The respiratory center not only ensures the rhythmic alternation of inhalation and exhalation, but is also capable of changing the depth and frequency of respiratory movements, thereby adapting pulmonary ventilation to the current needs of the body. Environmental factors, for example the composition and pressure of atmospheric air, ambient temperature, and changes in the state of the body, for example during muscle work, emotional arousal, etc., affecting the metabolic rate, and, consequently, oxygen consumption and carbon dioxide release, affect the functional state of the respiratory center. As a result, the volume of pulmonary ventilation changes.
Like all other processes of automatic regulation of physiological functions, the regulation of breathing is carried out in the body based on the feedback principle. This means that the activity of the respiratory center, which regulates the supply of oxygen to the body and the removal of carbon dioxide formed in it, is determined by the state of the process it regulates. The accumulation of carbon dioxide in the blood, as well as the lack of oxygen, are factors that cause excitation of the respiratory center.
The importance of blood gas composition in the regulation of breathing was shown by Frederick through an experiment with cross-circulation. To do this, two dogs under anesthesia had their carotid arteries and separately jugular veins cut and cross-connected (Figure 2). After this connection and clamping of other neck vessels, the head of the first dog was supplied with blood not from its own body, but from the body of the second dog, the head of the second dog is from the body of the first.
If the trachea of one of these dogs is clamped and thus suffocating the body, then after a while it stops breathing (apnea), while the second dog experiences severe shortness of breath (dyspnea). This is explained by the fact that compression of the trachea in the first dog causes an accumulation of CO 2 in the blood of its body (hypercapnia) and a decrease in oxygen content (hypoxemia). Blood from the first dog's body enters the second dog's head and stimulates its respiratory center. As a result, increased breathing occurs - hyperventilation - in the second dog, which leads to a decrease in CO 2 tension and an increase in O 2 tension in the blood vessels of the body of the second dog. The oxygen-rich, carbon-dioxide-poor blood from this dog's body goes first to the head and causes apnea.
Figure 2 - Scheme of Frederick's cross-circulation experiment
Frederick's experience shows that the activity of the respiratory center changes with changes in the tension of CO 2 and O 2 in the blood. Let's consider the effect on breathing of each of these gases separately.
The importance of carbon dioxide tension in the blood in the regulation of respiration. An increase in carbon dioxide tension in the blood causes excitation of the respiratory center, leading to an increase in ventilation of the lungs, and a decrease in carbon dioxide tension in the blood inhibits the activity of the respiratory center, which leads to a decrease in ventilation of the lungs. The role of carbon dioxide in the regulation of breathing was proven by Holden in experiments in which a person was in a confined space of a small volume. As the oxygen content of the inhaled air decreases and the carbon dioxide content increases, dyspnea begins to develop. If you absorb the released carbon dioxide with soda lime, the oxygen content in the inhaled air can decrease to 12%, and there is no noticeable increase in pulmonary ventilation. Thus, the increase in the volume of ventilation of the lungs in this experiment is due to an increase in the content of carbon dioxide in the inhaled air.
In another series of experiments, Holden determined the volume of ventilation of the lungs and the content of carbon dioxide in the alveolar air when breathing a gas mixture with different contents of carbon dioxide. The results obtained are shown in Table 1.
breathing muscle gas blood
Table 1 - Volume of lung ventilation and carbon dioxide content in alveolar air
The data presented in Table 1 show that simultaneously with an increase in the content of carbon dioxide in the inhaled air, its content in the alveolar air, and therefore in the arterial blood, increases. At the same time, there is an increase in ventilation of the lungs.
The experimental results provided convincing evidence that the state of the respiratory center depends on the carbon dioxide content in the alveolar air. It was revealed that an increase in CO 2 content in the alveoli by 0.2% causes an increase in ventilation of the lungs by 100%.
A decrease in the carbon dioxide content in the alveolar air (and, consequently, a decrease in its tension in the blood) reduces the activity of the respiratory center. This occurs, for example, as a result of artificial hyperventilation, i.e., increased deep and frequent breathing, which leads to a decrease in the partial pressure of CO 2 in the alveolar air and the tension of CO 2 in the blood. As a result, breathing stops. Using this method, i.e., by performing preliminary hyperventilation, you can significantly increase the time of voluntary breath holding. This is what divers do when they need to spend 2...3 minutes under water (the usual duration of voluntary breath-holding is 40...60 seconds).
The direct stimulating effect of carbon dioxide on the respiratory center has been proven through various experiments. Injection of 0.01 ml of a solution containing carbon dioxide or its salt into a certain area of the medulla oblongata causes increased respiratory movements. Euler exposed isolated cat medulla oblongata to carbon dioxide and observed that this caused an increase in the frequency of electrical discharges (action potentials), indicating excitation of the respiratory center.
The respiratory center is influenced increasing the concentration of hydrogen ions. Winterstein in 1911 expressed the view that the excitation of the respiratory center is caused not by carbonic acid itself, but by an increase in the concentration of hydrogen ions due to an increase in its content in the cells of the respiratory center. This opinion is based on the fact that increased respiratory movements are observed when not only carbonic acid, but also other acids, such as lactic acid, are introduced into the arteries supplying the brain. Hyperventilation, which occurs with an increase in the concentration of hydrogen ions in the blood and tissues, promotes the release of part of the carbon dioxide contained in the blood from the body and thereby leads to a decrease in the concentration of hydrogen ions. According to these experiments, the respiratory center is a regulator of the constancy of not only the carbon dioxide tension in the blood, but also the concentration of hydrogen ions.
The facts established by Winterstein were confirmed in experimental studies. At the same time, a number of physiologists insisted that carbonic acid is a specific irritant of the respiratory center and has a stronger stimulating effect on it than other acids. The reason for this turned out to be that carbon dioxide penetrates more easily than the H+ ion through the blood-brain barrier, which separates the blood from the cerebrospinal fluid, which is the immediate environment that bathes the nerve cells, and more easily passes through the membrane of the nerve cells themselves. When CO 2 enters the cell, H 2 CO 3 is formed, which dissociates with the release of H+ ions. The latter are the causative agents of the cells of the respiratory center.
Another reason for the stronger effect of H 2 CO 3 compared to other acids is, according to a number of researchers, that it specifically affects certain biochemical processes in the cell.
The stimulating effect of carbon dioxide on the respiratory center is the basis of one measure that has found application in clinical practice. When the function of the respiratory center is weakened and the resulting insufficient supply of oxygen to the body, the patient is forced to breathe through a mask with a mixture of oxygen and 6% carbon dioxide. This gas mixture is called carbogen.
Mechanism of action of increased CO voltage 2 and increased concentration of H+ ions in the blood during respiration. For a long time it was believed that an increase in carbon dioxide tension and an increase in the concentration of H+ ions in the blood and cerebrospinal fluid (CSF) directly affect the inspiratory neurons of the respiratory center. It has now been established that changes in CO 2 voltage and the concentration of H + ions affect respiration, exciting chemoreceptors located near the respiratory center that are sensitive to the above changes. These chemoreceptors are located in bodies with a diameter of about 2 mm, located symmetrically on both sides of the medulla oblongata on its ventrolateral surface near the exit site of the hypoglossal nerve.
The importance of chemoreceptors in the medulla oblongata can be seen from the following facts. When these chemoreceptors are exposed to carbon dioxide or solutions with an increased concentration of H+ ions, stimulation of respiration is observed. Cooling of one of the chemoreceptor bodies of the medulla oblongata entails, according to Leschke’s experiments, the cessation of respiratory movements on the opposite side of the body. If the chemoreceptor bodies are destroyed or poisoned by novocaine, breathing stops.
Along with With chemoreceptors of the medulla oblongata in the regulation of breathing, an important role belongs to chemoreceptors located in the carotid and aortic bodies. This was proven by Heymans in methodologically complex experiments in which the vessels of two animals were connected so that the carotid sinus and carotid body or the aortic arch and aortic body of one animal were supplied with the blood of another animal. It turned out that an increase in the concentration of H + ions in the blood and an increase in CO 2 voltage cause excitation of carotid and aortic chemoreceptors and a reflex increase in respiratory movements.
There is evidence that 35% of the effect is caused by inhalation of air With high carbon dioxide content are due to the effect on chemoreceptors of an increased concentration of H + ions in the blood, and 65% are the result of an increase in CO 2 voltage. The effect of CO 2 is explained by the rapid diffusion of carbon dioxide through the chemoreceptor membrane and a shift in the concentration of H + ions inside the cell.
Let's consider the effect of lack of oxygen on breathing. Excitation of the inspiratory neurons of the respiratory center occurs not only when the carbon dioxide tension in the blood increases, but also when the oxygen tension decreases.
Reduced oxygen tension in the blood causes a reflex increase in respiratory movements, acting on the chemoreceptors of the vascular reflexogenic zones. Direct evidence that a decrease in oxygen tension in the blood excites the chemoreceptors of the carotid body was obtained by Gaymans, Neal and other physiologists by recording bioelectric potentials in the sinocarotid nerve. Perfusion of the carotid sinus with blood with reduced oxygen tension leads to increased action potentials in this nerve (Figure 3) and increased respiration. After the destruction of chemoreceptors, a decrease in oxygen tension in the blood does not cause changes in respiration.
Figure 3 - Electrical activity of the sinus nerve (according to Neil) A- when breathing atmospheric air; B- when breathing a gas mixture containing 10% oxygen and 90% nitrogen. 1 - recording of electrical activity of the nerve; 2 - recording of two pulse fluctuations in blood pressure. Calibration lines correspond to pressure values of 100 and 150 mmHg. Art.
Recording Electrical Potentials B shows continuous frequent impulses that occur when chemoreceptors are irritated by a lack of oxygen. High-amplitude potentials during periods of pulse increases in blood pressure are caused by impulses of the pressoreceptors of the carotid sinus.
The fact that the irritant of chemoreceptors is a decrease in oxygen tension in the blood plasma, and not a decrease in its total content in the blood, is proven by the following observations of L. L. Shik. When the amount of hemoglobin decreases or when it is bound by carbon monoxide, the oxygen content in the blood is sharply reduced, but the dissolution of O 2 in the blood plasma is not impaired and its tension in the plasma remains normal. In this case, the chemoreceptors are not excited and breathing does not change, although oxygen transport is sharply impaired and the tissues experience a state of oxygen starvation, since not enough oxygen is delivered to them by hemoglobin. When atmospheric pressure decreases, when the oxygen tension in the blood decreases, chemoreceptors are excited and breathing increases.
The nature of changes in breathing with an excess of carbon dioxide and a decrease in oxygen tension in the blood is different. With a slight decrease in oxygen tension in the blood, a reflex increase in the breathing rhythm is observed, and with a slight increase in carbon dioxide tension in the blood, a reflex deepening of respiratory movements occurs.
Thus, the activity of the respiratory center is regulated by the effect of an increased concentration of H+ ions and increased CO 2 tension on the chemoreceptors of the medulla oblongata and on the chemoreceptors of the carotid and aortic bodies, as well as the effect on the chemoreceptors of these vascular reflexogenic zones of decreased oxygen tension in the arterial blood.
Causes of a newborn's first breath are explained by the fact that in the womb, gas exchange of the fetus occurs through the umbilical vessels, which are in close contact with the maternal blood in the placenta. The cessation of this connection with the mother at birth leads to a decrease in oxygen tension and the accumulation of carbon dioxide in the blood of the fetus. This, according to Barcroft, irritates the respiratory center and leads to inhalation.
For the first breath to occur, it is important that the cessation of embryonic respiration occurs suddenly: when the umbilical cord is slowly clamped, the respiratory center is not excited and the fetus dies without taking a single breath.
It should also be taken into account that the transition to new conditions causes irritation of a number of receptors in the newborn and the flow of impulses through the afferent nerves, increasing the excitability of the central nervous system, including the respiratory center (I. A. Arshavsky).
The importance of mechanoreceptors in the regulation of breathing. The respiratory center receives afferent impulses not only from chemoreceptors, but also from pressoreceptors of the vascular reflexogenic zones, as well as from mechanoreceptors of the lungs, respiratory tract and respiratory muscles.
The influence of pressoreceptors of vascular reflexogenic zones is found in the fact that an increase in pressure in the isolated carotid sinus, connected to the body only by nerve fibers, leads to inhibition of respiratory movements. This also happens in the body when blood pressure rises. On the contrary, when blood pressure decreases, breathing becomes faster and deeper.
Impulses coming to the respiratory center via the vagus nerves from the lung receptors are important in the regulation of breathing. The depth of inhalation and exhalation largely depends on them. The presence of reflex influences from the lungs was described in 1868 by Hering and Breuer and formed the basis for the idea of reflex self-regulation of breathing. It manifests itself in the fact that when you inhale, impulses arise in the receptors located in the walls of the alveoli, reflexively inhibiting inhalation and stimulating exhalation, and with a very sharp exhalation, with an extreme degree of decrease in lung volume, impulses arise that arrive to the respiratory center and reflexively stimulate inhalation . The presence of such reflex regulation is evidenced by the following facts:
In the lung tissue in the walls of the alveoli, i.e. in the most extensible part of the lung, there are interoreceptors, which are the perceiving irritations of the endings of the afferent fibers of the vagus nerve;
After cutting the vagus nerves, breathing becomes sharply slower and deeper;
When the lung is inflated with an indifferent gas, for example nitrogen, under the obligatory condition that the vagus nerves are intact, the muscles of the diaphragm and intercostal spaces suddenly stop contracting, and inhalation stops before reaching the usual depth; on the contrary, when air is artificially suctioned from the lung, the diaphragm contracts.
Based on all these facts, the authors came to the conclusion that stretching of the pulmonary alveoli during inspiration causes irritation of the lung receptors, as a result of which the impulses coming to the respiratory center through the pulmonary branches of the vagus nerves become more frequent, and this reflexively excites the expiratory neurons of the respiratory center, and, consequently, entails the occurrence of exhalation. Thus, as Hering and Breuer wrote, “every breath, as it stretches the lungs, itself prepares its end.”
If you connect the peripheral ends of the cut vagus nerves to an oscilloscope, you can record action potentials that arise in the receptors of the lungs and travel along the vagus nerves to the central nervous system not only when the lungs are inflated, but also when air is artificially suctioned from them. During natural breathing, frequent currents of action in the vagus nerve are detected only during inhalation; during natural exhalation they are not observed (Figure 4).
Figure 4 - Currents of action in the vagus nerve during stretching of the lung tissue during inhalation (according to Adrian) From top to bottom: 1 - afferent impulses in the vagus nerve: 2 - recording of breathing (inhalation - up, exhalation - down); 3 - timestamp
Consequently, the collapse of the lungs causes reflex irritation of the respiratory center only with such strong compression of them, which does not happen during normal, ordinary exhalation. This is observed only with a very deep exhalation or sudden bilateral pneumothorax, to which the diaphragm reflexively reacts by contracting. During natural breathing, the receptors of the vagus nerves are stimulated only when the lungs are stretched and reflexively stimulate exhalation.
In addition to the mechanoreceptors of the lungs, mechanoreceptors of the intercostal muscles and the diaphragm take part in the regulation of breathing. They are excited by stretching during exhalation and reflexively stimulate inhalation (S.I. Frankstein).
Relationships between inspiratory and expiratory neurons of the respiratory center. There are complex reciprocal (conjugate) relationships between inspiratory and expiratory neurons. This means that excitation of inspiratory neurons inhibits expiratory ones, and excitation of expiratory neurons inhibits inspiratory ones. Such phenomena are partly due to the presence of direct connections that exist between the neurons of the respiratory center, but mainly they depend on reflex influences and on the functioning of the pneumotaxis center.
The interaction between neurons of the respiratory center is currently represented as follows. Due to the reflex (through chemoreceptors) action of carbon dioxide on the respiratory center, excitation of inspiratory neurons occurs, which is transmitted to the motor neurons innervating the respiratory muscles, causing the act of inhalation. At the same time, impulses from the inspiratory neurons arrive at the pneumotaxis center located in the pons, and from it, through the processes of its neurons, impulses arrive at the expiratory neurons of the respiratory center of the medulla oblongata, causing excitation of these neurons, cessation of inhalation and stimulation of exhalation. In addition, excitation of expiratory neurons during inhalation is also carried out reflexively through the Hering-Breuer reflex. After transection of the vagus nerves, the flow of impulses from the mechanoreceptors of the lungs stops and expiratory neurons can be excited only by impulses coming from the pneumotaxis center. The impulse stimulating the exhalation center is significantly reduced and its stimulation is somewhat delayed. Therefore, after cutting the vagus nerves, inhalation lasts much longer and is replaced by exhalation later than before cutting the nerves. Breathing becomes rare and deep.
Similar changes in breathing with intact vagus nerves occur after transection of the brainstem at the level of the pons, separating the pneumotaxis center from the medulla oblongata (see Figure 1, Figure 5). After such a transection, the flow of impulses stimulating the exhalation center also decreases, and breathing becomes rare and deep. In this case, the exhalation center is excited only by impulses reaching it via the vagus nerves. If in such an animal the vagus nerves are also transected or the propagation of impulses along these nerves is interrupted by cooling them, then excitation of the exhalation center does not occur and breathing stops in the phase of maximum inspiration. If after this the conductivity of the vagus nerves is restored by warming them, then excitation of the exhalation center periodically occurs again and rhythmic breathing is restored (Figure 6).
Figure 5 - Diagram of nerve connections of the respiratory center 1 - inspiratory center; 2 - pneumotaxis center; 3 - expiratory center; 4 - mechanoreceptors of the lung. After moving along the lines / and // separately, the rhythmic activity of the respiratory center is preserved. With simultaneous cutting, breathing stops during the inhalation phase.
Thus, the vital function of breathing, possible only with the rhythmic alternation of inhalation and exhalation, is regulated by a complex nervous mechanism. When studying it, attention is drawn to the multiple support for the operation of this mechanism. Excitation of the inspiratory center occurs both under the influence of an increase in the concentration of hydrogen ions (increased CO 2 tension) in the blood, causing excitation of the chemoreceptors of the medulla oblongata and chemoreceptors of the vascular reflexogenic zones, and as a result of the influence of reduced oxygen tension on the aortic and carotid chemoreceptors. Excitation of the exhalation center is due to both reflex impulses coming to it via the afferent fibers of the vagus nerves, and the influence of the inhalation center through the pneumotaxis center.
The excitability of the respiratory center changes under the action of nerve impulses arriving along the cervical sympathetic nerve. Irritation of this nerve increases the excitability of the respiratory center, which intensifies and speeds up breathing.
The influence of sympathetic nerves on the respiratory center partly explains changes in breathing during emotions.
Figure 6 - The effect of turning off the vagus nerves on breathing after cutting the brain at the level between the lines I and II(see Figure 5) (by Stella) A- recording of breathing; b- nerve cooling mark
1) oxygen
3) carbon dioxide
5) adrenaline
307. Central chemoreceptors involved in the regulation of respiration are localized
1) in the spinal cord
2) in the pons
3) in the cerebral cortex
4) in the medulla oblongata
308. Peripheral chemoreceptors involved in the regulation of respiration are mainly localized
1) in the organ of Corti, aortic arch, carotid sinus
2) in the capillary bed, aortic arch
3) in the aortic arch, carotid sinus
309. Hyperpnea after voluntary breath holding occurs as a result
1) reducing CO2 tension in the blood
2) decrease in O2 tension in the blood
3) an increase in O2 tension in the blood
4) an increase in CO2 tension in the blood
310. Physiological significance of the Hering-Breuer reflex
1) in stopping inhalation during protective respiratory reflexes
2) in an increase in respiratory rate with increasing body temperature
3) in regulating the ratio of depth and frequency of breathing depending on lung volume
311. Contractions of the respiratory muscles stop completely
1) when separating the pons from the medulla oblongata
2) with bilateral transection of the vagus nerves
3) when the brain is separated from the spinal cord at the level of the lower cervical segments
4) when the brain is separated from the spinal cord at the level of the upper cervical segments
312. The cessation of inhalation and the beginning of exhalation is due primarily to the influence of receptors
1) chemoreceptors of the medulla oblongata
2) chemoreceptors of the aortic arch and carotid sinus
3) irritant
4) juxtacapillary
5) stretched lungs
313. Dyspnea (shortness of breath) occurs
1) when inhaling gas mixtures with a high (6%) carbon dioxide content
2) weakening of breathing and stopping it
3) insufficiency or difficulty breathing (heavy muscular work, pathology of the respiratory system).
314. Gas homeostasis in high altitude conditions is maintained due to
1) decreased oxygen capacity of the blood
2) decrease in heart rate
3) decrease in breathing rate
4) increase in the number of red blood cells
315. Normal inhalation is ensured by contraction
1) internal intercostal muscles and diaphragm
2) internal and external intercostal muscles
3) external intercostal muscles and diaphragm
316. Contractions of the respiratory muscles completely stop after transection of the spinal cord at the level
1) lower cervical segments
2) lower thoracic segments
3) upper cervical segments
317. Increased activity of the respiratory center and increased ventilation of the lungs causes
1) hypocapnia
2) normocapnia
3) hypoxemia
4) hypoxia
5) hypercapnia
318. An increase in pulmonary ventilation, which is usually observed when rising to a height of more than 3 km, leads to
1) to hyperoxia
2) to hypoxemia
3) to hypoxia
4) to hypercapnia
5) to hypocapnia
319. The receptor apparatus of the carotid sinus controls the gas composition
1) cerebrospinal fluid
2) arterial blood entering the systemic circulation
3) arterial blood entering the brain
320. The gas composition of the blood entering the brain controls the receptors
1) bulbar
2) aortic
3) carotid sinuses
321. The gas composition of the blood entering the systemic circulation controls the receptors
1) bulbar
2) carotid sinuses
3) aortic
322. Peripheral chemoreceptors of the carotid sinus and aortic arch are sensitive, mainly
1) to an increase in O2 and CO2 voltage, a decrease in blood pH
2) to an increase in O2 voltage, a decrease in CO2 voltage, an increase in blood pH
3) decreasing O2 and Co2 tension, increasing blood pH
4) decrease in O2 voltage, increase in CO2 voltage, decrease in blood pH
DIGESTION
323. What components of food and products of its digestion enhance intestinal motility?(3)
· Black bread
· White bread
324. What is the main role of gastrin:
Activates pancreatic enzymes
Converts pepsinogen to pepsin in the stomach
Stimulates the secretion of gastric juice
· Inhibits pancreatic secretion
325. What is the reaction of saliva and gastric juice during the digestion phase:
· pH of saliva 0.8-1.5, pH of gastric juice 7.4-8.
saliva pH 7.4-8.0, gastric juice pH 7.1-8.2
Saliva pH 5.7-7.4, gastric juice pH 0.8-1.5
saliva pH 7.1-8.2, gastric juice pH 7.4-8.0
326. The role of secretin in the digestion process:
· Stimulates the secretion of HCI.
· Inhibits bile secretion
Stimulates the secretion of pancreatic juice
327. How do the following substances affect the motility of the small intestine?
Adrenaline enhances, acetylcholine inhibits
Adrenaline inhibits, acetylcholine enhances
Adrenaline has no effect, acetylcholine enhances
Adrenaline inhibits, acetylcholine has no effect
328. Fill in the missing words, choosing the most correct answers.
Stimulation of parasympathetic nerves....................... the amount of saliva secretion with ………………………… concentration of organic compounds.
Increases, low
· Reduces, high
· Increases, high.
· Reduces, low
329. Under the influence of what factor do insoluble fatty acids turn into soluble fatty acids in the digestive tract:
Under the influence of pancreatic juice lipase
Under the influence of gastric juice lipase
Under the influence of bile acids
Under the influence of hydrochloric acid of gastric juice
330. What causes swelling of proteins in the digestive tract:
Bicarbonates
Hydrochloric acid
· Intestinal juice
331. Name which of the substances listed below are natural endogenous stimulants of gastric secretion. Choose the most correct answer:
Histamine, gastrin, secretin
Histamine, gastrin, enterogastrin
Histamine, hydrochloric acid, enterokinase
· Gastrin, hydrochloric acid, secretin
11. Will glucose be absorbed in the intestine if its concentration in the blood is 100 mg%, and in the intestinal lumen is 20 mg%:
· Will not
12. How will intestinal motor function change if atropine is administered to a dog:
· Bowel motor function will not change
There is a weakening of intestinal motor function
There is an increase in intestinal motor function
13. What substance, when introduced into the blood, causes inhibition of the secretion of hydrochloric acid in the stomach:
Gastrin
· Histamine
· Secretin
Products of protein digestion
14. Which of the following substances enhances the movement of intestinal villi:
· Histamine
· Adrenaline
· Willikinin
· Secretin
15. Which of the following substances enhances gastric motility:
Gastrin
Enterogastron
Cholecystokinin-pancreozymin
16. Select from the substances listed below the hormones that are produced in the duodenum:
· Secretin, thyroxine, villikinin, gastrin
· Secretin, enterogastrin, villikinin, cholecystokinin
· Secretin, enterogastrin, glucagon, histamine
17. Which option comprehensively and correctly lists the functions of the gastrointestinal tract?
Motor, secretory, excretory, absorption
Motor, secretory, absorption, excretory, endocrine
Motor, secretory, absorption, endocrine
18. Gastric juice contains enzymes:
· Peptidases
Lipase, peptidases, amylase
· Proteases, lipase
· Proteases
19. An involuntary act of defecation is carried out with the participation of a center located:
In the medulla oblongata
In the thoracic spinal cord
In the lumbosacral spinal cord
In the hypothalamus
20. Choose the most correct answer.
Pancreatic juice contains:
Lipase, peptidase
Lipase, peptidase, nuclease
Lipase, peptidase, protease, amylase, nuclease, elastase
Elastase, nuclease, peptidase
21. Choose the most correct answer.
Sympathetic nervous system:
· Inhibits gastrointestinal motility
· Inhibits secretion and motility of the gastrointestinal tract
· Inhibits gastrointestinal secretion
· Activates motility and secretion of the gastrointestinal tract
· Activates gastrointestinal motility
23. The flow of bile into the duodenum is limited. It will lead to:
Impaired protein breakdown
Impaired carbohydrate breakdown
To inhibition of intestinal motility
· Impaired fat breakdown
25. The centers of hunger and satiety are located:
· In the cerebellum
In the thalamus
In the hypothalamus
29. Gastrin is formed in the mucous membrane:
Body and fundus of the stomach
· Antrum
Greater curvature
30. Gastrin stimulates mainly:
Main cells
· Mucous cells
Parietal cells
33. Motility of the gastrointestinal tract is stimulated by:
Parasympathetic nervous system
Sympathetic nervous system
Respiratory system. Breath.
Choose one correct answer:
A) does not change B) narrows C) expands
2.
Number of cell layers in the wall of the pulmonary vesicle:
A) 1 B) 2 C) 3 D) 4
3.
Shape of the diaphragm during contraction:
A) flat B) domed C) elongated D) concave
4.
The respiratory center is located in:
A) medulla oblongata B) cerebellum C) diencephalon D) cerebral cortex
5.
Substance that causes activity of the respiratory center:
A) oxygen B) carbon dioxide C) glucose D) hemoglobin
6.
A section of the tracheal wall that lacks cartilage:
A) front wall B) side walls C) rear wall
7.
The epiglottis closes the entrance to the larynx:
A) during a conversation B) when inhaling C) when exhaling D) when swallowing
8.
How much oxygen is contained in exhaled air?
A) 10% B) 14% C) 16% D) 21%
9.
An organ that does not participate in the formation of the wall of the chest cavity:
A) ribs B) sternum C) diaphragm D) pericardial sac
10.
Organ that does not line the pleura:
A) trachea B) lung C) sternum D) diaphragm E) ribs
11.
The Eustachian tube opens at:
A) nasal cavity B) nasopharynx C) pharynx D) larynx
12.
The pressure in the lungs is greater than the pressure in the pleural cavity:
A) when inhaling B) when exhaling C) in any phase D) when holding your breath while inhaling
14.
The walls of the larynx are formed:
A) cartilage B) bones C) ligaments D) smooth muscles
15.
How much oxygen is contained in the air of the lung vesicles?
A) 10% B) 14% C) 16% D) 21%
16.
The amount of air that enters the lungs during a quiet inhalation:
A) 100-200 cm 3 B) 300-900 cm 3 C) 1000-1100 cm 3 D) 1200-1300 cm 3
17.
The membrane that covers the outside of each lung:
A) fascia B) pleura C) capsule D) basement membrane
18.
During swallowing occurs:
A) inhale B) exhale C) inhale and exhale D) hold your breath
19
. Amount of carbon dioxide in atmospheric air:
A) 0.03% B) 1% C) 4% D) 6%
20. Sound is formed when:
A) inhale B) exhale C) hold your breath while inhaling D) hold your breath while exhaling
21.
Does not take part in the formation of speech sounds:
A) trachea B) nasopharynx C) pharynx D) mouth E) nose
22.
The wall of the pulmonary vesicles is formed by tissue:
A) connective B) epithelial C) smooth muscle D) striated muscle
23.
Shape of the diaphragm when relaxed:
A) flat B) elongated C) dome-shaped D) concave into the abdominal cavity
24.
Amount of carbon dioxide in exhaled air:
A) 0.03% B) 1% C) 4% D) 6%
25.
Airway epithelial cells contain:
A) flagella B) villi C) pseudopods D) cilia
26
. The amount of carbon dioxide in the air of the pulmonary bubbles:
A) 0.03% B) 1% C) 4% D) 6%
28.
With an increase in chest volume, pressure in the alveoli:
A) does not change B) decreases C) increases
29
. Amount of nitrogen in atmospheric air:
A) 54% B) 68% C) 79% D) 87%
30.
Outside the chest is located:
A) trachea B) esophagus C) heart D) thymus (thymus gland) E) stomach
31.
The most frequent respiratory movements are characteristic of:
A) newborns B) children 2-3 years old C) teenagers D) adults
32. Oxygen moves from the alveoli to the blood plasma when:
A) pinocytosis B) diffusion C) respiration D) ventilation
33
. Number of breathing movements per minute:
A) 10-12 B) 16-18 C) 2022 D) 24-26
34
. A diver develops gas bubbles in his blood (the cause of decompression sickness) when:
A) slow rise from depth to the surface B) slow descent to depth
C) rapid ascent from depth to the surface D) rapid descent to depth
35.
Which laryngeal cartilage protrudes forward in men?
A) epiglottis B) arytenoid C) cricoid D) thyroid
36.
The causative agent of tuberculosis belongs to:
A) bacteria B) fungi C) viruses D) protozoa
37.
Total surface of the pulmonary vesicles:
A) 1 m 2 B) 10 m 2 C) 100 m 2 D) 1000 m 2
38.
The concentration of carbon dioxide at which poisoning begins in a person:
39
. The diaphragm first appeared in:
A) amphibians B) reptiles C) mammals D) primates E) humans
40. The concentration of carbon dioxide at which a person experiences loss of consciousness and death:
A) 1% B) 2-3% C) 4-5% D) 10-12%
41.
Cellular respiration occurs in:
A) nucleus B) endoplasmic reticulum C) ribosome D) mitochondria
42.
The amount of air for an untrained person during a deep breath:
A) 800-900 cm 3 B) 1500-2000 cm 3 C) 3000-4000 cm 3 D) 6000 cm 3
43.
The phase when the lung pressure is above atmospheric:
A) inhale B) exhale C) inhale hold D) exhale hold
44.
Pressure that begins to change during breathing earlier:
A) in the alveoli B) in the pleural cavity C) in the nasal cavity D) in the bronchi
45.
A process that requires the participation of oxygen:
A) glycolysis B) protein synthesis C) fat hydrolysis D) cellular respiration
46.
The airways do not include the organ:
A) nasopharynx B) larynx C) bronchi D) trachea E) lungs
47 . Does not apply to the lower respiratory tract:
A) larynx B) nasopharynx C) bronchi D) trachea
48.
The causative agent of diphtheria is classified as:
A) bacteria B) viruses C) protozoa D) fungi
49. Which component of exhaled air is found in greater quantities?
A) carbon dioxide B) oxygen C) ammonia D) nitrogen E) water vapor
50.
The bone in which the maxillary sinus is located?
A) frontal B) temporal C) maxillary D) nasal
Answers: 1b, 2a, 3a, 4a, 5b, 6c, 7d, 8c, 9d, 10a, 11b, 12c, 13c, 14a, 15b, 16b, 17b, 18d, 19a, 20b, 21a, 22b, 23c, 24c, 25g, 26g, 27c, 28b, 29c, 30g, 31a, 32b, 33b, 34c, 35g, 36a, 37c, 38c, 39c, 40g, 41g, 42c, 43b, 44a, 45g, 46d, 47b, 48a, 49g , 50v
The main function of the respiratory system is to ensure gas exchange of oxygen and carbon dioxide between the environment and the body in accordance with its metabolic needs. In general, this function is regulated by a network of numerous CNS neurons that are connected to the respiratory center of the medulla oblongata.
Under respiratory center understand a set of neurons located in different parts of the central nervous system, ensuring coordinated muscle activity and adaptation of breathing to the conditions of the external and internal environment. In 1825, P. Flourens identified a “vital node” in the central nervous system, N.A. Mislavsky (1885) discovered the inspiratory and expiratory parts, and later F.V. Ovsyannikov described the respiratory center.
The respiratory center is a paired formation consisting of an inhalation center (inspiratory) and an exhalation center (expiratory). Each center regulates the breathing of the same side: when the respiratory center on one side is destroyed, respiratory movements on that side cease.
Expiratory department - part of the respiratory center that regulates the process of exhalation (its neurons are located in the ventral nucleus of the medulla oblongata).
Inspiratory department- part of the respiratory center that regulates the process of inhalation (localized mainly in the dorsal part of the medulla oblongata).
The neurons of the upper part of the pons, regulating the act of breathing, were called pneumotaxic center. In Fig. Figure 1 shows the location of the neurons of the respiratory center in various parts of the central nervous system. The inhalation center is automatic and in good shape. The exhalation center is regulated from the inhalation center through the pneumotaxic center.
Pneumotaxic complex- part of the respiratory center, located in the area of the pons and regulating inhalation and exhalation (during inhalation it causes excitation of the exhalation center).
Rice. 1. Localization of respiratory centers in the lower part of the brain stem (posterior view):
PN - pneumotaxic center; INSP - inspiratory; ZKSP - expiratory. The centers are double-sided, but to simplify the diagram, only one is shown on each side. Transection along line 1 does not affect breathing, along line 2 the pneumotaxic center is separated, below line 3 respiratory arrest occurs
In the structures of the bridge, two respiratory centers are also distinguished. One of them - pneumotaxic - promotes a change from inhalation to exhalation (by switching excitation from the center of inspiration to the center of exhalation); the second center exerts a tonic effect on the respiratory center of the medulla oblongata.
The expiratory and inspiratory centers are in a reciprocal relationship. Under the influence of the spontaneous activity of the neurons of the inspiratory center, the act of inhalation occurs, during which mechanoreceptors are excited when the lungs are stretched. Impulses from mechanoreceptors travel through the afferent neurons of the excitatory nerve to the inspiratory center and cause excitation of the expiratory center and inhibition of the inspiratory center. This ensures a change from inhalation to exhalation.
In the change from inhalation to exhalation, the pneumotaxic center is of significant importance, which exerts its influence through the neurons of the expiratory center (Fig. 2).
Rice. 2. Scheme of nerve connections of the respiratory center:
1 - inspiratory center; 2 — pneumotaxic center; 3 - expiratory center; 4 - mechanoreceptors of the lung
At the moment of excitation of the inspiratory center of the medulla oblongata, excitation simultaneously occurs in the inspiratory section of the pneumotaxic center. From the latter, along the processes of its neurons, impulses come to the expiratory center of the medulla oblongata, causing its excitation and, by induction, inhibition of the inspiratory center, which leads to a change in inhalation to exhalation.
Thus, the regulation of breathing (Fig. 3) is carried out thanks to the coordinated activity of all parts of the central nervous system, united by the concept of the respiratory center. The degree of activity and interaction of the parts of the respiratory center is influenced by various humoral and reflex factors.
Vehicle respiratory center
The ability of the respiratory center to be automatic was first discovered by I.M. Sechenov (1882) in experiments on frogs under conditions of complete deafferentation of animals. In these experiments, despite the fact that afferent impulses did not enter the central nervous system, potential fluctuations were recorded in the respiratory center of the medulla oblongata.
The automaticity of the respiratory center is evidenced by Heymans' experiment with an isolated dog's head. Her brain was cut at the level of the pons and deprived of various afferent influences (the glossopharyngeal, lingual and trigeminal nerves were cut). Under these conditions, the respiratory center did not receive impulses not only from the lungs and respiratory muscles (due to the preliminary separation of the head), but also from the upper respiratory tract (due to the transection of these nerves). Nevertheless, the animal retained rhythmic movements of the larynx. This fact can only be explained by the presence of rhythmic activity of the neurons of the respiratory center.
The automation of the respiratory center is maintained and changed under the influence of impulses from the respiratory muscles, vascular reflexogenic zones, various intero- and exteroceptors, as well as under the influence of many humoral factors (blood pH, carbon dioxide and oxygen content in the blood, etc.).
The influence of carbon dioxide on the state of the respiratory center
The effect of carbon dioxide on the activity of the respiratory center is especially clearly demonstrated in Frederick's experiment with cross-circulation. In two dogs, the carotid arteries and jugular veins are cut and connected crosswise: the peripheral end of the carotid artery is connected to the central end of the same vessel of the second dog. The jugular veins are also cross-connected: the central end of the jugular vein of the first dog is connected to the peripheral end of the jugular vein of the second dog. As a result, blood from the first dog's body goes to the second dog's head, and blood from the second dog's body goes to the first dog's head. All other vessels are ligated.
After such an operation, the trachea was clamped (suffocated) in the first dog. This led to the fact that after some time an increase in the depth and frequency of breathing was observed in the second dog (hyperpnea), while the first dog experienced respiratory arrest (apnea). This is explained by the fact that in the first dog, as a result of compression of the trachea, there was no exchange of gases, and the content of carbon dioxide in the blood increased (hypercapnia occurred) and the oxygen content decreased. This blood flowed to the head of the second dog and influenced the cells of the respiratory center, resulting in hyperpnea. But in the process of enhanced ventilation of the lungs, the content of carbon dioxide in the blood of the second dog decreased (hypocapnia) and the oxygen content increased. Blood with a reduced carbon dioxide content entered the cells of the respiratory center of the first dog, and the irritation of the latter decreased, leading to apnea.
Thus, an increase in the content of carbon dioxide in the blood leads to an increase in the depth and frequency of breathing, and a decrease in the content of carbon dioxide and an increase in oxygen leads to a decrease in it until breathing stops. In those observations when the first dog was allowed to breathe various gas mixtures, the greatest change in breathing was observed with an increase in the carbon dioxide content in the blood.
Dependence of the activity of the respiratory center on the gas composition of the blood
The activity of the respiratory center, which determines the frequency and depth of breathing, depends primarily on the tension of gases dissolved in the blood and the concentration of hydrogen ions in it. The leading importance in determining the amount of ventilation of the lungs is the tension of carbon dioxide in the arterial blood: it, as it were, creates a request for the required amount of ventilation of the alveoli.
To denote increased, normal and decreased carbon dioxide tension in the blood, the terms “hypercapnia”, “normocapnia” and “hypocapnia” are used, respectively. The normal oxygen content is called normoxia, lack of oxygen in the body and tissues - hypoxia, in blood - hypoxemia. There is an increase in oxygen tension hyperxia. A condition in which hypercapnia and hypoxia exist simultaneously is called asphyxia.
Normal breathing at rest is called eipnea. Hypercapnia, as well as a decrease in blood pH (acidosis) are accompanied by an involuntary increase in pulmonary ventilation - hyperpnea, aimed at removing excess carbon dioxide from the body. Ventilation of the lungs increases mainly due to the depth of breathing (increasing tidal volume), but at the same time the breathing frequency also increases.
Hypocapnia and an increase in blood pH levels lead to a decrease in ventilation, and then to respiratory arrest - apnea.
The development of hypoxia initially causes moderate hyperpnea (mainly as a result of an increase in respiratory rate), which, with an increase in the degree of hypoxia, is replaced by a weakening of breathing and its cessation. Apnea due to hypoxia is deadly. Its cause is a weakening of oxidative processes in the brain, including in the neurons of the respiratory center. Hypoxic apnea is preceded by loss of consciousness.
Hypercainia can be caused by inhaling gas mixtures with carbon dioxide content increased to 6%. The activity of the human respiratory center is under voluntary control. Voluntary holding of breath for 30-60 s causes asphyxial changes in the gas composition of the blood; after the cessation of the delay, hyperpnea is observed. Hypocapnia is easily caused by voluntary increased breathing, as well as excessive artificial ventilation (hyperventilation). In a awake person, even after significant hyperventilation, respiratory arrest usually does not occur due to the control of breathing by the anterior parts of the brain. Hypocapnia is compensated gradually over several minutes.
Hypoxia is observed when rising to a height due to a decrease in atmospheric pressure, during extremely hard physical work, as well as when breathing, circulation and blood composition are impaired.
During severe asphyxia, breathing becomes as deep as possible, auxiliary respiratory muscles take part in it, and an unpleasant feeling of suffocation occurs. This kind of breathing is called dyspnea.
In general, maintaining a normal blood gas composition is based on the principle of negative feedback. Thus, hypercapnia causes an increase in the activity of the respiratory center and an increase in ventilation of the lungs, and hypocapnia causes a weakening of the activity of the respiratory center and a decrease in ventilation.
Reflex effects on breathing from vascular reflexogenic zones
Breathing responds especially quickly to various irritations. It quickly changes under the influence of impulses coming from extero- and interoreceptors to the cells of the respiratory center.
The receptors can be irritated by chemical, mechanical, temperature and other influences. The most pronounced mechanism of self-regulation is a change in breathing under the influence of chemical and mechanical stimulation of vascular reflexogenic zones, mechanical stimulation of the receptors of the lungs and respiratory muscles.
The sinocarotid vascular reflexogenic zone contains receptors that are sensitive to the content of carbon dioxide, oxygen and hydrogen ions in the blood. This is clearly shown in Heymans' experiments with an isolated carotid sinus, which was separated from the carotid artery and supplied with blood from another animal. The carotid sinus was connected to the central nervous system only by a neural pathway - Hering's nerve was preserved. With an increase in the content of carbon dioxide in the blood washing the carotid body, excitation of the chemoreceptors in this zone occurs, as a result of which the number of impulses going to the respiratory center (to the center of inspiration) increases, and a reflex increase in the depth of breathing occurs.
Rice. 3. Regulation of breathing
K - bark; GT - hypothalamus; Pvts — pneumotaxic center; APC - respiratory center (expiratory and inspiratory); Xin - carotid sinus; BN - vagus nerve; CM - spinal cord; C 3 -C 5 - cervical segments of the spinal cord; Dfn - phrenic nerve; EM - expiratory muscles; MI - inspiratory muscles; Mnr - intercostal nerves; L - lungs; Df - diaphragm; Th 1 - Th 6 - thoracic segments of the spinal cord
An increase in the depth of breathing also occurs when carbon dioxide affects the chemoreceptors of the aortic reflexogenic zone.
The same changes in breathing occur when the chemoreceptors of the named reflexogenic zones of the blood with an increased concentration of hydrogen ions are stimulated.
In those cases when the oxygen content in the blood increases, the irritation of the chemoreceptors of the reflexogenic zones decreases, as a result of which the flow of impulses to the respiratory center weakens and a reflex decrease in the respiratory rate occurs.
A reflex stimulus of the respiratory center and a factor influencing breathing is a change in blood pressure in the vascular reflexogenic zones. With an increase in blood pressure, the mechanoreceptors of the vascular reflexogenic zones are irritated, resulting in reflex respiratory depression. A decrease in blood pressure leads to an increase in the depth and frequency of breathing.
Reflex influences on breathing from the mechanoreceptors of the lungs and respiratory muscles. A significant factor causing the change in inhalation and exhalation are influences from the mechanoreceptors of the lungs, which was first discovered by Hering and Breuer (1868). They showed that every inhalation stimulates exhalation. During inhalation, stretching of the lungs irritates the mechanoreceptors located in the alveoli and respiratory muscles. The impulses that arise in them along the afferent fibers of the vagus and intercostal nerves come to the respiratory center and cause excitation of expiratory and inhibition of inspiratory neurons, causing a change in inhalation to exhalation. This is one of the mechanisms of self-regulation of breathing.
Similar to the Hering-Breuer reflex, reflex influences on the respiratory center are carried out from the receptors of the diaphragm. During inhalation in the diaphragm, when its muscle fibers contract, the endings of the nerve fibers are irritated, the impulses arising in them enter the respiratory center and cause the cessation of inhalation and the occurrence of exhalation. This mechanism is especially important during increased breathing.
Reflex influences on breathing from various receptors of the body. The considered reflex influences on breathing are permanent. But there are various short-term effects from almost all the receptors in our body that affect breathing.
Thus, when mechanical and temperature stimuli act on the exteroreceptors of the skin, breath holding occurs. When cold or hot water hits a large surface of the skin, breathing stops on inhalation. Painful irritation of the skin causes a sharp inhalation (scream) with simultaneous closure of the vocal tract.
Some changes in the act of breathing that occur when the mucous membranes of the respiratory tract are irritated are called protective respiratory reflexes: coughing, sneezing, holding your breath when exposed to strong odors, etc.
Respiratory center and its connections
Respiratory center called a set of neural structures located in various parts of the central nervous system, regulating rhythmic coordinated contractions of the respiratory muscles and adapting breathing to changing environmental conditions and the needs of the body. Among these structures, vital parts of the respiratory center are distinguished, without the functioning of which breathing stops. These include sections located in the medulla oblongata and spinal cord. In the spinal cord, the structures of the respiratory center include motor neurons that form their axons, the phrenic nerves (in the 3-5 cervical segments), and motor neurons that form the intercostal nerves (in the 2-10 thoracic segments, while the aspiratory neurons are concentrated in the 2-10 thoracic segments). 6th, and expiratory ones - in the 8th-10th segments).
A special role in the regulation of breathing is played by the respiratory center, represented by sections localized in the brain stem. Some of the neuronal groups of the respiratory center are located in the right and left halves of the medulla oblongata in the region of the bottom of the fourth ventricle. There is a dorsal group of neurons that activate the inspiratory muscles, the inspiratory section, and a ventral group of neurons that primarily control exhalation, the expiratory section.
Each of these sections contains neurons with different properties. Among the neurons of the inspiratory region there are: 1) early inspiratory - their activity increases 0.1-0.2 s before the onset of contraction of the inspiratory muscles and lasts during inspiration; 2) full inspiratory - active during inspiration; 3) late inspiratory - activity increases in the middle of inspiration and ends at the beginning of exhalation; 4) neurons of the intermediate type. Some neurons in the inspiratory region have the ability to spontaneously excite rhythmically. Neurons with similar properties are described in the expiratory section of the respiratory center. The interaction between these neural pools ensures the formation of the frequency and depth of breathing.
An important role in determining the nature of the rhythmic activity of the neurons of the respiratory center and breathing belongs to the signals coming to the center along afferent fibers from receptors, as well as from the cerebral cortex, limbic system and hypothalamus. A simplified diagram of the nerve connections of the respiratory center is shown in Fig. 4.
Neurons of the inspiratory region receive information about the tension of gases in arterial blood, blood pH from vascular chemoreceptors, and cerebrospinal fluid pH from central chemoreceptors located on the ventral surface of the medulla oblongata.
The respiratory center also receives nerve impulses from receptors that control the stretching of the lungs and the condition of the respiratory and other muscles, from thermoreceptors, pain and sensory receptors.
Signals received by the neurons of the dorsal part of the respiratory center modulate their own rhythmic activity and influence their formation of streams of efferent nerve impulses transmitted to the spinal cord and further to the diaphragm and external intercostal muscles.
Rice. 4. Respiratory center and its connections: IC - inspiratory center; PC—inspection center; EC - expiratory center; 1,2- impulses from stretch receptors of the respiratory tract, lungs and chest
Thus, the respiratory cycle is triggered by inspiratory neurons, which are activated due to automaticity, and its duration, frequency and depth of breathing depend on the influence on the neural structures of the respiratory center of receptor signals sensitive to the level of p0 2, pC0 2 and pH, as well as on others intero- and exteroceptors.
Efferent nerve impulses from inspiratory neurons are transmitted along descending fibers in the ventral and anterior part of the lateral cord of the white matter of the spinal cord to a-motoneurons that form the phrenic and intercostal nerves. All fibers leading to the motor neurons innervating the expiratory muscles are crossed, and of the fibers following the motor neurons innervating the inspiratory muscles, 90% are crossed.
Motor neurons, activated by the flow of nerve impulses from the inspiratory neurons of the respiratory center, send efferent impulses to the neuromuscular synapses of the inspiratory muscles, which provide an increase in the volume of the chest. Following the chest, the volume of the lungs increases and inhalation occurs.
During inhalation, stretch receptors in the airways and lungs are activated. The flow of nerve impulses from these receptors along the afferent fibers of the vagus nerve enters the medulla oblongata and activates expiratory neurons that trigger exhalation. This closes one circuit of the breathing regulation mechanism.
The second regulatory circuit also starts from the inspiratory neurons and conducts impulses to the neurons of the pneumotaxic section of the respiratory center, located in the pons of the brain stem. This department coordinates the interaction between inspiratory and expiratory neurons of the medulla oblongata. The pneumotaxic department processes information received from the inspiratory center and sends a stream of impulses that excite the neurons of the expiratory center. Streams of impulses coming from the neurons of the pneumotaxic department and from the stretch receptors of the lungs converge on the expiratory neurons, excite them, and the expiratory neurons inhibit (but according to the principle of reciprocal inhibition) the activity of the inspiratory neurons. The sending of nerve impulses to the inspiratory muscles stops and they relax. This is enough for a calm exhalation to occur. With increased exhalation, efferent impulses are sent from expiratory neurons, causing contraction of the internal intercostal muscles and abdominal muscles.
The described scheme of nerve connections reflects only the most general principle of regulation of the respiratory cycle. In reality, afferent signal flows from numerous receptors of the respiratory tract, blood vessels, muscles, skin, etc. arrive to all structures of the respiratory center. They have an excitatory effect on some groups of neurons, and an inhibitory effect on others. The processing and analysis of this information in the respiratory center of the brain stem is controlled and corrected by the higher parts of the brain. For example, the hypothalamus plays a leading role in changes in breathing associated with reactions to painful stimuli, physical activity, and also ensures the involvement of the respiratory system in thermoregulatory reactions. Limbic structures influence breathing during emotional reactions.
The cerebral cortex ensures the inclusion of the respiratory system in behavioral reactions, speech function, and the penis. The presence of influence of the cerebral cortex on the parts of the respiratory center in the medulla oblongata and spinal cord is evidenced by the possibility of arbitrary changes in the frequency, depth and holding of breathing by a person. The influence of the cerebral cortex on the bulbar respiratory center is achieved both through the cortico-bulbar pathways and through the subcortical structures (stropallidal, limbic, reticular formation).
Oxygen, carbon dioxide and pH receptors
Oxygen receptors are already active at normal levels of pO 2 and continuously send streams of signals (tonic impulses) that activate inspiratory neurons.
Oxygen receptors are concentrated in the carotid bodies (the bifurcation area of the common carotid artery). They are represented by type 1 glomus cells, which are surrounded by supporting cells and have synaptic connections with the endings of the afferent fibers of the glossopharyngeal nerve.
Type 1 glomus cells respond to a decrease in pO 2 in arterial blood by increasing the release of the mediator dopamine. Dopamine causes the generation of nerve impulses in the endings of the afferent fibers of the pharyngeal nerve, which are conducted to the neurons of the inspiratory section of the respiratory center and to the neurons of the pressor section of the vasomotor center. Thus, a decrease in oxygen tension in arterial blood leads to an increase in the frequency of sending afferent nerve impulses and an increase in the activity of inspiratory neurons. The latter increase ventilation of the lungs, mainly due to increased breathing.
Receptors sensitive to carbon dioxide are present in the carotid bodies, aortic bodies of the aortic arch, and also directly in the medulla oblongata - central chemoreceptors. The latter are located on the ventral surface of the medulla oblongata in the area between the exit of the hypoglossal and vagus nerves. Carbon dioxide receptors also perceive changes in the concentration of H + ions. Receptors of arterial vessels respond to changes in pCO 2 and blood plasma pH, and the flow of afferent signals from them to inspiratory neurons increases with an increase in pCO 2 and (or) a decrease in arterial blood plasma pH. In response to the receipt of more signals from them to the respiratory center, ventilation of the lungs reflexively increases due to deepening of breathing.
Central chemoreceptors respond to changes in pH and pCO 2, cerebrospinal fluid and intercellular fluid of the medulla oblongata. It is believed that central chemoreceptors predominantly respond to changes in the concentration of hydrogen protons (pH) in the interstitial fluid. In this case, a change in pH is achieved due to the easy penetration of carbon dioxide from the blood and cerebrospinal fluid through the structures of the blood-brain barrier into the brain, where, as a result of its interaction with H 2 0, carbon dioxide is formed, dissociating with the release of hydrogen gases.
Signals from central chemoreceptors are also carried to the inspiratory neurons of the respiratory center. The neurons of the respiratory center themselves exhibit some sensitivity to shifts in the pH of the interstitial fluid. A decrease in pH and accumulation of carbon dioxide in the cerebrospinal fluid is accompanied by activation of inspiratory neurons and an increase in pulmonary ventilation.
Thus, the regulation of pCO 0 and pH are closely related both at the level of effector systems that influence the content of hydrogen ions and carbonates in the body, and at the level of central nervous mechanisms.
With the rapid development of hypercapnia, the increase in ventilation of the lungs is only approximately 25% caused by stimulation of the peripheral chemoresceptors of carbon dioxide and pH. The remaining 75% is associated with activation of the central chemoreceptors of the medulla oblongata by hydrogen protons and carbon dioxide. This is due to the high permeability of the blood-brain barrier to carbon dioxide. Since the cerebrospinal fluid and intercellular fluid of the brain have a much lower capacity of buffer systems than blood, an increase in pCO2 similar in magnitude to blood creates a more acidic environment in the cerebrospinal fluid than in the blood:
With prolonged hypercapnia, the pH of the cerebrospinal fluid returns to normal due to a gradual increase in the permeability of the blood-brain barrier to HC03 anions and their accumulation in the cerebrospinal fluid. This leads to a decrease in ventilation, which has developed in response to hypercapnia.
An excessive increase in the activity of pCO 0 and pH receptors contributes to the emergence of subjectively painful, painful sensations of suffocation and lack of air. This is easy to verify if you hold your breath for a long time. At the same time, with a lack of oxygen and a decrease in p0 2 in arterial blood, when pCO 2 and blood pH are maintained normal, a person does not experience discomfort. The consequence of this may be a number of dangers that arise in everyday life or when a person breathes gas mixtures from closed systems. Most often they occur with carbon monoxide poisoning (death in a garage, other household poisonings), when a person, due to the absence of obvious sensations of suffocation, does not take protective actions.
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