed into the resulting between two cells; With their help, segmented granulocyte quickly penetrates into the space under the endothelial cell, K-paradium, as it were, is peeled, and the hole above it is closed by connecting again the cells of the endothelium - segmented granulocyte turns out to be between the endothelium and the basal membrane (Fig. 1, a). The following obstacle is the basal membrane - segmented granulocyte overcomes, apparently, according to the thixotropy mechanism (isothermal reversible decrease in the viscosity of the colloidal p-ra), i.e. the membrane gel transition to the sol with a slight touch of granulocyte to the membrane. The granulocyte easily overcomes the sol, it turns out in the tissue outside the vessel (Fig. 1, b), and the basal membrane is again restored to a dense gel.

With trans-endothelial emigration, agranulocytes are initially glued to the endothelial cell, the activity of the K-Roy is sharply rising; The financing processes arising from the membrane of the endothelial cell as to capture the mononuclear cell from all sides, absorb it by forming a large vacuole and thrown into the basal membrane. Then, according to the mechanism of thixotropy, mononuclear cells penetrate through the basal membrane into the perivascular space and are mixed up to the exudate.

With V. From the vessels in the fabric, erythrocytes are also published (see Diapened). They pass the vessel wall passively with a sharp increase in vascular permeability, which is observed in highly toxic infections (plague, Siberian ulcers), damage to the walls of the vessels of the tumor, radiation sickness, etc.

The exit from the segmented granulocyte vessel and the progress towards the hearth damage to I. I. Meschnikov explained Hemotaxis, that is, the effect on the leukocytes of substances that caused V. or those formed in the focus (see Taxis). Menkin (V. Menkin, 1937) allocated so-called from inflammatory fabric. leutarataxin, causing positive chemotaxis segmented granulocytes; Positive chemotaxis is more pronounced in segmented granulocytes, less- in agranulocytes.

The most important phenomenon of V. is phagocytosis (see), carried out by cells - phagocytes; These include segmented granulocytes - microphages and agranulocytes - macrophages (see), in the cytoplasm of which the process of intracellular digestion is carried out. A positive role is revealed in the phagocytosis processes of aluminum, chromium, iron and calcium ions, opsonins (see).

It has been established that various particles and bacteria invagine the Phagocyte shell; In the cytoplasm of phagocyte, the invaginated part of the shell with the material in it is cleaved, forming a vacuol or phageosoma. In the fusion of the phageosomes with a lysosome, a phagelicosome (secondary lysosome) is formed, K-Paradise with acidic hydrolase performs intracellular digestion. At the time of phagocytosis, the activity of lysosomal proteolytic enzymes, especially acid phosphatases, collagenase, cathelins, arylsulfatase A and B, etc., thanks to the same enzymes, the dead fabrics are blocked by the same enzymes; The removal of decay products from the focus of V. occurs by phagocytosis.

With the help of pinocytosis phenocytosis, the droplets of the liquid and macromolecules, for example, ferritin, protein, antigen (see Pinocytosis) take place. Nosel (G. Nossal, 1966) showed that Antigen Salmonella, labeled with radioactive iodine and introduced into the bunny organism, is absorbed by macrophages in micropinocytosis. The antigen molecules in the cytoplasm of the macrophage are exposed to lysosomal hydrolase, which leads to the release of antigenic determinants. The latter are complexized with RNA macrophages, and then information about the antigen is transmitted to lymphocytes, which are transformed into plasma cells that form antibodies. Thus, the intracellular digestion of the antigen is completed with an immunogenic process (see Immunoorphology), and a protective and immunogenic function of the inflammatory response is carried out, cell and humoral immunity occurs during the K-Roy.

However, along with the completed phagocytosis in the macrophages, for example, with some infections, phagocytosis unfinished, or endocytobiosis, when phagocyted bacteria or viruses are not exposed to complete digestion, and sometimes even begin to multiply in the cytoplasm of the cell. Endocyteobiosis is explained by the disadvantage or even the absence of antibacterial cationic proteins in the lysosomes of macrophages, which reduces the digestible ability of lysosomal enzymes.

As a result of changes in microcirculation, increasing the vascular permeability and the next exudation of plasma proteins, water, salts and emigration of blood cells in tissues, the liquid is rich in protein (from 3 to 8%) liquid - exudate (see). Exudate can accumulate in serous cavities, between fibrous structures of the organ of organ, in subcutaneous tissue, which leads to an increase in the volume of inflamed tissue. Exudate consists of a liquid part and cell mass, contains tissue decay products. The nature of the exudate is not homogeneous: with a small degree of permeability of the vessels in the exudate, albumin prevails, some cells, with a significant permeability - globulin, fibrin, many cells.

The dynamics of the cellular changes of the exudate shows that under the influence of treatment, the number of neutrophils is initially reduced, and the number of monocytes increases, a large number of macrophages appear. The shift in the exudate segmenocyte segmenocytes is considered to be a favorable prognostic sign.

Proliferation (reproduction) cells It is the final, reparative phase V. The reproduction of cells occurs in ch. arr. Due to the mesenchymal elements of stroma, as well as elements of parenchyma organs. The stem cells of the connective tissue are multiplied - polyblasts, or lymphoid cells, adventitial and endothelial cells of small vessels, reticular lymph cells, nodes, small and large lymphoblasts (see granulation fabric, connecting tissue). With their differentiation in the focus of V., mature and specialized cells appear: fibroblasts, fibrocytes, fat and plasma cells, which are differentiated from their predecessors - plasmoblasts and large and small lymphocytes; New capillaries arise. During proliferation (see) there is also an exudation of neutrophilic, eosinophilic, basophilic leukocytes and lymphocytes, etc.; In this connection, lymphoid, plasma-cell, eosinophilic and other infiltrates are distinguished.

Cell elements in the inflammatory focus are subjected to transformation processes. Segmented granulocytes that fulfill their phagocytic function, quickly die. The lymphocytes are part of the part die, we are transformed into plasma cells, which are gradually dying, leaving the product of their secretion - hyaline balls. Puffy cells die, blood monocytes that have fallen into tissues become macrophages clearing the focus of V. from cell detritus, and luminous lymph current into regional lymph, nodes where they also die. Polyblasts and their differentiation products are the most persistent cellular forms in the inflammatory focus - epithelioid cells, fibroblasts and fibrocytes. Sometimes many-nuclear giant cells arising from epithelioid and proliferating endothelial cells appear. With the participation of fibroblasts there is an active synthesis of collagen. The cytoplasm of fibroblasts becomes a pironinophilic, that is, enriched with ribonucleotoproteis, forming a matrix for collagen. Completed by V. Education of mature fibrous connective tissue.

Exchange disorders arising in the focus of V., according to Lindner (J. Lindner, 1966), can be divided into catabolic and anabolic processes.

Catabolic processes are manifested by physiol disorders, the equilibrium of the main substance of the connective tissue: the processes of depolymerization of protein-mucopolysaccharide complexes, the formation of decay products, the appearance of free amino acids, the omnovy Kt (which leads to acidosis), amino marshares, polypeptides, low molecular weight polysaccharides. Such disorganization of the interstitial substance enhances the vascular tissue permeability, exudation; This is accompanied by the deposition of blood proteins, including fibrinogen, between collagen fibrils and protofibrils, which contributes, in turn, the change in the properties of collagen.

Protective reactions of the organism are largely determined by the anabolic processes and the degree of their intensity. These processes in V. are expressed in an increase in the synthesis of RNA and DNA, the synthesis of the main intertaround substance and cell enzymes, including hydrolytic. Histhop. Studies conducted by the Lindner on the study of enzymes in the cells in the focus of V., showed that monocytes, macrophages, gigantic cells, segmented granulocytes show especially greater enzymatic activity from the moment of appearance in the focus. The activity of hydro-Lases, which are markers lysosoma, increases, which suggests the increase in the activity of lysosomes in the focus in fibroblasts, the granulocytes increases the activity of redox enzymes, which increase the conjugate tissue respiration process and oxidative phosphorylation.

The early appearance of cells rich in hydrolylase (lysosomes), and above all segmented granulocytes, can be considered as one of the manifestations of catabolic processes due to the need for increased processing of decay products; At the same time, it contributes to anabolic processes.

Regulation factors and flow

B. is considered as a local tissue reaction, at the same time its emergence and flow are largely determined. common state organism. The general principle of self-regulation with feedback is presented at the cell level. However, adaptive reactions within the cell have an independent value as long as functional systems The whole organism, reflecting the complex complex of self-regulation of cells and organs, retain its relatively stable state. In violation of this state, adaptive and compensatory mechanismsrepresenting complex neurohumoral reactions. This should be kept in mind when analyzing local features Development of the focus of V.

The character V. can affect both hormonal and nerve factors. Non-ry hormones have very important for inflammatory reaction, ch. arr. The hormones of the adrenal cortex and pituitary gland, which is convincingly shown in the experiment and in the clinic by the Canadian pathologist G. Selre. It has been established that somatotropic hormone pituitary deoxykorticosterone acetate and aldosterone are able to increase the inflammatory "potential" of the body, that is, to strengthen V., although they can not call it on themselves. Mineralocorticoids, affecting the electrolyte composition of the tissues, have a pro-inflammatory action (activate V.). Along with this, glucocorticoids (hydrocortisone and others), adrenocorticotropic hormone, not possessing bactericidal properties, have an anti-inflammatory effect, reducing the inflammatory response. Cortizon, delaying the development of the earliest signs V. (hyperemia, exudation, cell emigration), prevents edema; This property of cortisone is widely used in practical medicine. Cortizon deprives the connective tissue of obese cells (large lymphocytes and polyblasts), in connection with this, there is a depletion of connective tissue with fat cells. Perhaps this is based on the anti-inflammatory effect of the cortisone, since, in the absence of obese cells, the activity of launch factors V., for example, histamine formed from granules of fat cells is largely reduced.

Influence nerve factors On V. studied not enough. However, it is known that in violation peripheral innervation, especially sensitive, V. acquires a sluggish, protracted character. Eg trophic ulcers limbs arising from the wounds of the spinal cord or sedal Nerva, Salurate very long. This is due to the fact that metabolic processes are disturbed in tissues, deprived of sensitive innervation, and alteractive changes are increasing, vascular permeability increases and swelling increases.

Wedge, the flow of V. depends on the set of factors. Especially great importance for the flow V. has the condition of the reactive readiness of the body, the degree of sensitization. In some cases, especially with increased sensitivity, V. flows sharply, in others - takes a protracted course, acquiring the nature of subacute or chronic. There is also a wavy flow of V., when the periods of sinking the process alternate with exacerbations; Outbreaks of the inflammatory process are possible for a number of years, for example, with brucellosis, tuberculosis, collagen diseases. In these cases, during the disease, the period (phase) of the hypersensitivity of the immediate type is replaced by a period of slow motion hypersensitivity. In the phases of hypersensitivity, exudative and even necrotic changes with a pronounced reaction of the microcirculation system are dominated. As V. or the transition of the process in a subacute form, vascular phenomena subsides to the fore, the phenomena of proliferation are dominant at the hron. B. When hron, abscess, for example, along with the formation of a pus, there are pronounced proliferative phenomena right up to the development of mature connective tissue. At the same time, proliferative nodules with a very weakly pronounced vascular-exudative reaction arise primary with some infectious diseases with acute stream (abdominal and raw materials, malaria, tularemia).

When hron, inflammation with the wave-like clinium, the picture can be very motley depending on the predominance of a phase V., and in tissues are possible both old and fresh morphol, changes.

Main clinical signs

Five classic wedges, signs characteristic of acute V. External Pokrov, maintain their meaning, passing the test by time and obtaining modern pathophysioli. and morphol, characteristic: red, swelling, pain, temperature increase, function disorder. With hron. V. And V. internal organs of some of these signs may be absent.

Redness - very bright wedge, a sign of V., due to inflammatory hyperemia, the expansion of arterioles, veins, capillaries, slowing down blood current; As the blood current is slowed down, the al-red painting of the inflamed tissue is made blue. Inflammatory hyperemia is combined with alteration of tissue, increased vascular permeability, exudation and cell proliferation, i.e., with the whole complex of tissue changes, characteristic of V.

Swelling In v. due to the initial period of the consequences of the vascular reaction and the formation of infiltration and perifocal edema, developing particularly easily around the hearth, surrounded by loose tissue; In later periods V. matters and proliferation.

Pain - Permanent satellite V., resulting from irritation by exudite the endings of sensitive nerves or ne-fish physiologically active substances, for example, by Kinin.

Temperature increase It develops with an enhanced inflow of arterial blood, as well as as a result of raising metabolism in the focus of V.

Violation of function On the soil V. arises, as a rule, always; Sometimes it can be limited to the disorder of the functions of the affected fabric, but the whole body suffers more often, especially when V. occurs in vital important organs.

The main forms of inflammation

According to Morfol, the signs are distinguished by three forms in.: Alteractive, exudative, productive (proliferative).

Alteractive inflammation

Alteractive inflammation is characterized by the predominance of tissue damage, although the exudation and proliferation also take place. This species V. is also called parenchymal, since it is observed most often in parenchymal organs (myocardium, liver, kidneys, skeletal muscles).

The alteration is expressed by various types of dystrophy of the parenchyma of the organ and stroma, ranging from the muddy swelling of the cytoplasm and ending with necrobiotic and necrotic changes, which can occur in the organ of the organ and in the intermediate tissue in the form of fibrinoid swelling and fibrinoid necrosis.

Alteractive V. With the predominance of necrobiotic changes is called necrotic V. Such type V. is observed with an allergic reaction of an immediate type (see allergies), as well as when exposed to strong toxic substances. When exposed to the body toxins of bacteria, for example, diphtheria, an allestrative V. myocardium arises, which is expressed by the appearance of myocardials in various layers, especially in the subendocardial zone, folk dystrophy folotic decay of the miofibrill until the occurrence of heavy cases Necrosis foci; The same is observed with an allergic myocardium (color. Fig. 1). The vascular meteorchimal and proliferative reaction are weakly expressed.

In the liver alteractive V. is observed in infectious hepatitis, under exposure, for example, chloroform, carbon tetrachloride and is expressed by muddy swelling and adhesive dystrophy of hepatocytes, an increase in their size and size of the liver as a whole.

In the kidney, Alteractive V. is expressed by the grainy dystrophy of the epithelium of the proximal and distal nephrone departments up to the epithelium necrosis with a weakly pronounced vascular-mesenchymal reaction.

Exodes of Alteractive V. are determined by the intensity and depth of tissue damage. With a mild dystrophy after eliminating the cause that caused V., there comes a complete restoration of tissues; Plots of irreversible damage to parenchyma are replaced by a connective tissue (eg, after diphtheria myocarditis, cardiosclerosis develops).

Exudative inflammation

Exquidative inflammation is characterized by the predominance of the reaction of the microcirculation system, ch. arr. its venular department, on the processes of alteration and proliferation. There is an exudation of liquid plasma parts, emigration of blood cells, i.e., the formation of exudate. For an exudative V. Typically a variety of morfol, and wedge, manifestations, since, depending on the degree of violation of vascular permeability, the nature of the exudate may be different. In this regard, Exudative V. may be serous, catarrhal, fibrinous (brunt and diphteritic), purulent, rotten, hemorrhagic, mixed.

Serous inflammation It is characterized by accumulation in tissues, more often in serous cavities, a slightly turbid, almost transparent exudate containing from 3 to 8% serum protein, and in a sediment - single segmented granulocytes and solid cells of serous shells.

The cause of serous V. may be thermal (burns), chemical, infectious (especially viruses), endocrine, allergic agents. This form V. is more often developing in serous cavities (serous pleurisy, peritonitis, pericarditis, arthritis, etc.), less often in parenchymal organs - myocardium, liver, kidneys.

Serous V. Myocardium is expressed by the accumulation of exudate between beams muscular fibers, around capillaries; in the liver - in the surroundinusoid spaces (disseasses); In the kidneys (for serous glomerulite) - in the lumen of the Capsules of the Gulf (Capsules of the Sillyansky - Bowman). In the easy, serous effusion accumulates in the lumen alveoli (color. Fig. 2). When skin burns, serous effusion accumulates under the epidermis, which leads to the formation of large bubbles. In serous shells there are hyperemia, they become dull, lose their characteristic shine.

Serous effusion may occur around the foci of purulent V. (for example, with a jaw periostite) or around a tuberculous focus, increasing the area of \u200b\u200bthe defeat, is so called. Perifocal V.

Serous V. Usually proceeds. For large quantities Dropping is hampered by cardiac activity, arises respiratory failure, limited the mobility of the joints, etc.

The outcome of serous V., if it has not passed into purulent or hemorrhagic, mainly favorable. Serous exudate is easily absorbed and leaves no traces or a small thickening of serous shells is formed. In myocardium and liver, small sections of sclerosis on the soil of the proliferation of fibroblasts and the formation of collagen fibers can occur.

Catarial inflammation (Qatar) It develops on mucous membranes and is characterized by the formation of liquid, often transparent exudate with an admixture of a large amount of mucus, the mucous glands are isolated in an increased amount. Exudate contains leukocytes, lymphocytes and lunned epithelial cells and usually as it should flow along the mucous membrane. Such are the catarrhal rhinitis, rhinosinusitis, gastritis, enterocolit. According to the nature of the exudate, that is, on the predominance of certain elements in the exudate, they speak about serous, mucous membrane or purulent cattle. V. The mucous membrane often begins with a serous Qatar, which goes into the mucous, then into purulent.

Causes are very diverse. Microbes, thermal and chemical are important. Irriters and others. Qatars can occur when weakening the protective forces of the body, when saprophyte bacteria, vegetative on mucous membranes, become pathogenic.

Catarial V. may leak acutely and chronically. For acute flow The mucous membrane looks full, swollen, covered with liquid exudate. A sharp serous and mucous Qatar lasts two to three weeks and usually passes without leaving the consequences. With purulent Qatar on the mucous membrane, erosion, ulcers may occur. When HRON, Qatar In some cases, the mucous membrane can remain nobuchish for a long time and becomes thickened, different polyps (hypertrophic Qatar) can appear on it, in other cases - the mucous membrane is highly thinned (atrophic Qatar).

Fibrinous inflammation It is characterized by liquid exudate, in a short time, the fibrinogen is accumulated in a short time, translated when contact with damaged tissues into fibrin, as a result of which the exudate is compacted. The etiology of fibrous V. is diverse: it can be caused by microbes (diphtheria stick, dysenteric microbes, tuberculosis mycobacteria, etc.), viruses, endogenous poisons (eg, at Uremia) and exogenous (eg, Sumle) origin. Fibrinous V. is localized on serous and mucous membranes, less often - in the depths of the organ. Fibrinic V. is usually acute, but in some cases it can take a hron, the flow or flow wavely.

Fig. 12. Truck inflammation of the lung in the stage of gray compelling.

On the surface of the serous shells, fibrin falls in the form of nailed masses, and on the surface of the mucous membranes - in the form of a solid film (color. Fig. 3). In the lumen of the pulmonary alveoli, fibrin falls in the form of fibrinous traffic jams, for example, with a bruboral pneumonia (color. Fig. 7), as a result of which the lung fabric becomes a dense and its consistency resembles a liver (color. Fig. 12).

Serous shells acquire a dim view, they formed a naval bleaching of fibrin, soldered with a serous shell (eg, fibrinous pericarditis - Fig. 2). On the mucous membranes, fibrinous impositions in some cases are located loose, superficially, easily separated, in others - tightly soldered with the subject to cloth, which depends on the depth of damage and on the nature of the epithelium of the mucous membrane. Thus, the relationship of the prismatic epithelium with a weak and fibrin that is subject to fabric, even falling in the depths of the submembraty layer, forms the loose film (eg, on the mucous membrane of the stomach, intestines, trachea, bronchi).

Fig. 10. Difsteritic tonsillitis and bitter tracheitis. The surface of the almonds and the mucous membrane is covered with film overlap.

The flat epithelium is densely connected to the connecting tissue, and the fibrin film is therefore tightly soldered with the mucous membrane, although fibrin and falls in the surface layer of the flat epithelium (between the cells preserved during damage), which is observed, for example, on the mucous membrane of the tonsils, oral cavity, esophagus. Due to these features, fibrinous V. (Chern. Fig. 10) is divided into diphtheritic (tightly seated films) and a brunt (loosely seated films).

Diphestic V. It takes more hard: microbes are multiplied under tightly seated films, highlighting a large amount of toxin; Films can close the respiratory tract, for example, during the diphtheria of the language, which can cause asphyxia. With a brunette, V. Films are easily separated, intoxication is less pronounced, but the danger of blockage respiratory tract Also not excluded.

Fibrinic V. refers to the number of heavy forms in.; Its forecast is largely determined by the localization of the process and the depth of the lesion of the tissue, and the outcome of the fibrinous V. serous and mucous membranes is different. The serous sheaths of the fibrin mass are partially subjected to enzymatic melting, most of the processes of the organization, i.e., the germination of a young connective tissue on the side of the cambial layers of visceral and parietal serous shells, in connection with which the connecting blocks (spikes) are formed, which can be broken The function of the organ.

On the mucous membranes, fibrinous films are usually rejected by autolysis (see), deploying around the focus, and demarcation V. On the site of the rejected film, the defect of the mucous membrane is formed, the depth of the fibrin depth is determined by the depth of the fibrin. The healing of ulcers sometimes happens quickly, but in some cases (especially in the thick intestine with dysentery) is delayed for long time. IN pulmonary alveoli The fibrinous exudate at a favorable flow of trapped pneumonia is subjected to a lithic decay and is solved, in rare cases, the exudate germinates with cells of young connective tissue, the K-paradium gradually matures, and the sclerosis fields occur, which is indicated as the lung carnification.

Purulent inflammation characterized by liquid exudate containing albumin and globulines, and sometimes fibrin yarn; In the sediment - neutrophils, predominantly broken (purulent tales). Such a product V.- Mudny, with a greenish tinge liquid - is called Mouth (see). The etiology of purulent V. Dobinal knowledge: It can be caused by bacteria (staphylococci, streptococci, gonococci, meningococci, less often Salmonella Tifa, tuberculosis mycobacteria, etc.), pathogenic fungi or to be aseptic caused by Chem. substances. Purulent V. may occur in any tissue and organ, serous cavities, in the skin (Fig. 3). It can be sharp and chronic, in some cases very heavy.

Morphologically purulent V. can have two forms - abscess (see) and phlegmon (see) and accompanied by hystolysis (tissue melting). The abscess may occur primary (the cavity is formed as a result of the melting of the tissue), as well as by embolism during septicopemia, for example, the focal purulent V. myocardium with the formation of an abscess (china. Fig. 8).

Acute spilled purulent V. (phlegmon) has an inclination to spread over interfascial layers, interstitial slits (color Fig. 4); Under the phlegmon zel.-Kish. The path in the infiltrate is a lot of eosinophils (color. Fig. 5).

When hron, the form of V. The purulent focus is surrounded by a dense fibrous capsule; In the exudate, along with purulent calves are in a small amount of lymphocytes, macrophages and plasma cells. Periods of exacerbation of V., the formation of a fistula with the expiration of pus. The accumulation of purulent exudate in some utensils of the body is indicated as emphasis (see).

In the outcome of acute purulent V. In favorable cases, the process is occurring, it is possible to heal even large uluses by replacing their cavity with a granulation tissue, gradually maturing into the scar, which remains on the site of abscess. Cron, purulent V. may leak very long and lead to amyloidosis (see). In unfavorable cases, purulent focus is not delivered, the purulent process goes to lymph, vessels and veins, which leads to the generalization of the process, sometimes up to sepsis (see).

Pinged inflammation (gangrenoz, omphorosal) develops due to participation in the form of exudative V. putrid bacteria (pathogenic anaerobov). Pinged V. is a greater danger to the body and can occur in those organs, to-rye contact with environmental (See Gangrena, Ludwig Angina). Inflamed fabrics are subjected to putrid decomposition, acquire a dirty-green color, become flabs, as if they are sprawling with the formation of bad smelling gases (see anaerobic infection).

Hemorrhagic inflammation It is characterized by the presence of different amounts of erythrocytes in the excess. Hemorrhagic character may take any kind of V. (serous, fibrinous, purulent), which depends on the high degree of increasing permeability, up to the destruction of microcirculation vessels. This species V. occurs when exposed to high-voluminous microbes; With the plague, the Siberian ulcer, the toxic influenza, the hemorrhagic focus of V. resembles hemorrhage. Hemorrhagic exudate is observed in serous cavities at malignant tumors. This species V. is a sign of very severe illness; The outcome of it depends on the main disease.

Mixed inflammation forms are observed when weakening the protective forces of the body, the addition of a secondary infection, for example. Staphilococci. In these cases, purulent or fibrinous can be connected to the serous exudate, then B. is called serous-purulent, serous-fibrinous, etc. Mixed nature may have a catarrhal V. Particularly unfavorable prognostic sign is the transformation of serous exudate into hemorrhagic, which always indicates On the attachment of severe infection or progression of a malignant tumor.

Productive inflammation

This form is also called proliferative inflammation, since it is characterized by the predominance of breeding (proliferation) of cell elements of the affected tissue. The alteration and exudation are weakly expressed, recognized with difficulty; Segmented granulocytes are single.

Productive V. may be caused by primary biol., Piz. and chemical. Factors or observed in the transition of acute V. into chronic.

Productive V. flows, as a rule, chronically, but may be sharp, for example, granulomatous V. In the abdominal and rapid tit, with vasculitis various etiology etc.

The basis of the productive V. is the reproduction of young cells of local connecting tissue, as well as cubbial cells of blood capillaries, with differentiation of forming new capillaries. All pronounced cells of V. Cells have both local, histiogenic and hematogenic origin. For example, in the focus of V. You can see large and small lymphocytes, monocytes, as well as in a small amount of eosinophilic and basophils that have occasionally from the current. As cell ripen in the focus of V. remains macrophages, fibroblasts, fibrocytes, lymphoid, single plasma and obese cells. Productive V. How would fibroblasts come true; They secrete tropocalegned - the precursor of collagen fibrous connective tissue, K-paradium remains at the focus of the productive V.

Exodues of productive inflammation are different. May come full resorption of cell infiltrate; However, it is formed more often on the site of infiltrate as a result of the ripening of mesenchymal cells included in the infiltration of mesenchymal cells, connective tissue fibers are formed and rutters occur.

There are two varieties of productive in.: Non-specific and specific. In nonspecific productive V. Proliferating cells are located in inflamed tissue diffuser; Morfol, a specific picture, which caused V. pathogen, not. With a specific productive V. Cellular composition of the exudate, cell grouping and the process cycle are characteristic of the pathogen B. Specific V. Most of the same is characteristic. Infectious granulov - nodules consisting of elements of granulation tissue.

Intermediate inflammationor interstitial, usually has a hron, the flow and is characterized by the fact that the inflammatory infiltration is formed in the surrounding vessels of a stroma of organ (myocardium, liver, kidneys, lungs, transverse muscles, uterus, endocrine glands). The infiltrate consisting of a variety of cells is diffuse, capturing the entire organ, or by individual foci mainly around the vessels (color. Fig. 9). In some cases, a kind of cell type prevails; Sometimes infiltrate consists of lymphocytes and macrophages and reminds V. on an immune basis. In some kinds of intermediate V. accumulates a large number of plasma cells secreting gamma globulins. With the death of plasma cells, the products of their livelihoods remain in the tissues in the form of freely lying fuchsinophilic spherical formations - the so-called. Hyalin balls, or Russevsky Taurus. In the outcome of the intermediate productive V. Developed sclerosis (see) or cirrhosis (see).

The formation of granules (nodules) occurs as a result of the reproduction of cells in the intermediate tissue of the organ under the influence of the pathogenic factor. These nodules may consist of a variety of mesenchymal cells or from one type of cells; Sometimes they are located in close touch With small vessels and even form in the artery wall. The diameter of the granuloma usually does not exceed 1-2 mm, but can reach 2 cm. In the center of the granuloma, sometimes cellular or tissue dedrites are found, in K-ROM, it is sometimes possible to identify the causative agent of the disease, and on the periphery of the Detriton in different ratios are lymphoid macrophages, epithelioid, plasma-plasma And obese cells, among the to-ry, it is possible to detect multi-core giant cells. Usually granulomas are poor capillaries.

The formation in the tissues of the granulul reflects protective and immune processes, which develop in infectious diseases, and to a certain extent determines the dynamics of the immunol, the process from the beginning of the fabric damage to the final stage of the disease, expressing the scarring of the granul.

The formation of the granuloma is observed under a number of acute infectious diseases (abdominal and raw materials, tularemia, viral encephalitis, rabies) and some hron, diseases (rheumatism, brucellosis, mycoses, sarcoidosis, tuberculosis, syphilis, etc.).

In some hron, the infectious diseases of the granuloma are acquired to a certain measure characteristic of the morphol, structure and dynamics of development. In this regard, they are denoted as follows: tuberculosis - with tuberculosis, gum - during syphilis, lepreger - with lepreing, nodules - during the sappa and rhinoscler. With listed diseases V. proceeds specifically, i.e., only this disease is peculiar; In the granulomas of a specific V. Cellular composition is quite similar, the most characteristic epithelioid and multi-core giant cells: Pirogov - Langhanes cells - in tuberculous granuloma; cells, or balls, virghova - in leprine; Mikulich cells - with scler and others.

Fig. 11. Miliary tuberculous lung granulomas.

The specificity of the granulul is determined not only by their morphol, the structure (color. Fig. 6), but also the characteristics of the wedge. flows and pathologan manifestations of V. (china. Fig. 11). In some cases, the granulomas for tuberculosis, syphilis and pumping have so much in structure that without special painting of the pathogen, the diagnosis may be difficult; Therefore, with morphol, the diagnosis of a specific V. is very important to the clinical and anatomical analysis of the disease in general.

For abdominal Tife Granulomas are formed in group lymph, follicles (peyer plaques), in Ileo-cecal lymph, nodes, liver, spleen, bone marrow. They arise from proliferating reticular cells capable of phagocytic typhoid salmonella; These nodule clusters are then subject to necrosis. The process of formation of granuloma, including the formation of a scar, takes 4-5 weeks. (see abdominal typhoid).

Granulomas with rapid tites arise in C. n. s., especially in oblong brain At the olive level, in a close connection with small vessels, the productive and destructive endotromoscalite characteristic of the raped typhoid is observed (see a rapid epidemic title). Granuloma-similar structures, but with a less pronounced lesion of vessels arise in C. n. from. for viral encephalitis and rabies.

In rheumatism, granulomas occur in the connecting tissue of myocardium, heart valves, in the near-hand fabric, in the almond capsule; They are constructed from large with basophilic cytoplasm of a macrophageal type of cells, the accumulation of to-rye is considered as a reaction to the processes of disorganization of the connective tissue (see rheumatism).

With tularemia, granuloma develops in regional lesion lesion lesions, nodes. In the center of the granuloma - the focus of necrosis, on the periphery - shaft from epithelioid and lymphoid cells and a large number of segmented granulocytes; Sometimes there are many-nuclear giant cells (see Tularemia).

With brucellosis granulomas have a different structure. In some cases, in the center of the granuloma and around the circle, there is an accumulation of epithelioid and giant multi-core cells, in others - in the center of the granuloma of necrosis and the periphery epithelioid and giant cells (see brucellosis); Morfol, the picture is very similar to a tuberculous granuloma.

Sarcoidosis is characterized by the formation of a granuloma, built from epithelioid and giant cells without signs of necrosis in the center (see sarcoidosis).

When healing the granulum is formed small, barely noticeable rutters (see Granuloma).

The formation of polyps and poisonous - Productive V. mucous membranes. At the same time, the cells of stroma and prismatic epithelium are growing, polyps of inflammatory origin (hypertrophic Qatar) are formed; Such, for example, polypotic rhinitis, colitis, etc. On the mucous membranes, on the boundary of the prismatic and flat epithelium, for example, in the rear pass, on the genitals, from the growths of the flat epithelium are sharply dingens (see warts). The separated mucous membranes is annoying and macerating a flat epithelium, in the stroma causes a hron. B., K-Roe stimulates to further grow stroma and epithelium (see papilloma, polyp, polyposis).

A favorable course of B. is determined by the perfection of phagocytosis processes, the formation of antibodies, proliferation of connective tissue cells, eliminating the inflammatory hearth. Such an adequate response is characteristic of a healthy organism and is called normergic. However, the development of all components of V., the flow and outcome also depend on the state of the body: from preceding diseases, age, intensity of metabolism, etc.

Wedge, observations show that often the same pathogen in one person does not cause any reaction, and the other is a very stormy local and general reaction, sometimes leading to death.

Described, for example, cases of diphtheria, when in the family, one person died from severe toxic manifestation of the disease, and other family members were either completely ill, or they had an infection in an erased form of illness, although everyone had one source of infection.

It has been established that, depending on the reactivity of the body, V. may be hypergic, arising in a sensitized organism (see allergies), or hypoergic, which is observed in the presence of immunity to agent V.

There is a lot of observations when the picture V. does not correspond to the usual, normgic type and depends not so much on the toxicity of the pathogen, how much from the inadequately strict reaction of the affected organism, which can be caused by preliminary sensitization (see). This type of V. is called allergic inflammation.

In an experiment in animals infected with the diphtheria wand after sensitizing horse serum, the disease occurs very violently and peculiarly compared to nonsense animals. What is different from the normergic course of the disease is associated with the sensitization of the body, it was also noted in the works on anaphylaxis of G. P. Sakharov (1905), according to the tuberculin reaction K. Pirka (1907), in studies on the morphology of allergic reactions A. I. Apricos (1938) and R. Ressla (1935), in the works of Development V. in Ontogenesis H. N. Sirotinin (1940).

Immune inflammation

Research F. Berenet (1962), R. V. Petrova (1968) found that the rate V. may increase or slow down depending on the state of cell and humoral immunity, i.e., with a changed reactivity of the body, V. acquires features that distinguish it From the Nerftergic V. So, the introduction into the body as an antigen of the protein substance leads to the development of increased sensitivity and with a re-introduction of even the insignificant dose of the same substance develops an inadequate total or local response with a clear difference from the normergic reaction - the inconsistency between the low dose of the antigen and very Stormy reaction of the body (see anaphylaxis, artus phenomenon).

Such a reaction is called a hypergic, v.-hyperoergic, or a reaction of an increased sensitivity of an immediate type: it develops in tissue 1-2 hours after re-administering the antigen. The cause of V. with the hypersensitivity of the immediate type is the immune complexes, which consist of an antibody circulating antibody to the antigen introduced earlier, newly introduced into the tissue of the antigen and activated complement. Cocrin (CH. Cochrane, 1963) showed that the immune complexes have a cytopathic and leukotaxic effect: they are fixed in the vessel wall, especially the postcase veul, damage it, increasing permeability and leukeodiapes.

With an allergic V., which occurs by the type of reaction of the hypersensitivity of the immediate type, from the tissues is released so called. Inflammatory protease (rich in sulfhydryl groups), sharply increase the vascular permeability and stimulating emigration of segmented granulocytes. In this type of V. both in the experiment and in human pathology, there is a significant damage to the tissue, a very pronounced reaction of the microcirculatory channel, the abundant emigration of segmented granulocytes, plasma impregnation and fibrinoid necrosis of the walls of small vessels and the surrounding vessels of tissues, swelling, hemorrhage, t. e. A characteristic picture of necrotic V. The immune nature of this is developing. It is confirmed by the detection of immune complexes determined by the Kun method in the focus (see Immunofluorescence).

Electronic microscopic and immunochim. Schirasava studies (H. Schirasawa, 1965) show the following sequence of tissue changes in the heater of Ishiergic V. Immediate type: 1) The formation of immune precipitates (antigen - antibody complexes) in the wing of Vole; 2) Combination with complement; 3) chemotaxic action of precipitates for segmented granulocytes and accumulation of them near veins and capillaries; 4) phagocytosis and digestion of immune complexes segmented granulocytes using lysosomes enzymes; 5) the release of lysosomal enzymes and the formation of vazoactive substances; 6) Damage to the vascular wall with subsequent hemorrhage, edema and necrosis.

Hypergic inflammation, i.e. V., which flows on an immune basis, is observed in patients prone to allergic reactions, naire, during drug intolerance, in acute phase The flow of collagen diseases, with hay fever, etc.

There is another type of enhanced sensitivity of the body - the hypersensitivity of the slow-type type; It is based on the manifestations of not humoral, but cellular immunity. In this case, the local response in the tissues of the sensitized organism occurs after 12 or more hours after the re-administration of the corresponding antigen. Such a reaction is usually observed in the infected tuberculosis mycobacterium of children after the intradermal administration of tuberculin, therefore the reaction of the hypersensitivity of the slow-type type is also called the reaction of tuberculin type. The main role in the focus of this V. owns T-lymphocytes and macrophages. Lymphocytes are representatives of the population of thymus lymphocytes, they migrate from lymphoid organs into blood and back (recycling lymphocytes), as if they find antigen in the tissues and are carried out pathogenic effect on the tissue. Lymphocytes come into contact with rich acid phosphatase by macrophages and, as if mutually informing each other about the nature of the antigen. Changes in the microcirculatory line in the focus of V. At the same time, the type of reaction is expressed very weakly, segmented granulocytes are absent, the signs of V. are expressed indiscriminately. Meanwhile, V., which flows by the type of slower hypersensitivity, is observed under a number of severe autoimmune diseases (in the skin, liver, kidneys, etc.). Having a weakly pronounced wedge, and morphol, dynamics, and ends with sclerosis.

Often histol, the picture at the hron, intermediate V. in humans resembles a delayed type reaction (predominantly in the infiltrate of lymphocytes and macrophages); B. Takes a protracted flow, reflecting autoimmune processes occurring in the body. The same type of V. is observed when forming a granul. In some cases, the granulomas perform the function of macrophages against the antigen, in the other - granuloma, as it would be intended for resorption of tissue decay products in a focus of immune damage (eg, rheumatic granuloma).

B., developing on an immune basis, can manifest itself in mixed formWhen the boundaries between the two types of hypeergic V. are difficult to establish.

Differentiation of inflammation and morphologically similar processes

In the developed form, V. does not represent large difficulties for wedge, and morphol, diagnosis. However, only morphol, the criterion cannot be limited when V. is recognized, especially its individual forms; It is necessary to take into account the whole complex of manifestations, including wedge, data. In the body there are such fabric and vascular cellular reactions, as, for example, with a slow-type hypersensitivity, when it is difficult to detect all signs in the tissues: for example, there is no pronounced reaction of microcirculation vessels, there are no segmented granulocytes or, as it is observed in the wall The stomach in the rug of digestion, a lot of segmented granulocytes as a manifestation of distribution leukocytosis. It is known that under the postpartum involution of the uterus in the glandular organs, you can detect infiltrates from lymphoid cells as an expression of metabolic shifts. The expressed proliferation of plasmoblasts and plasmocytes in immunogenesis (bone marrow, lymph, nodes, spleen, spleen, is not described. watch iron) As an expression of a protective reaction that manifests the production of antibodies. In near the loching tissue, the foci of non-acid surge blood formation, resembling inflammatory infiltration, are described.

Large difficulties arise in the distinction of inflammatory and dystrophic processes, inflammatory proliferation of cells and proliferation of non-inflammatory cells, in particular tumor.

Exodes and inflammation value for the body

Exodes V. Different and depend on the cause, state of the body and structure of the body. The death of vital tissues with the most severe consequences for the body is possible. However, the inflamed tissue is gradually declared from the surrounding healthy tissue, the products of the tissue decay are subjected to enzymatic cleavage and are resubped by phagocytosis, absorbed by the capillaries of the newly formed lymph. network. Due to the cell proliferation, the focus of V. is gradually replaced by a granulation tissue (see). If there was no significant damage to the tissue, there may be a complete recovery. With a significant defect on the site of the focus of V. As a result of ripening of the granulation tissue, the scar is formed (see). In organs and tissues there may remain certain pathol, changes (thickening and spikes of serous shells, overgrowth of serous cavities, scars in organs), violating the function of the rosy organ in difficult cases, sometimes - the whole organism. So, for example, fibrinous effusion on the surface of the serous shells, in the lumen of the alveoli may resolve or, with its significant accumulation, exposed to an organization and a connective tissue transformation. Diffuse intermediate productive V. Usually ends with diffuse sclerosis of the organ (eg, cardiosclerosis). When healing a large number of granuloma, for example, in myocardium during rheumatism, significant fields of cardiosclerosis are formed, which adversely affect the activities of the heart. In cases where the connective tissue has arisen and squeezes the parenchyma, the organ is deformed, which is usually accompanied by a restructuring of its structure and regeneration phenomena (see). Such a process is denoted as cirrhosis of the organ, for example, cirrhosis of the liver, nephrotyrrosis, pneumocyrous.

Inflammation is an important defendant and in the general biological plan, a rather expedient reaction developed in the process of phylogenesis; This reaction was gradually complicated in the process of evolution of living organisms (see the body's protective reactions, adaptive reactions). B. carries protection against the effects of the pathogenic factor in the form of a kind of biol, barrier, which is expressed by the phenomenon of phagocytosis and the production of cellular and humoral immunity. However, this is automatic reaction, it is carried out using self-regulation mechanisms using reflex and humoral influences. As an adaptive reaction, V. under certain conditions, may be acquired sometimes harmful importance for the body: with V. There is damage to tissues, with some shapes up to necrosis.

Due to the inflammatory response, the focus of damage from the entire body, the emigration of white blood cells to the hearth of V. and phagocytosis, the elimination of malicious began. Proliferation of lymphocytes and plasma cells contributes to the production of antibodies and an increase in local and general immunity. At the same time, it is well known that the accumulation of exudate with V. can be very dangerous. So, for example, the exudate in the alveoli at pneumonia already from the very beginning its occurrence has a harmful effect on the body, since gas exchange, education on the mucous membrane of the larynx fibrinous effusion causes a narrowing of the lumen, annoying larynx receptors, which is accompanied by a larynx muscle spasm and May lead to asphyxia (see). Phagocytosis can be unfinished: phagocyte, which absorbed bacteria, but not able to digest it, becomes a carrier of infection by the body.

Violations in V. Not only local; usually arises I. general reaction organism, expressed by fever, leukocytosis, accelerated Roe, change of protein and carbohydrate exchange, the phenomena of general intoxication of the body, which in turn changes the reactivity of the body.

I. I. Mesnikov in 1892 wrote: "... the healing force of nature, the main element of which constitutes inflammatory reactions, is not even a fixture that has reached perfection. Private diseases and cases of premature death are proven enough. " And further: "This imperfection made the necessary active intervention of a person who is dissatisfied with the function of its natural healing force." The imperfection of the "healing force" of nature makes the necessary surgical intervention and the use of therapeutic agents aimed at strengthening the protective and compensatory reactions of the organism and the liquidation of V.

V. underlies many diseases, therefore is one of the most important problems of experimental and wedge, medicine. It is studied at all levels of biol, structures, starting with molecular, subcet, cellular and ending with a holistic organism. Ethiol, factors, biochemical, changes, morphophysiol are investigated. Characteristics, tissue reactivity and body as a whole, Wedge, Painting V. An Special section arose in the development of the problem of V.- Pharmacology V.- Study of the mechanisms of action of mediators V., with the participation of C-rye, various stages of the inflammatory response are implemented; Active anti-inflammatory drugs are sought, which hovering the release of these mediators, which, consequently contributing to the sink V.

Bibliography: ADO A. D. Patophysiology Phagocytov, M., 1961, Bibliogr.; Alekseev O. V. and Chernukh A. M. Neuro-Capillary connections in myocardium rats, Bull. Experiments, biol, and honey., Vol. 74, No. 12, p. 96, 1972, bibliogr.; Alpern D. E. Inflammation (pathogenesis questions), M., 1959, Bibliogr.; Voronin V. V. Inflammation, Tbilisi, 1959, bibliogr.; Inflammation, immunity and hypersensitivity, per. from English, ed. G. 3. Movet, M., 1975; Kongeim I. General pathology, per. with him., Vol. 1, St. Petersburg, 1887; M E N-K INV. Dynamics of inflammation, per. from English, M., 1948, bibliogr.; Mesnikov I. I. Essays of the current state of the question of inflammation, St. Petersburg., 1897; He, lectures on comparative pathology of inflammation, M., 1947; P.S. S. Role gumoral factors peptide and protein nature in the regulation of capillary permeability, Vestn. AMN USSR, № 9, p. 21, 1962; Pigarevsky V. E. Cytochemistry of antibacterial cationic leukocyte proteins with phagocytosis and inflammation, arch. Patol., Vol. 37, No. 9, p. 3, 1975, bibliogr.; Polycar A. Inflammatory reactions and their dynamics, per. with Franz., Novosibirsk, 1969, bibliogr.; Strasov A. I. Controversial issues in the teaching on inflammation, arch. Patol., Vol. 34, No. 10, p. 73, 1972, bibliogr.; Chernukh A. M. Infectious focus of inflammation, M., 1965, Bibliogr.; Chernukh A. M., Aleksandrov P. N. and Alekseev O. V. M! Ikrocyarkul, M., 1975, Bibliogr.; C O T R A N R. S. The Fine Structure of the Microvasculature in Relation to Normal and Alterated Permeability, in the book: Physical Bases of Circulatory Transport, Ed. By E. B. Reeve a. A. C. Guyton, p. 249, Philadelphia-L., 1967, Bibliogr.; H i R S C H J. G. Phagocytosis, Ann. Rev. Microbiol., V. 19, p. 339, 1965, BIBLIOGR.; The Inflammatory Process, ED. By B. W. Zweifach a. o., v. 1 - 3, N. Y .-- L., 1974; Mediators of Inflamation, ED. by G. Weissmann, N. Y., 1974; M I 1 E S A. A. Large Molecular Substances AS Mediators of the Inflammatory Reaction, Ann. N. Y. ACAD. Sci., V. 116, p. 855, 1964; M i 1 ES A. A. a. Wilhelm D. L. Globulins affecting Capillary Permeability, In the book: Polypeptides Which Effect Smooth Muscles a. Blood Vessels, ED. By M. Schach-Ter, p. 309, Oxford a. o., 1960, bibliogr.; Rocha E Silva M. Chemical Mediators of the Acute Inflammatory Reaction, Ann. N. Y. ACAD. Sci., V. 116, p. 899, 1964; Selye H. The Mast Cells, Washington, 1965, Bibliogr.; Spector W. G. Activation of A Globulin System Controlling Capillarry Permeability In Inflammation, J. Path. BACT., V. 74, p. 67, 1957, BIBLIOGR.; He, Substances Which Affect Capillary Permeability, Pharmacol. Rev., v. 10, p. 475, 1958, BIBLIOGR.; Spector W. G. a. Willoughby D. A. THE INFLAMMATORY RESPONCE, BACT. Rev., v. 27, p. 117,1963; They, The Pharmacology of Inflamation, L., 1968; Willoughby D. A. a. Walters M. N. THE EFFECT OF RIBONUCLEIC ACID (RNA) on Vascular Permeability and Its Possible Relation to Lnpf, J. Path. BACT., V. 90, p. 193, 1965.

A. I. Strakov, A. M. Chernukh.

Inflammation I. Inflammatio (Inflammatio)

protective-adaptive local organism On the action of various damaging factors, one of the most frequent forms of the body responding to pathogenic stimuli.

The causes of V. are diverse. It can be caused by various factors: biological (for example, bacteria, viruses), physical (high and low temperature, mechanical, etc.), chemical (for example, the effects of acids, alkalis). Classical signs of V. are: redness, temperature rise, swelling, and function disruption. However, in many cases, only a part of these signs is expressed.

Inflammation begins with alteration (cells and tissues), which is the result of direct action etiological factor. At the same time, a number of changes occurred in the cell that arising in the components of the cytoplasm, the core of the cell and its membrane, to pronounced dystrophic processes and even complete destruction of cells and tissues. Alteration phenomena are observed both in the parenchyma and in stroma. Primary entails the release of biologically active substances (inflammation mediators) in the affected tissues. These substances, differing in origin, chemical nature and action features, play the role of a starting link in the chain of the inflammatory process mechanisms and are responsible for its various components. The release of inflammation mediators may be the immediate result of the damaging effect of pathogenic factors, but to a large extent this mediated process arising under the influence of lysosomal hydrolytic enzymes that are released from lysosomes during the destruction of their membrane. Lizosomes are called the "starting pad of inflammation", because Lizosomal hydrolytic split all types of macromolecules that are part of animal tissues (, nucleic acids, lipids). Under the influence of lysosomal hydrolytic enzymes, a connective tissue frame of microsusuds continues. Inflammation, both cellular and humoral origin, accumulating as V., are increasingly deepening the alteration of tissue. Thus, the most powerful histamine causes the expansion of the micrososcience, an increase in their permeability. It is contained in the granules of labrocytes (fat cells), as well as in basophilas and is released during the granulation of these cells. Another cell mediator - serotonin , Enhances the vascular. Its source are. To cellular mediators V. belongs formed in lymphocytes, prostaglandins, etc. From humoral mediators have the greatest importance (, Callidin), expanding the prokapillary arterioles that increase the permeability of the wall of the capillaries and participating in the formation pain sensations. - A group of neurovoactive polypeptides resulting from a cascade of chemical reactions, the starting mechanism of which is the activation of the XII blood coagulation factor. Lizosomal hydrolytic enzymes can be attributed to mediators. They not only stimulate the formation of other mediators, but also act as mediators, participating in phagocytosis and hemotaxis.

Under the influence of mediators B. The following is formed, the main link of the mechanism of inflammation is a hyperemic reaction (see hyperemia) , Characterized by an increase in vascular permeability and violation of the rheological properties of blood. Vascular reaction with V. is expressed in a sharp expansion of the microvascular bed, primarily the capillaries, both active and passive (see microcirculation) . It is this vascular reaction that determines the first sign of V. - Redness and its features (diffuse, respectableness from neighboring tissues, etc.). In contrast to various types of arterial hyperemia (thermal, reactive, etc.), the expansion of capillaries in V. depends not as much from the inflow of blood in arterial segments, how many from local (primary) mechanisms. The latter refers to the expansion of the prokapillary microscopes under the influence of vasodilative mediators B. and the increase in pressure in them, which causes an increase in the lumen of active capillaries and the opening of the lumen of previously not functioning. This is facilitated by changing the mechanical properties of a loose connective tissue frame of the capillary bed. The diffuse expansion of the capillaries joins the reflex arterial both in the focus of inflammation, and according to its periphery, developing on the axon-reflex mechanism (ie, the reflex, which is carried out on the axon branchings). In this initial period of the inflammatory process (after 2-3 c.after the impact of the damaging factor), due to the increase in the total cross-sectional area of \u200b\u200bthe vascular bed, the intensity of the blood flow increases in the affected area, despite the reduction of its linear velocity. At this stage, the strengthening of blood flow in the field of inflammation determines the second sign V. - Increased local temperature (heat).

Subsequent links of the process are characterized by the appearance of not only chain reactions, but also "vicious circles", in which pathological phenomena followed each other, accompanied by the deepening of their severity. This is seen by the example of such an inherent rheological phenomenon, as erythrocytes (the formation of erythrocyte conglomerates) in microsudes. The slowdown of blood flow creates conditions for aggregation of erythrocytes, and the aggregation of red blood cells, in turn, further reduces the circulation rate.

In B., other changes in rheological properties occur, which ultimately lead to an increase in blood coagulation and thrombosis. Erythrocyte units and thrombots (thrombocyte clots), partially or completely closing the clearance of vessels, serve as one of the main reasons that the slowdown in places goes into the prestance and. The growing phenomena of venous hyperemia and stagnation are gradually joined to arterial hyperemia. The development of venous hyperemia is also associated with the compression of veins and lymphatic vessels (up to lymphostasis) accumulated in the surrounding tissues with inflammatory liquid - Exudate OM . The third sign of V. - swelling depends on the accumulation of exudate in the tissues. With an increase in the volume of tissue, nerve endings occurs, as a result, the fourth sign of V. - pain occurs. It is manifested by the yield of components of blood - water, salts, proteins, as well as uniform elements (emigration) from blood vessels of the tissue. The emigration of leukocytes is due to both purely physical (hemodynamic) and biological patterns. When slowing down the blood flow, the transition of leukocytes from the axial layer of blood elements in the wall (plasma) layer occurs in full compliance with the physical laws of the particles weighted in the current fluid; A decrease in the difference in the speeds of movement in axial and wall layers causes a decrease in the pressure difference between them, and as lighter compared to the erythrocytes, as it were, are discarded to the inner shell of the blood vessel. In places there is a particularly strong slowdown of blood current (the transition of capillaries to Venules), where the bloodstream becomes wider, forming "bay", the regional arrangement of leukocytes goes into the edible standing, they begin to attach to the wall of the blood vessel, which is covered with a flake layer. After that, the leukocytes form thin protoplasmic processes -, with the help of which they penetrate through the inter-hendothelial slots, and then through the basal membrane - beyond the blood vessel. It is possible that there is a transcellorular path of the emigration of leukocytes, i.e. Through the cytoplasm of endothelial cells, emigrated leukocytes in the focus of V. continues to be active (migration), and mainly towards chemical stimuli. They may be products of proteolysis of fabrics or livelihoods of microorganisms. This property of leukocytes move towards certain substances (hemotaxisisisu) I.I. Mechnikov attached the leading importance at all stages of moving leukocytes from the blood in the tissue. In the future, it turned out that when leukocytes passed through a vascular wall played a minor role. In the focus of V. The main leukocytes is to absorb and digest the foreign particles ().

The exudation primarily depends on the increase in the permeability of the microcosuds and an increase in the hydrodynamic blood pressure in them. The increase in the permeability of the micrososcience is associated with the deformation of the normal pathways of permeability through the endothelial wall of the vessels and the appearance of new ones. Due to the expansion of micrososudes and, possibly, the contractual structures (myofibrils) of endothelial cells, the cracks between them increase, forming the so-called small pores, and even channels, or large pores, can appear in the endothelial cell. In addition, the V. is activated by the transfer of substances by microwiecular transport - active "swallowing" endothelial cells of the smallest bubbles and plasma drops (micropinocytosis), their conducts through cells on the opposite direction and pushing out of its limits. The second factor that causes the process of exudation is an increase in blood pressure in the capillary network, it is primarily the result of an increase in the lumen of the prokapillary and larger leading arterial vessels, from which the resistance and consumption of energy (ie, pressure) decrease in them, and therefore remains More "unspent" energy.

In the indispensable link V. is () cells, especially expressed in the final stages of inflammation, when recovery processes are performed on the foreground. Local cambial cells (predecessor cells) are involved in proliferative processes, primarily mesenchymal cells, which give rise to fibroblasts, synthesizing (main part of the scar tissue); Advential, endothelial cells, as well as cells of hematogenic origin - and T-lymphocytes and monocytes are breeding. Part of the cells that make up their phagocytic function, dies, the other is subjected to a number of transformations. For example, monocytes are transformed into histiocytes (macrophages), and macrophages may be a source of epithelioid cells, of which the so-called gigantic single or multi-core cells occur (see the mononuclear phagocite system) .

Depending on the nature of the prevailing local changes, the allestrative, exudative and productive, V. with Alteractive V., are expressed by the phenomena of damage - and necrosis. They are more often observed in parenchymal organs (liver, kidneys, etc.).

Exudative V. is characterized by the predominance of exudation processes. Depending on the nature of the exudate, serous, catarrhal, fibrinous, purulent and hemorrhagic inflammation is distinguished. In serous, V. contains from 3 to 8% serum protein and single leukocytes (serous exudate). Serous V., as a rule, is sharp, localizes more often in serous cavities; Serous exudate is easily absorbed, V. practically does not leave traces. Catarial V. Develops on mucous membranes. Proceeds acute or chronically. Serous or purulent exudate with admixture of mucus is distinguished. Fibrinic V. occurs on serous or mucous membranes; It is usually sharp. Contains a lot of fibrin, which in the form of a film can freely lie on the surface of the mucous membrane or serous shell or be saved with the subject to the surface. Fibrinic V. refers to the number of severe inflammation forms; Its outcome depends on the localization and depth of tissue damage. Purulent V. can develop in any fabric and organ; The course is acute or chronic, can take the form of abscess or phlegmon; The process is accompanied by hystolysis (melting) tissue. Exudate contains mainly leukocytes in a state of decay. When the content in the exudate of a large number of red blood cells, inflammation is called hemorrhagic. It is characterized by a sharp increase in the permeability of blood vessels and even a violation of the integrity of their walls. Any V. may take a character.

Productive (proliferative) V., as a rule, leakschronically : The phenomena of reproduction of cell elements of affected tissues prevail. Frequent outcome is the formation of a scar.

Inflammation depends on the body's immunological reactivity, so it may have a clinically completely different flow and outcome. If the inflammatory response has a normal character, i.e. Such which is observed most often, speak of a normergic V. If the inflammatory process flows sluggishly, acquires a protracted character with a weakly pronounced basic signs of V., it is called hypo-ergic inflammation. In some cases, the damaging agent causes an extremely stormy inflammatory response, inadequate strength and dose. Such V., called hypergic, most characteristic of the state of allergies (allergy) .

Exodus V. is determined by the nature and intensity of the inflammatory agent, the form of the inflammatory process, its localization, dimensions of the affected area and the reactivity of the body (the organism reactivity) . V. is accompanied by the death of cell elements in the event that necrosis covers significant areas, especially in vital organs; The consequences for the body can be the most severe. The focus is selected more often from the surrounding healthy tissue, the products of the tissue decay are subjected to enzymatic cleavage and phagocytic resorption, and the inflammatory focus as a result of cell proliferation is filled with granular tissue. If the area of \u200b\u200bdamage is small, there may be a complete restoration of the previous tissue (see Regeneration) , With a more extensive lesion at the site of the defect is formed.

From the point of view of biological expediency, the inflammatory process has a dual nature. One side. B. - Protective-adaptive reaction developed in the process of evolution. Thanks to her, he is delivering herself from malicious factors located in the focus of V., prevents the process to generalize. This is achieved with the help of various mechanisms. So, venous and lymphatic stagnation and stasis, the occurrence of thromboms prevent the dissemination of the process outside the affected area. In the exudent formed there are components that can bind, fix and destroy bacterial; Phagocytosis is carried out by emigrated leukocytes, the proliferation of lymphocytes and plasma cells contributes to the production of antibodies and an increase in local and general immunity. In the proliferation stage, a protective shaft is formed from granulation tissue. At the same time, V. can have a destructive and life-threatening effect. In the V. Zone, the death of cell elements always occurs. The accumulated exudate can cause enzymatic melting of the tissue, their compression with circulatory impairment and power. Exudate and fabric decay products cause intoxication, metabolic disorders. The inconsistency of V. Value for the body dictates the need to distinguish between the phenomena of a protective nature from the elements of the separation of compensatory mechanisms.

Bibliography: Alpern D.E. Inflammation. (Questions of pathogenesis), M., 1959, Bibliogr.; General man, ed. A.I. Strukov et al., M., 1982; Stops A.I. and Chernukh A.M. Inflammation, BME, 3rd ed., Vol. 4, p. 413, m, 1976; Chernukh A.M. Inflammation, M., 1979, Bibliogr.

II. Inflammatio (Inflammatio)

protective-adaptive reaction of a holistic organism on the action of the pathogenic stimulus, manifested by the development of the tissue damage or the body changes and an increase in vascular permeability in combination with the tissue dystrophy and cell proliferation.

Inflammation of allergic (I. Allergica;. V. hypergic) - V., in which tissues and organs are caused by the formation of an allergen complex with antibodies or sensitized lymphocytes; It is characterized by the sharp and sharp severity of phenomena V., not corresponding to the body caused by the same factor without preliminary sensitization of the body.

Alteractive inflammation (i. Alterativa; Lat. Altero, Alteratum change, do others) - V., characterized by the predominance of dystrophic-necrotic changes of organs and tissues.

Aseptic inflammation (i. Aseptica; Sin. V. Reactive) - V., arising without the participation of microbes.

Gangrenoz inflammation (I. Gangraenosa) - Alteractive V., flowing in the form of gangrenes of tissues and organs; Characteristic, for example, for anaerobic infection.

Hemorrhagic inflammation (I. HaemorRhagica) - Exudative V., in which the exudate contains many erythrocytes.

Inflammation of hypergergic (i. hyperergica) - see the inflammation of allergic.

Inflammation of hypoergic (i. hypoergica) - V., characterized by sluggish and long flow with a predominance, as a rule, alteration and almost full absence cell infiltration and proliferation.

Inflammation of grinding (i. Putrida; Sin. V. Izoroznaya) - V., arising from a pendant infection; It is characterized by decomposition of tissues with the formation of bad smelling gases.

Inflammation purulent (i. Purulenta) - Exudative V., characterized by the formation of purulent exudate and the melting of tissue (cell) elements in the inflammation site; As a rule, it is caused by glorodic microorganisms.

Inflammation of demarcation (Franz. Démarcation distinction; Sin.: V. Defense, V. Protective, V. Limiting) - V., arising at the border of necrosis foci with unchanged fabric sites.

The inflammation is deskvamative (I. Desquamativa) - Alteractive V., characterized by the lunch of the epithelium of the skin, mucous membranes of the gastrointestinal tract or respiratory tract.

Inflammation of defense (i. Defensiva; Lat. Defensio Protection) - see inflammation demarcation.

Diffeter inflammation (i. Diphtherica; Sin. - Constitue) - fibrinous V. mucous membranes, characterized by deep necrosis and impregnation of necrotic fibrin masses, which leads to the formation of difficult films.

Inflammation protective (i. Defensiva) - see inflammation demarcation.

Inflammation of interstitial (i. Interstitialis; Sin. V. Interchnyh) - V. With predominant localization in intermediate fabric, stroma parenchimato organs.

Inflammation of catarrhal-hemorrhagic (I. Catarrhalis HaemorRhagica) - Catarial V., characterized by the presence of erythrocytes in exudate.

Catar and purulent inflammation (i. Catarrhalis Purulenta; Sin.) - Catarial V., characterized by the formation of purulent exudate.

Catarish-desquamative inflammation (I. Catarrhalis Desquamativa) - Catarial V., characterized by massive lunch of the epithelium.

Catarial inflammation (i. Catarrhalis; Sin.) - V. mucous membranes, characterized by the formation of abundant exudate of various nature (serous, mucous, purulent, serous-hemorrhagic, etc.) and its swelling on the surface of the mucous membrane.

Inflammation Cataro-Serous (I. Catarrhalis Serosa; Sin.) - Catarial V., characterized by the formation of serous exudate.

Big inflammation (I. CROUPOSA) - a type of fibrinic V., characterized by shallow necrosis and the impregnation of necrotic masses of fibrin, which leads to the formation of easily separated films.

Intermediate inflammation - See inflammation interstitial.

Inflammation of normergic (i. Normergica) - V., resulting in a pre-sensitized organism and characterized by morphologically and clinically complete correspondence in the intensity of the tissue reaction by the power of pathogenic stimulus.

Inflammation limitating - See inflammation demarcation.

Parenchimato inflammation (I. ParenchyMatosa) - Alteractive V. in a parenchymal organ.

Inflammation of perifocal (i. PeriFocalis) - V., arising in the circumference of the focus of fabric damage or an imagined in a foreign body.

Inflammation productive (i. Productiva; Sin. V. Proliferative) - V., characterized by the predominance of phenomena of the proliferation of cellular elements.

Inflammative productive specific (I. Productiva Specifica) - V.p., in which the proliferation of cell elements occurs with the formation of a granulomatic specific for this disease; It is characteristic of some infectious diseases.

Proliferative inflammation (I. PROLIFERATIVA) - see inflammatory inflammation.

Inflammation of reactive (i. Reactiva) - see the inflammation aseptic.

Inflammation of the face (i. ErySipelatosa) - a kind of alteractively exudative V. Skin, less often mucous membranes, observed during the feeling and characterized by a rapid flow, the formation of subepidermal bubbles,. Flegmons, necrosis sites.

Serous inflammation (i. Serosa) - Exudative V., characterized by the formation of serous exudate in the tissues; It is observed more often in serous cavities.

Inflammation of fibrinous (i. Fibrinosa) - Exudative V. mucous and serous shells, less frequently parenchymal organs, characterized by the formation of a rich fibrin of exudate, which is coagulated to form fibrous masses and fibrin films.

Inflammation of physiological (I. Physiological) is a type of aseptic exudative V., arising in the body in the process of carrying out normal physiological functions (for example, serous-hemorrhagic deskvamative menstrual, leukocyte mucous membranes of the gastrointestinal tract after meals).

Inflammation of phlegmonous (I. Phlegmonosa) is a variety of purulent V., in which purulent exudate spreads between tissue elements, in intermushny layers, subcutaneous tissue, along the vascular-nerve beams, along the tendons and fascia, impregnating and exhausting tissue.

Inflammation of phlegmon-ulcery (I. Phlegmonosa ulcerosa) is a kind of phlegmosny V., characterized by the ulceration of the affected tissues; It is observed mainly in the walls of the gastrointestinal tract.

Exudative inflammation (I. Exsudativa) - V., characterized by the predominance of the education of exudate by the processes of alteration and proliferation.

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First medical care. - M.: Large Russian Encyclopedia. 1994 3. encyclopedic Dictionary Medical terms. - M.: Soviet Encyclopedia. - 1982-1984.

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Inflammation is a complex protective and adaptive response of the body to various harmful effects, manifested by local changes in the affected body and changes in the entire body.

Inflammation is a typical pathological process aimed at eliminating the pathogenic stimulus and restoring damaged tissue. Inflammation carries elements not only pathology, but also physiology.

The development of inflammation is closely associated with the reactivity of the body. Reduced reactivity causes a slowdown and weakening of the development of inflammation (among the elderly, people with reduced food, at avitaminosis, etc.). On the other hand, inflammation affects the state of the reactivity of the entire body, causing a fever, leukocytosis in humans and other changes in reactivity.

Maintenance exterior signs Inflammation on the skin and mucous membranes in humans were described in antiquity of hippocrates: red and a tumor with heat and pain with a function of function.

The development of inflammation in the internal organs is not always accompanied by the indicated signs.

The causes of inflammation can be:

1) physical factors: injuries, burns, frostbite, ionizing radiation, etc.;

2) Chemical factors: acids, alkalis, poisoning substances, technical fluids, etc.;

3) biological factors: Microbes, viruses, immune complexes, etc.

The development of inflammation is determined not only by the impact of these factors, but also the peculiarities of the reactivity of the body.

Inflammation can be expressed by the formation of a microscopic focus or an extensive area, not only focal, but also diffuse character. Sometimes inflammation occurs in the tissue system, then they talk about systemic inflammatory lesions (for example, rheumatic disease, systemic vasculitis, etc.).

3 Inflammation - the pathological process arising in response to the action of various pathogenic factors, characteristic signs of inflammation is: hyperemia, swelling, pain, violation of functions. The reasons: 1. Physical (radiation); 2. Biological (viruses); 3. endogenous; 4. Mechanical (cuts, fractures). The standard stages of the inflammatory process are developing on the cause of inflammation and localization: 1. Alteration (damage); 2. Exudition (vessels and tissue response); 3. Proliferation (recovery). Nature is damage to any factor, the starting mechanism for the development of inflammation. The biologically active substances are released - inflammatory mediators: histamine, sulfur, factors activating platelets.

Excudation process. At first there is a spasm of vessels, then arterial hyperemia, due to the inflow of blood. This is manifested by redness, an increase in temperature. Calculation of cells in the focus of inflammation is called - infiltrate.

Proliferation. This is the final phase in the development of inflammation. The reproduction of cells in the focus of inflammation is manifested.

The nomenclature of inflammatory diseases: Russian IT is added to designate the presence of an inflammatory process to the authority name. (Gastritis, cystitis, bronchitis, hepatitis, pancreatitis).

Forms of inflammatory diseases: Depending on the predominance of one or another stage of the inflammatory process, 3 groups of inflammatory processes are distinguished: 1. Alteractive; 2. Exudative; 3. Proliferative (productive).

Alteractive inflammation - the aggressive component of the inflammatory process prevails (damaging). (hepatitis, myocarditis). These inflammations are more often ending with necrosis. Exudative inflammation - characterized by the yield of liquid blood, proteins, shaped elements of blood beyond the limits of the vascular bed, i.e. Education exudate. 1. Serous inflammation - characterized by the presence in the exudate of albumin (pleura, pericardium, intestines - serous shells). 2. Fibrous inflammation - the presence of fibrinogen in the exisudate

There are 2 forms of fibrous inflammation: 1. Brewing - fibrous masses are easily separated from tissues; 2. Difteric - fibrous masses for the separation form ulcers.

Together with leukocytes in the inflammation zone penetrates a liquid rich in protein. As a result, pus is formed. Structure Pota: leukocytes (living, dead), fat droplets, spree products of affected fabrics.

Causes of purulent inflammations: infection of tissues of glottering m / o (streptococci, staphylacocci).

Views: Abscess - cavity filled with pus. Further, with increasing emigration of leukocytes, there is a melting and a leacuation of tissues, which leads to the formation of the cavity filled with pus. A small abscess breaks outward, and the large is revealed surgically. Phlegmons - Pouring fabrics by gently. Phlegmon can be on: bundles, muscles, tendons, subcutaneous fatty cells. It is treated by injuries of antibiotics or ingestion. Hemorrhagic inflammation - in the exudate in large numbers contained erythrocytes (chopsticks of the plague, Siberian ulcers) abundant allocation mucus (runny nose, throat, but not ODS) proliferative inflammation - this type of inflammation is characterized by chronic inflammatory processes (rheumatism, myocarditis, syphilis, gonorrhea).

If you notice these five signs of inflammation - you urgently need to consult a doctor.

The inflammatory process is a serious pathology that can not be treated independently

From a little age in the office of uncle or aunt in a white coat, a frightened child hears these strange words: rhinitis, sinusitis, or, for example, tormylit. With the age of mysterious diagnoses with the end of "IT" added in the medical card of almost every person. Do you know that all these "its" denote one thing: inflammation of a particular body. The doctor tells jade - it means that the kidneys have witnessed, arthritis - your joint was dry. Absolutely each structure in the human body may be affected by the inflammatory process. And your body early early and actively starts to tell you about it.

Five signs of inflammation were allocated in ancient times, when not only special medical devices for diagnostics did not exist, and did not even go about a simple analysis of blood.

Knowing these five characteristic signs of inflammation, you will also be able to identify your illness without any additional methods:

1. Tumor - swelling

Any inflammatory process in the human body begins with the penetration of provoking agent into it. It can be bacteria, virus, foreign body, chemical or other "provocateur". The body immediately reacts to an unexpected guest, sending its guards to him - leukocyte cells, which are not happy to him and instantly enter the battle. In terms of the accumulation of the exudate, infiltrate is formed. In the inflammatory process, you will definitely see swelling.

2. Rubor - Red

As a result of the death of damaged cells in the body, special substances are released - inflammation mediators. They, first of all, react blood vessels located in the surrounding tissues. To slow down blood flow, they expand, filled with blood and the result of this is the occurrence of redness. In this way, Redness is another characteristic sign of inflammation.

3. Calor - temperature rise

The extension of the vessels is the mandatory component of any inflammatory process also because on the battlefield it is necessary to remove. The influx of blood brings oxygen into place and the necessary building materials, and all decay products - takes. As a result of such active work in the field of inflammation, it becomes very hot. The third mandatory sign of inflammation is to increase the temperature.

4. Dolor - pain

The fact that somewhere in the body is actively fighting the pest, it is necessary to inform the brain, and this is the best way to make any bright and expressive signal. For this, in almost every plot of our body there are special bells - nerve endings. The pain is the best signal for the brain, as a result of which a person understands - in a certain area of \u200b\u200bhis body something happens.

5. FUNCTIO LAESA - function violation

The above signs of inflammation in the amount give another important symptom of this pathological process - violation of the function of the affected structure.In the field of hostilities, life cannot continue in the usual way.Therefore, inflammation is always accompanied by the functional failure of the affected organ. In some cases, this can be very dangerous for the body, for example, in inflammatory processes of heart, kidneys or other vital organs.

If you notice these five signs of inflammation - you urgently need to consult a doctor.

Remember that the inflammatory process is a serious pathology that cannot be treated independently. Consultation of a qualified specialist and the selection of an effective treatment regimen will help your body become a winner in the battle with inflammation.published