Central and peripheral chemoreceptors, their role in the regulation of respiration. Regulation of respiration Chemoreceptors of the respiratory center respond to concentration
Central chemoreceptors located on the ventral surface of the medulla oblongata and are sensitive to the level of carbon dioxide and hydrogen ions in the cerebrospinal fluid. Provides stimulation of respiratory neurons, because maintain a constant afferent flow and participate in the regulation of the frequency and depth of breathing when the gas composition of the cerebrospinal fluid changes.
Peripheral receptors localized in the bifurcation area carotid artery and aortic arches in special glomus (glomeruli). Afferent fibers go as part of the vagus and glossopharyngeal nerves to the respiratory center. They respond to a decrease in oxygen tension, an increase in the level of carbon dioxide and hydrogen ions in the blood plasma. Meaning : provide a reflex increase in breathing when the blood gas composition changes.
Secondary sensory receptors, vascular, non-adaptive, always active, increase with changes.
A particularly strong stimulus for chemoreceptors is the combination of hypercapnia and hypoxemia. These are natural changes in the gas composition of the blood during physical activity, which lead to a reflex increase in pulmonary ventilation.
Hypercapnia- increase in voltage carbon dioxide in blood plasma.
Hypoxemia- voltage drop oxygen in blood plasma.
During hypoxemia, growth in glomus tissue reduces the permeability of K channels of the receptor membrane → depolarization → opening of voltage-dependent Ca channels and diffusion of Cf ions into the cell.
Ca → DOPA exocytosis. In the area of contact of the receptor membrane with the end of the sensitive nerve fiber → activity in the fibers of the sinocarotid nerve (Hering’s nerve is part of the glossopharyngeal nerve) → to the DC through the neurons of the nuclei of the solitary tract → increase in pulmonary ventilation.
The role of airway receptors in the regulation of breathing.
The role of mechanoreceptors
1. Lung stretch receptors localized in the smooth muscle layer of the airways (trachea, bronchi), connected by thick afferent myelin fibers to the neurons of the respiratory center, and pass as part of the vagus nerve. When you inhale, the lungs stretch and the lung stretch receptors are activated, impulses go to the respiratory center, inhalation is inhibited, and exhalation is stimulated. If the vagus nerves are cut, breathing becomes slower and deeper. Meaning : regulate the frequency and depth of breathing, are not active during quiet breathing; low threshold.
2. Irritant receptors are located in the epithelial and subepithelial layers of the airways and are connected to the respiratory center by thin myelin fibers. Are high-threshold and quickly adapting . During quiet breathing they are not active. They react to large changes in lung volume (collapse and overextension), as well as to air irritants (ammonia, smoke) and dust. Causes rapid breathing - shortness of breath. Bimodal receptors (mechano. + chemo.)
3. Juxtacapillary receptors - are located in the interstitial tissue of the alveoli. They are activated when the amount of tissue fluid increases. Their activity increases with pathology (pneumonia, pulmonary edema). Form frequent and shallow breathing.
4. Mechanoreceptors of the nasopharynx, larynx, trachea. When they are excited (dust, mucus), a reflexive defensive reaction occurs - coughing. Afferent pathways pass through the trigeminal and glossopharyngeal nerves.
5. Mechanoreceptors of the nasal cavity. When they are irritated, a protective reflex occurs - sneezing.
6. Olfactory receptors in the nasal cavity. When irritated, a “sniffing” reaction occurs - short, frequent breaths.
PHYSIOLOGY OF DIGESTION, METABOLISM AND ENERGY
Food motivation. Digestion in the oral cavity. Regulation of salivation.
Digestion- a set of processes that ensure grinding and splitting nutrients into components that lack species specificity and are capable of being absorbed into the blood or lymph and participating in metabolism. The digestion process follows food consumption, and food consumption is a consequence of purposeful eating behavior, which is based on the feeling of hunger. Hunger and associated eating behavior are considered as a motivation aimed at eliminating the discomfort associated with a lack of nutrients in the blood. The central structure that triggers food motivation is hypothalamus . In its lateral part there are nuclei, the stimulation of which causes a feeling of hunger.
Functions of the oral cavity
1. Capturing and holding food (a person puts food in the mouth or sucks it in).
2. Analysis of food using oral receptors.
3. Mechanical grinding of food (chewing).
4. Wetting food with saliva and initial chemical treatment.
5. Transfer of the food bolus into the pharynx (oral phase of the act of swallowing).
6. Protective (barrier) - protection from pathogenic microflora.
A person has three pairs of large salivary glands (parotid, submandibular and sublingual) and many small glands in the mucous membrane of the palate, lips, cheeks, and tip of the tongue. The salivary glands contain two types of cells: mucous membranes- produce a viscous secretion rich in mucin, and serous- produce a liquid secretion rich in enzymes. The sublingual gland and small glands produce saliva continuously (associated with speech function), and the submandibular and parotid gland- only when they are excited.
Composition and properties of saliva
0.5-2.0 liters of saliva are produced per day. The osmotic pressure of saliva is always less than the osmotic pressure of blood plasma (saliva hypotonic blood plasma). The pH of saliva depends on its volume: with a small amount of saliva secreted, it is slightly acidic, and with a large volume, it is slightly alkaline (pH = 5.2-8.0).
Water wets the food bolus and dissolves some of its components. Wetting is necessary to facilitate the swallowing of a bolus of food, and its dissolution is necessary for the interaction of food components with the taste buds of the oral cavity. The main enzyme in saliva is alpha amylase- causes the cleavage of glycosidic bonds of starch and glycogen through intermediate stages of dextrins to maltose and sucrose. Mucus (mucin) is represented by mucopolysaccharides and glycoproteins, making the food bolus slippery, which makes it easier to swallow.
Mechanisms of saliva formation
The formation of saliva occurs in two stages:
1. The formation of primary saliva occurs in the acini. Water, electrolytes, and low molecular weight organic substances are filtered into the acini. High molecular weight organic substances are formed by the cells of the salivary glands.
2. B salivary ducts the composition of primary saliva changes significantly due to the processes of secretion (potassium ions, etc.) and reabsorption (sodium, chlorine ions, etc.). Secondary (final) saliva enters the oral cavity from the ducts.
Regulation of saliva formation is carried out reflexively.
Oral receptors
They prepare the entire gastrointestinal tract for the intake of food. There are four types of receptors:
1. Flavoring - are secondary sensory receptors and are divided into four types: they cause the sensation of sweet, sour, salty and bitter.
2. Mechanoreceptors - primary sensory, sensation of solid or liquid food, readiness of a bolus of food for swallowing.
3. Thermoreceptors - primary sensory, sensation of cold, hot.
4. Painful - primary sensory, activated when the integrity of the oral cavity is violated.
Afferent fibers from the receptors enter the brainstem as part of the trigeminal, facial, glossopharyngeal and vagus nerves.
Efferent innervation of the salivary glands
ñ Parasympathetic innervation - the mediator acetylcholine is released at the nerve endings, which interacts with M-cholinergic receptors and causes the release large quantities liquid saliva, rich in enzymes and poor in mucin.
ñ Sympathetic innervation - the mediator norepinephrine is released at the nerve endings, which interacts with alpha-adrenergic receptors and causes the release of a small amount of thick and viscous saliva, rich in mucin.
Regulation of salivation
1. Conditioned reflexes - occur with the participation of the cerebral cortex and hypothalamic nuclei, and arise when distant receptors are stimulated (visual, auditory, olfactory).
2. Unconditioned reflexes - occur when receptors in the oral cavity are irritated.
The act of swallowing
Swallowing is the process of food passing from the mouth to the stomach. The act of swallowing is carried out according to the program. F. Magendie divided the act of swallowing into three stages:
ñ Oral stage (voluntary) is triggered from mechanoreceptors and chemoreceptors of the oral cavity (the food bolus is ready for swallowing). Coordinated movement of the muscles of the cheeks and tongue propels the bolus of food to the root of the tongue.
ñ Pharyngeal stage (partially voluntary) is triggered from the mechanoreceptors of the root of the tongue. The tongue moves the bolus of food into the pharynx. The muscles of the pharynx contract, while at the same time the soft palate rises and the entrance to the nasal cavity from the pharynx closes. The epiglottis closes the entrance to the larynx and the upper esophageal sphincter opens.
ñ Esophageal stage (involuntary) triggered by mechanoreceptors of the esophagus. The muscles of the esophagus sequentially contract while the underlying muscles relax. The phenomenon is called peristaltic waves.
The swallowing center is located in the medulla oblongata and has connections with the spinal cord. When swallowing, the activity of the respiratory and cardioinhibitory centers is inhibited (heart rate increases).
The tension in arterial blood O 2 and CO 2, as well as pH, as is already known, depends on ventilation of the lungs.
But, in turn, they are factors influencing the intensity of this ventilation, that is, they affect the activity of the DC.
Frederico's experience with cross-circulation. In two dogs, the carotid arteries were crossed with the jugular veins while the vertebral arteries were ligated. As a result, the head of the first dog was supplied with the blood of the second dog, and the head of the second dog with the blood of the first. If the first dog's trachea was compressed (causing asphyxia), then the second dog experienced hyperpnea. In the first dog, despite an increase in pCO 2 and a decrease in pO 2, apnea occurs.
Reason: the carotid artery of the first dog received blood from the second dog, whose blood pCO 2 decreased as a result of hyperventilation. This influence is carried out not directly on its neurons, but through special chemoreceptors located:
1. In central structures (central, medullary, bulbar chemoreceptors).
2. On the periphery (arterial chemoreceptors).
From these receptors, the respiratory center receives afferent signaling about the gas composition of the blood.
In this way, unique regulatory feedback circuits are formed, the activity of which is aimed at maintaining hemostasis and matching the respiratory function with the metabolic needs of the body.
The role of central chemoreceptors. Central chemoreceptors are located in the PM. Perfusion of the PM site in the area where these receptors are located with a solution with a low pH leads to a sharp increase in respiration, and with an increase in pH, to a weakening of respiration.
Two receptor fields were discovered in the PM. They are designated by the letters M and L. Between them there is a large field S. The neurons of this field are insensitive to pH. The destruction of the S field leads to a loss of sensitivity of the M and L fields to pH. It is believed that afferent pathways from chemoreceptors to the DC pass here.
Under natural conditions, central chemoreceptors are constantly stimulated by H + contained in the intercellular fluid of the brain stem, which is very similar in composition to the cerebrospinal fluid. The concentration of H + in it depends on the tension of CO 2 in the arterial blood. A decrease in pH by 0.01 causes an increase in ventilation by 4 l/min.
At the same time, central chemoreceptors also respond to changes in pCO 2, but to a lesser extent than changes in pH. It is believed that the main chemical factor influencing central chemoreceptors is the H + content in the intercellular fluid of the brain stem, and the effect of CO 2 is associated with the formation of these ions.
The role of arterial chemoreceptors. O 2 , CO 2 and H + can act on the structures of the NS not only centrally, directly, but also by exciting peripheral chemoreceptors.
The most important of them are:
1. Paraganglia located at the site of division of the common carotid artery into internal and external, called carotid bodies (innervated by branches of the glossopharyngeal nerve).
2. Paraganglia of the aortic arch, the so-called aortic bodies (innervated by fibers of the vagus).
Chemoreceptors of these zones are excited when pCO 2 increases and pO 2 and pH decrease. This can be shown by perfusion of the indicated sections of the arteries with blood, changing its parameters pO 2, pCO 2, pH, while recording changes in the bioelectrical activity of afferent fibers. It has been shown that the effect of O 2 on the respiratory center is mediated exclusively by peripheral chemoreceptors.
As for CO 2 and H + , they have a predominantly central effect, although with shifts in pCO 2 and pH, the impulse from the chemoreceptors changes, but only slightly, which indicates a relatively small influence of these factors on the DC mediated by peripheral chemoreceptors.
Thus, DC neurons are maintained in a state of activity by impulses coming from central (bulbar) and peripheral (arterial) chemoreceptors that respond to changes in 3 parameters of arterial blood:
1. Decrease in pO 2 (hypoxemia);
2. Increased pCO 2 (hypercapnia);
3. Decrease in pH (acidosis).
The main stimulus for breathing is hypercapnic. The higher the pCO 2 (and pH is associated with it) in arterial blood and intercellular fluid, the higher the excitation of bulbar chemosensitive structures and arterial chemoreceptors, the higher the ventilation of the lungs.
The hypoxic stimulus is of lesser importance in the regulation of respiration (the steepness of the drop in pO 2 in the blood occurs only when pO 2 drops below 60-70 mm Hg).
But a particularly strong stimulus to the central respiratory mechanism is the combined effect of hypoxemia and hypercapnia (and associated acidosis). This is quite understandable: increased oxidative processes in the body are associated with:
· with increased absorption of O 2 ;
· with increased formation of CO 2 ;
· with increased formation of acidic metabolic products.
This requires an increase in ventilation volume.
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 principle feedback. 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.
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 rapid 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 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.
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.
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 for opposite side bodies. If the chemoreceptor bodies are destroyed or poisoned by novocaine, breathing stops.
Along with With chemoreceptors of the medulla oblongata play an important role in the regulation of breathing 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.
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.
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 influence of an increased concentration of H+ ions and increased CO 2 voltage 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 the above
The importance of mechanoreceptors in the regulation of breathing. The respiratory center receives afferents impulses not only from chemoreceptors, but also from pressoreceptors of 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. On the contrary, when blood pressure decreases, breathing becomes faster and deeper.
Impulses coming to the respiratory center through the vagus nerves from lung receptors. 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 slow and deep;
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.”
In addition to lung mechanoreceptors, take part in the regulation of breathing mechanoreceptors of the intercostal muscles and diaphragm. 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 influx of impulses from the mechanoreceptors of the lungs stops and expiratory neurons can only be excited 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.
Thus, it is vital important function 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.
Related information.
Main function 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 nerve s). 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 jugular vein 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 great importance with 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 exposed to cold or hot water on a large surface of the skin, breathing stops on inspiration. 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. After 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 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 diagram of nerve connections reflects only the most general principle 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 level 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.
Regulation of breathing is carried out through reflex reactions resulting from the excitation of specific receptors embedded in the lung tissue, vascular reflexogenic zones and other areas. The central apparatus for regulating breathing is represented by the formations of the spinal cord, medulla oblongata and overlying parts of the nervous system. The main function of breathing control is carried out by respiratory neurons in the brain stem, which transmit rhythmic signals in the spinal cord to the motor neurons of the respiratory muscles.
Respiratory nerve center - this is a set of neurons of the central nervous system that ensures the coordinated rhythmic activity of the respiratory muscles and constant adaptation external respiration to changing conditions inside the body and in environment. The main (working) part of the respiratory nerve center is located in the medulla oblongata. It distinguishes two sections: inspiratory(inhalation center) and expiratory(exhalation center). The dorsal group of respiratory neurons of the medulla oblongata consists mainly of inspiratory neurons. They partially give rise to descending pathways that come into contact with the motor neurons of the phrenic nerve. The ventral group of respiratory neurons sends predominantly descending fibers to the motor neurons of the intercostal muscles. In the anterior part of the pons, an area called pneumotaxic center. This center is related to the work of both its experimental and inspiratory departments. An important part of the respiratory nerve center is a group of neurons cervical spine spinal cord (III-IV cervical segments), where the nuclei of the phrenic nerves are located.
By the time the child is born, the respiratory center is capable of producing a rhythmic change in the phases of the respiratory cycle, but this reaction is very imperfect. The fact is that the respiratory center is not yet formed at birth; its formation ends by 5-6 years of life. This is confirmed by the fact that it is by this period of children’s lives that their breathing becomes rhythmic and uniform. In newborns, it is unstable both in frequency and depth and rhythm. Their breathing is diaphragmatic and differs practically little during sleep and wakefulness (frequency from 30 to 100 per minute). In 1-year-old children, the number of respiratory movements during the day is within 50-60, and at night - 35-40 per minute, unstable and diaphragmatic. At the age of 2-4 years, the frequency becomes within 25-35 and is predominantly of the diaphragmatic type. In 4-6 year old children, the breathing rate is 20-25, mixed - chest and diaphragmatic. By 7–14 years it reaches a level of 19-20 per minute; at this time it is mixed. Thus, the final formation of the nerve center practically dates back to this age period.
How does the respiratory center get excited? One of the most important ways of its arousal is automation. There is no single point of view on the nature of automaticity, but there is evidence that secondary depolarization may occur in the nerve cells of the respiratory center (on the principle of diastolic depolarization in the heart muscle), which, reaching a critical level, gives a new impulse. However, one of the main ways to excite the respiratory nerve center is its irritation with carbon dioxide. In the last lecture, we noted that a lot of carbon dioxide remains in the blood flowing from the lungs. It functions as the main irritant of the nerve cells of the medulla oblongata. This is mediated through special education - chemoreceptors located directly in the structures of the medulla oblongata ( "central chemoreceptors"). They are very sensitive to the tension of carbon dioxide and the acid-base state of the intercellular brain fluid washing them.
Carbon dioxide can easily diffuse from blood vessels brain into the cerebrospinal fluid and stimulate the chemoreceptors of the medulla oblongata. This is another way to excite the respiratory center.
Finally, its excitation can also be carried out reflexively. We conditionally divide all reflexes that ensure the regulation of breathing into: intrinsic and associated.
Own reflexes of the respiratory system - These are reflexes that originate in the organs of the respiratory system and end there. First of all, this group of reflexes includes the reflex act from lung mechanoreceptors. Depending on the location and type of perceived irritation, the nature of reflex responses to irritation, three types of such receptors are distinguished: tension receptors, irritant receptors and juxtacapillary receptors of the lungs.
Lung stretch receptors are located mainly in the smooth muscles of the airways (trachea, bronchi). There are about 1000 such receptors in each lung and they are connected to the respiratory center by large myelinated afferent fibers of the vagus nerve with high speed carrying out. The direct stimulus of this type of mechanoreceptor is internal tension in the tissues of the walls of the airways. As the lungs stretch during inhalation, the frequency of these impulses increases. Inflation of the lungs causes a reflex inhibition of inhalation and a transition to exhalation. When the vagus nerves are cut, these reactions stop, and breathing becomes slower and deeper. These reactions are called reflexes Goering-Breuer. This reflex is reproduced in an adult when the tidal volume exceeds 1 liter (during physical exertion, for example). It is of great importance in newborns.
Irritant receptors or quickly adapting mechanoreceptors of the airways, receptors of the mucous membrane of the trachea and bronchi. They respond to sudden changes in lung volume, as well as when the mucous membrane of the trachea and bronchi is exposed to mechanical or chemical irritants (dust particles, mucus, vapors of caustic substances, tobacco smoke, etc.). Unlike pulmonary stretch receptors, irritant receptors have rapid adaptation. If tiny particles enter the respiratory tract foreign bodies(dust, smoke particles), activation of irritant receptors causes a cough reflex in a person. Its reflex arc is as follows - from the receptors, information through the upper laryngeal, glossopharyngeal, trigeminal nerve goes to the corresponding brain structures responsible for exhalation (urgent exhalation - cough). If the receptors of the nasal airways are stimulated in isolation, this causes another urgent exhalation - sneezing.
Juxtacapillary receptors - located near the capillaries of the alveoli and respiratory bronchi. The irritant of these receptors is an increase in pressure in the pulmonary circulation, as well as an increase in the volume of interstitial fluid in the lungs. This is observed with stagnation of blood in the pulmonary circulation, pulmonary edema, damage to the lung tissue (for example, with pneumonia). Impulses from these receptors are sent to the respiratory center via the vagus nerve, causing frequent shallow breathing. In case of illness, it causes a feeling of shortness of breath and difficulty breathing. There may be not only rapid breathing (tachypnea), but also a reflex narrowing of the bronchi.
There is also a large group of self-reflexes that originate from the proprioceptors of the respiratory muscles. Reflex from proprioceptors of intercostal muscles is carried out during inhalation, when these muscles, contracting, send information through the intercostal nerves to the expiratory section of the respiratory center and, as a result, exhalation occurs. Reflex from proprioceptors of the diaphragm carried out in response to its contraction during
inhalation, as a result, information flows through the phrenic nerves, first to the spinal nerve, and then to the medulla oblongata in the expiratory section of the respiratory center and exhalation occurs.
Thus, all of the respiratory system’s own reflexes occur during inhalation and end with exhalation.
Conjugate reflexes of the respiratory system – these are reflexes that begin outside of it. This group of reflexes, first of all, includes the reflex to couple the activities of the circulatory and respiratory systems. Such a reflex act begins from the peripheral chemoreceptors of the vascular reflexogenic zones. The most sensitive of them are located in the sinocarotid zone. Sinocarotid chemoreceptive conjugate reflex – occurs when carbon dioxide accumulates in the blood. If its voltage increases, then the most highly excitable chemoreceptors are excited (and they are located in this zone in the sinocarotid body), the resulting wave of excitation goes from them along the IX pair of cranial nerves and reaches the expiratory section of the respiratory center. Exhalation occurs, which increases the release of excess carbon dioxide into the surrounding space. Thus, the circulatory system (by the way, when this reflex act is carried out, it also works more intensely, the heart rate and blood flow speed increase) affects the activity of the respiratory system.
Another type of conjugate reflexes of the respiratory system is a large group exteroceptive reflexes. They originate from tactile (remember the reaction of breathing to touch, touch), temperature (heat - increases, cold - decreases respiratory function), pain (weak and medium-strength stimuli - increase, strong - depress breathing) receptors.
Proprioceptive conjugate reflexes respiratory system are carried out due to irritation of receptors of skeletal muscles, joints, ligaments. This is observed when performing physical activity. Why is this happening? If at rest a person needs 200-300 ml of oxygen per minute, then during physical activity this volume should increase significantly. Under these conditions, MO, the arteriovenous difference in oxygen, also increases. An increase in these indicators is accompanied by an increase in oxygen consumption. Then everything depends on the amount of work. If the work lasts 2-3 minutes and its power is high enough, then oxygen consumption continuously increases from the very beginning of work and decreases only after it stops. If the duration of work is longer, then oxygen consumption, increasing in the first minutes, is subsequently maintained at a constant level. Oxygen consumption increases the more the harder the physical work. The greatest amount of oxygen that the body can absorb in 1 minute during extremely hard work is called maximum oxygen consumption (MOC). The work in which a person reaches his MPC level should last no more than 3 minutes. There are many ways to determine MIC. For those who do not engage in sports or physical exercise in people, the MIC value does not exceed 2.0-2.5 l/min. In athletes it can be more than twice as high. MIC is an indicator aerobic performance of the body. This is a person’s ability to perform very hard physical work, providing their energy costs through oxygen absorbed directly during work. It is known that even a well-trained person can work with oxygen consumption at the level of 90-95% of his VO2 max for no more than 10-15 minutes. Those who have greater aerobic productivity achieve better results in work (sports) with relatively the same technical and tactical readiness.
Why does physical work increase oxygen consumption? Several reasons can be identified for this reaction: the opening of additional capillaries and an increase in blood in them, a shift in the hemoglobin dissociation curve to the right and down, and an increase in temperature in the muscles. In order for muscles to perform certain work, they need energy, the reserves of which are restored in them when oxygen is delivered. Thus, there is a relationship between the power of work and the amount of oxygen required for work. The amount of blood required for work is called oxygen demand. During heavy work, oxygen demand can reach up to 15-20 liters per minute or more. However, the maximum oxygen consumption is two to three times less. Is it possible to perform work if the minute oxygen reserve exceeds the MIC? To answer this question correctly, we need to remember why oxygen is used during muscle work. It is necessary for the restoration of energy-rich chemical substances, providing muscle contraction. Oxygen usually interacts with glucose, and when it oxidizes, it releases energy. But glucose can be broken down without oxygen, i.e. anaerobically, which also releases energy. In addition to glucose, there are other substances that can be broken down without oxygen. Consequently, muscle work can be ensured even if there is insufficient oxygen supply to the body. However, in this case, many acidic products are formed and oxygen is needed to eliminate them, because they are destroyed by oxidation. The amount of oxygen required to oxidize metabolic products formed during physical work is called oxygen debt. It occurs during work and is eliminated during recovery period after her. It takes from several minutes to an hour and a half to eliminate it. It all depends on the duration and intensity of the work. The main role in the formation of oxygen debt is lactic acid. To continue working when there is a large amount of it in the blood, the body must have powerful buffer systems and its tissues must be adapted to work when there is a lack of oxygen. This adaptation of tissues is one of the factors ensuring high anaerobic performance.
All this complicates the regulation of breathing during physical work, since oxygen consumption in the body increases and its lack in the blood leads to irritation of chemoreceptors. Signals from them go to the respiratory center, resulting in increased breathing. During muscular work, a lot of carbon dioxide is produced, which enters the blood and can act on the respiratory center directly through the central chemoreceptors. If a lack of oxygen in the blood leads mainly to increased breathing, then an excess of carbon dioxide causes it to deepen. During physical work, both of these factors act simultaneously, resulting in both increased and deepening of breathing. Finally, impulses coming from the working muscles reach the respiratory center and enhance its work.
When the respiratory center functions, all its parts are functionally interconnected. This is achieved by the following mechanism. When carbon dioxide accumulates, the inspiratory section of the respiratory center is excited, from which information goes to the pneumatic toxic section of the center, then to its expiratory section. The latter, in addition, is excited by a whole range of reflex acts (from receptors of the lungs, diaphragm, intercostal muscles, respiratory tract, vascular chemoreceptors). Due to its excitation through a special inhibitory reticular neuron, the activity of the inhalation center is inhibited and it is replaced by exhalation. Since the inhalation center is inhibited, it does not send further impulses to the pneumatic toxic department, and the flow of information from it to the exhalation center stops. At this point, carbon dioxide accumulates in the blood and the inhibitory influences from the expiratory part of the respiratory center are removed. As a result of this redistribution of the flow of information, the inhalation center is excited and inhalation replaces exhalation. And everything repeats itself again.
An important element in the regulation of breathing is the vagus nerve. It is through its fibers that the main influences on the exhalation center occur. Therefore, if it is damaged (as well as if the pneumatic toxic part of the respiratory center is damaged), breathing changes so that inhalation remains normal, but exhalation is sharply prolonged. This type of breathing is called vagus-dyspnea.
We have already noted above that when rising to a height, there is an increase in pulmonary ventilation due to stimulation of chemoreceptors in the vascular zones. At the same time, heart rate and MO increase. These reactions improve somewhat oxygen transport in the body, but not for long. Therefore, during a long stay in the mountains, as one adapts to chronic hypoxia, the initial (urgent) breathing reactions gradually give way to a more economical adaptation of the body’s gas transport system. Thus, in permanent residents of high altitudes, the respiratory response to hypoxia is sharply weakened ( hypoxic deafness) and pulmonary ventilation is maintained at almost the same level as in those living on the plain. But with long-term living in high altitude conditions, vital capacity increases, CK increases, there is more myoglobin in the muscles, and the activity of enzymes that ensure biological oxidation and glycolysis increases in the mitochondria. People living in the mountains, in addition, have reduced sensitivity of body tissues, in particular the central nervous system, to insufficient oxygen supply.
At altitudes of more than 12,000 m, the air pressure is very low and under these conditions even breathing pure oxygen does not solve the problem. Therefore, when flying at this altitude, pressurized cabins are required (airplanes, spaceships).
Sometimes a person has to work in conditions high blood pressure(diving work). At depth, nitrogen begins to dissolve in the blood and with a rapid rise from the depths it does not have time to be released from the blood, gas bubbles cause vascular embolism. The condition that arises in this case is called decompression sickness. It is accompanied by joint pain, dizziness, shortness of breath, and loss of consciousness. Therefore, nitrogen in air mixtures is replaced by insoluble gases (for example, helium).
A person can voluntarily hold his breath for no more than 1-2 minutes. After preliminary hyperventilation of the lungs, this breath holding increases to 3-4 minutes. However, prolonged diving, for example, after hyperventilation, is fraught with serious danger. A rapid drop in blood oxygenation can cause a sudden loss of consciousness, and in this state a swimmer (even an experienced one), under the influence of a stimulus caused by an increase in the partial tension of carbon dioxide in the blood, can inhale water and choke (drown).
So, at the end of the lecture, I must remind you that healthy breathing is through the nose, as little as possible, with a delay during inhalation and, especially, after it. Lengthening inhale, we stimulate the work of the sympathetic department of the autonomic nervous system, with all the ensuing consequences. By lengthening the exhalation, we retain more and longer carbon dioxide in the blood. And this turns out to be positive influence on the tone of blood vessels (reduces it), with all the ensuing consequences. Thanks to this, oxygen can in such a situation pass into the most distant microcirculation vessels, preventing the disruption of their function and the development of numerous diseases. Proper breathing is the prevention and treatment of a large group of diseases not only of the respiratory system, but also of other organs and tissues! Breathe for your health!
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