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Hering Breuer reflex physiology. Breathing reflex

Reflex regulation of breathing is carried out due to the fact that the neurons of the respiratory center have connections with numerous mechanoreceptors respiratory tract and alveoli of the lungs and receptors of vascular reflexogenic zones.
Lung receptors 1

The following types of mechanoreceptors are found in the human lungs:
airway smooth muscle stretch receptors; Pulmonary stretch receptors
irritant, or rapidly adapting, receptors of the mucous membrane of the respiratory tract;
J-receptors.
Pulmonary stretch receptors

It is believed that these receptors lie in the smooth muscles of the airways.
If the lungs are kept in an inflated state for a long time, then the activity of the stretch receptors changes little, which indicates their poor adaptability.
The impulse from these receptors travels along the large myelinated fibers of the vagus nerves. Transection of the vagus nerves eliminates reflexes from these receptors.
The main response to stimulation of pulmonary stretch receptors is a decrease in respiratory rate as a result of an increase in expiratory time. This reaction is called inflationary reflex Goering - Breuer. (i.e., arising in response to bloating)
Classic experiments have shown that inflation of the lungs leads to inhibition of further activity of the inspiratory muscles.
There is also a reverse reaction, i.e. an increase in this activity in response to a decrease in lung volume ( deflation reflex). These reflexes can serve as a mechanism of self-regulation based on the principle of negative feedback.
It was once believed that the Hering-Breuer reflexes play a major role in the regulation of ventilation, that is, the depth and frequency of breathing depend on them. The principle of such regulation could consist in modulating the work of the “inhalation interrupter” in the medulla oblongata by impulses from stretch receptors. Indeed, with bilateral cutting of the vagus nerves, deep, rare breathing is established in most animals. However, recent work has shown that in an adult, the Hering-Breuer reflexes do not operate until the tidal volume exceeds 1 liter (as, for example, with physical activity). Short-term bilateral blockade of the vagus nerves using local anesthesia in a awake person it does not affect either the frequency or depth of breathing. Some evidence suggests that these reflexes may be more important in newborns.



Reflexes from the nasal mucosa. Irritation of the irritant receptors of the nasal mucosa, for example, tobacco smoke, inert dust particles, gaseous substances, water causes narrowing of the bronchi, glottis, bradycardia, decreased cardiac output, narrowing of the lumen of blood vessels in the skin and muscles. The protective reflex occurs in newborns when briefly immersed in water. They experience respiratory arrest, preventing water from entering the upper respiratory tract.
Reflexes from the pharynx. Mechanical irritation of the receptors of the mucous membrane of the posterior part of the nasal cavity causes a strong contraction of the diaphragm, external intercostal muscles, and, consequently, inhalation, which opens the airway through the nasal passages (aspiration reflex). This reflex is expressed in newborns.
Reflexes from the larynx and trachea. Numerous nerve endings are located between epithelial cells mucous membrane of the larynx and main bronchi. These receptors are stimulated by inhaled particles, irritating gases, bronchial secretions, foreign bodies. All this causes a cough reflex, manifested in a sharp exhalation against the background of a narrowing of the larynx and a contraction of the smooth muscles of the bronchi, which persists for a long time after the reflex.
The cough reflex is the main pulmonary reflex of the vagus nerve.
Reflexes from bronchiole receptors. Numerous myelinated receptors are located in the epithelium of the intrapulmonary bronchi and bronchioles. Irritation of these receptors causes hyperpnea, bronchoconstriction, laryngeal contraction, and hypersecretion of mucus, but is never accompanied by a cough.
Receptors are most sensitive to three types of irritants: 1) tobacco smoke, numerous inert and irritating chemicals;
2) damage and mechanical stretching of the airways during deep breathing, as well as pneumothorax, atelectasis, and the action of bronchoconstrictors;
3) pulmonary embolism, pulmonary capillary hypertension and pulmonary anaphylactic phenomena.
Reflexes from J-receptors. In the alveolar septa, in contact with the capillaries, there are special J-receptors. These receptors are particularly sensitive to interstitial edema, pulmonary venous hypertension, microembolism, irritant gases and inhaled drugs, phenyl diguanide (when administered intravenously). Stimulation of J receptors initially causes apnea, then superficial tachypnea, hypotension and bradycardia.
Hering-Breuer reflexes.

Inflation of the lungs in an anesthetized animal reflexively inhibits inhalation and causes exhalation. Nerve endings located in the bronchial muscles play the role of lung stretch receptors. They are classified as slowly adapting lung stretch receptors, which are innervated by myelinated fibers vagus nerve.
The Hering-Breuer reflex controls the depth and frequency of breathing. In humans it has physiological significance with tidal volumes exceeding 1 liter (for example, during physical activity). In an awake adult, short-term bilateral vagus nerve blockade using local anesthesia does not affect the depth or rate of breathing.
In newborns, the Hering-Breuer reflex clearly manifests itself only in the first 3-4 days after birth.
Proprioceptive control of breathing. Receptors in the joints of the chest send impulses to the cerebral cortex and are the only source of information about chest movements and respiratory volumes.
The intercostal muscles, and to a lesser extent the diaphragm, contain a large number of muscle spindles. The activity of these receptors is manifested during passive muscle stretching, isometric contraction and isolated contraction of intrafusal muscle fibers. Receptors send signals to appropriate segments spinal cord. Insufficient shortening of the inspiratory or expiratory muscles increases impulses from muscle spindles, which, through γ-motoneurons, increase the activity of O-motoneurons and thus dose muscle effort.

Chemoreflexes of breathing. Horn and Prog in arterial blood humans and animals is maintained at a fairly stable level, despite significant changes in Oz consumption and CO2 emissions. Hypoxia and a decrease in blood pH (acidosis) cause increased ventilation (hyperventilation), and hyperoxia and an increase in blood pH (alkalosis) cause a decrease in ventilation (hypoventilation) or apnea. Control for normal content in internal environment the body's 02, CO2 and pH are carried out by peripheral and central chemoreceptors.

An adequate stimulus for peripheral chemoreceptors is a decrease in Po; arterial blood, to a lesser extent an increase in Pco2 and pH, and for central chemoreceptors - an increase in the concentration of H* in the extracellular fluid of the brain.

Arterial (peripheral) chemoreceptors. Peripheral chemoreceptors are located in the carotid and
aortic bodies. Signals from arterial chemoreceptors along the sinocarotid and aortic nerves initially arrive at the neurons of the nucleus of the solitary fasciculus medulla oblongata, and then switch to neurons of the respiratory center. The response of peripheral chemoreceptors to a decrease in Pao^ is very rapid, but nonlinear. Under Rao; within 80-60 mm rt. Art. (10.6-8.0 kPa) there is a slight increase in ventilation, and with Rao; below 50 mm Hg. Art. (6.7 kPa) severe hyperventilation occurs.

Paco2 and blood pH only potentiate the effect of hypoxia on arterial chemoreceptors and are not adequate stimuli for this type of respiratory chemoreceptors.

Response of arterial chemoreceptors and respiration to hypoxia. Lack of C>2 in arterial blood is the main irritant of peripheral chemoreceptors. Impulse activity in the afferent fibers of the sinocarotid nerve stops when Raod is above 400 mm Hg. Art. (53.2 kPa). In normoxia, the frequency of discharges of the sinocarotid nerve is 10% of their maximum reaction, which is observed when Raod is about 50 mm Hg. Art. and below - The hypoxic respiratory reaction is practically absent in the indigenous inhabitants of the highlands and disappears approximately 5 years later in the inhabitants of the plains after the beginning of their adaptation to the highlands (3500 m and above).

Central chemoreceptors. The location of the central chemoreceptors has not been definitively established. Researchers believe that such chemoreceptors are located in the rostral parts of the medulla oblongata near its ventral surface, as well as in various areas of the dorsal respiratory nucleus.

The presence of central chemoreceptors is proven quite simply: after transection of the sinocarotid and aortic nerves in experimental animals, the sensitivity of the respiratory center to hypoxia disappears, but the respiratory response to hypercapnia and acidosis is completely preserved. Transection of the brainstem immediately above the medulla oblongata does not affect the nature of this reaction.

An adequate stimulus for central chemoreceptors is a change H4 concentrations in the extracellular fluid of the brain. Function threshold regulator pH shifts in the area central chemoreceptors perform the structures of the blood-brain barrier, which separates the blood from extracellular fluid of the brain. Transport occurs through this barrier 02, CO2 and H^ between blood and extracellular brain fluid. Transport of СО3 and H+ from internal brain environment in plasma blood through structures of the blood-brain barrier regulated with the participation of the enzyme carbonic anhydrase.
50. Regulation of breathing at low and high atmospheric pressure.

Breathing at low atmospheric pressure. Hypoxia

Atmospheric pressure decreases as you rise in altitude. This is accompanied by a simultaneous decrease in the partial pressure of oxygen in the alveolar air. At sea level it is 105 mmHg. At an altitude of 4000 m it is already 2 times less. As a result, the oxygen tension in the blood decreases. Hypoxia occurs. When falling fast atmospheric pressure acute hypoxia is observed. It is accompanied by euphoria, a feeling of false well-being, and a rapid loss of consciousness. With a slow rise, hypoxia increases slowly. Symptoms of mountain sickness develop. Initially, weakness, rapid and deepening of breathing appears, headache. Then nausea and vomiting begin, weakness and shortness of breath increase sharply. As a result, loss of consciousness, cerebral edema and death also occur. Up to an altitude of 3 km, most people do not experience symptoms of altitude sickness. At an altitude of 5 km, changes in respiration, blood circulation, higher nervous activity. At an altitude of 7 km these phenomena intensify sharply. An altitude of 8 km is the maximum altitude for life; the body suffers not only from hypoxia, but also from hypocapnia. As a result of a decrease in oxygen tension in the blood, vascular chemoreceptors are excited. Breathing becomes faster and deeper. Carbon dioxide is removed from the blood and its voltage drops below normal. This leads to depression of the respiratory center. Despite hypoxia, breathing becomes rare and shallow. In the process of adapting to chronic hypoxia There are three stages. In the first, emergency, compensation is achieved by increasing pulmonary ventilation, increasing blood circulation, increasing the oxygen capacity of the blood, etc. At the stage of relative stabilization, changes in systems and the body occur that provide a higher and more beneficial level of adaptation. In the stable stage, the physiological parameters of the body become stable due to a number of compensatory mechanisms. Thus, the oxygen capacity of the blood increases not only due to an increase in the number of red blood cells, but also due to an increase in the 2,3-phosphoglycerate in them. Due to 2,3-phosphoglycerate, the dissociation of oxyhemoglobin in tissues is improved. Fetal hemoglobin appears, which has a higher ability to bind oxygen. At the same time, the diffusion capacity of the lungs increases and “functional emphysema” occurs. Those. reserve alveoli are included in breathing and the functional residual capacity increases. Energy metabolism decreases, but the intensity of carbohydrate metabolism increases.

Hypoxia is an insufficient supply of oxygen to tissues. Forms of hypoxia:

1. Hypoxemic hypoxia. Occurs when the oxygen tension in the blood decreases (decreases in atmospheric pressure, diffusion capacity of the lungs, etc.).

2. Anemic hypoxia. It is a consequence of a decrease in the blood’s ability to transport oxygen (anemia, carbon dioxide poisoning).

3. Circulatory hypoxia. Observed in cases of disturbances of systemic and local blood flow (heart and vascular disease).

4. Histotoxic hypoxia. Occurs when tissue respiration is impaired (cyanide poisoning).

Human breathing at elevated air pressure takes place at considerable depths under water during divers' work or during caisson work. Since the pressure of one atmosphere corresponds to the pressure of a column of water 10 m high, then in accordance with the depth of a person’s immersion under water in a diver’s spacesuit or in a caisson, air pressure is maintained according to this calculation. Man being in the atmosphere high blood pressure air, does not experience any respiratory distress. With high blood pressure atmospheric air a person can breathe if air enters his respiratory tract at the same pressure. In this case, the solubility of gases in a liquid is directly proportional to its partial pressure.

Therefore, when breathing air at sea level, 1 ml of blood contains 0.011 ml of physically dissolved nitrogen. At the air pressure that a person breathes, for example, 5 atmospheres, 1 ml of blood will contain 5 times more physically dissolved nitrogen. When a person switches to breathing at lower air pressure (as the caisson rises to the surface or a diver ascends), the blood and body tissues can only hold 0.011 ml of N2/ml of blood. The remaining amount of nitrogen passes from solution into a gaseous state. The transition of a person from a zone of increased pressure of inhaled air to a lower pressure must occur slowly enough so that the released nitrogen has time to be released through the lungs. If nitrogen, turning into a gaseous state, does not have time to be completely released through the lungs, which occurs when the caisson is quickly lifted or the diver’s ascent mode is violated, nitrogen bubbles in the blood can clog small vessels of the body tissues. This condition is called gas embolism. Depending on the location of the gas embolism (vessels of the skin, muscles, central nervous system, heart, etc.), a person experiences various disorders(pain in joints and muscles, loss of consciousness), which are generally called “decompression sickness.”

Located dorsally in the nucleus parabrachialis At the top of the pons, the pneumotaxic center transmits signals to the inhalation area. The main thing in the activity of this center is control over the “turn-off” point of the increasing inspiratory signal and the duration of the lung filling phase. With a strong pneumotaxic signal, inhalation can be shortened to 0.5 seconds, which corresponds to very low filling of the lungs; when the pneumotaxic signal is weak, inhalation may last 5 seconds or more, and the lungs will fill with more air.

Primary the task of the pneumotaxic center is a limitation of inhalation. In this case, a secondary effect occurs - an increase in breathing rate, because restricting inhalation shortens the duration of exhalation and the total period of each breathing cycle. A strong pneumotaxic signal can increase the respiratory rate to 30-40 per minute, while a weak pneumotaxic signal can reduce the rate to 3-5 breathing movements in a minute.

Ventral group of respiratory neurons

From two sides of the medulla oblongata- about 5 mm anterior and lateral to the dorsal group of respiratory neurons - lies the ventral group of respiratory neurons, located rostrally in the nucleus ambiguus and caudally in the nucleus retroambiguus. The functions of this group of neurons have some important differences from the functions of the respiratory neurons of the dorsal group.

1. During normal quiet breathing, the respiratory neurons of the ventral group remain almost completely inactive. Normal quiet breathing is caused only by the repetition of inspiratory signals from the dorsal group of respiratory neurons, transmitted mainly to the diaphragm, and exhalation occurs under the influence of elastic traction of the lungs and chest.
2. There is no evidence of the participation of respiratory neurons of the ventral group in the main rhythmic oscillation that regulates breathing.
3. When the impulse causing increased pulmonary ventilation becomes greater than normal, the generation of respiratory signals begins to proceed from the main oscillating mechanism in the dorsal group of neurons to the respiratory neurons of the ventral group. As a result, neurons of the ventral group will participate in the creation of additional impulses. 4. Electrical stimulation of some neurons of the ventral group causes inhalation, stimulation of others causes exhalation. Therefore, this group of neurons is involved in both the creation of inhalation and exhalation. They are especially important for creating powerful expiratory signals transmitted to the abdominal muscles during difficult exhalation. Thus, this group of neurons works primarily as a reinforcing mechanism when a large increase in pulmonary ventilation is required, especially during heavy physical activity.

Hering-Breuer stretch reflex

In addition to the central nervous mechanisms breathing regulation located within the brain stem, signals from receptors in the lungs also take part in the regulation of breathing. The most important are the stretch receptors located in the muscular areas of the walls of the bronchi and bronchioles of all parts of the lungs, which, in the event of overextension of the lungs, transmit signals through the vagus nerves to the dorsal group of respiratory neurons. These signals act on inspiration in the same way as signals from the pneumotaxic center do: when the lungs are overstretched, the stretch receptors activate feedback, which “turns off” the inhalation impulse and pauses inhalation. This is called the Hering-Breuer stretch reflex. The reflex also causes increased breathing, as do signals from the pneumotaxic center.

It appears that the person Hering-Breuer reflex is activated only after the tidal volume increases more than 3 times (becomes more than 1.5 l). It is believed that this reflex is mainly defense mechanism to prevent excessive stretching of the lungs and is not an important component in the normal regulation of breathing.

Distinguish constant and intermittent (episodic) reflex influences on functional state respiratory center.

Constant reflex influences arise as a result of irritation of alveolar receptors ( Hering-Breuer reflex ), lung root and pleura ( pulmothoracic reflex ), chemoreceptors of the aortic arch and carotid sinuses ( Heymans reflex ), proprioceptors respiratory muscles.

The most important reflex is Hering-Breuer reflex. The alveoli of the lungs contain stretch and collapse mechanoreceptors, which are sensitive nerve endings of the vagus nerve. Any increase in the volume of the pulmonary alveoli excites these receptors.

The Hering-Breuer reflex is one of the mechanisms of self-regulation of the respiratory process, ensuring a change in the acts of inhalation and exhalation. When the alveoli are stretched during inhalation, nerve impulses from stretch receptors travel along the vagus nerve to expiratory neurons, which, when excited, inhibit the activity of inspiratory neurons, which leads to passive exhalation. The pulmonary alveoli collapse, and nerve impulses from the stretch receptors no longer reach the expiratory neurons. Their activity decreases, which creates conditions for increasing the excitability of the inspiratory part of the respiratory center and the implementation of active inhalation.

In addition, the activity of inspiratory neurons increases with increasing concentration of carbon dioxide in the blood, which also contributes to the manifestation of inhalation.

Pulmothoracic reflex occurs when the receptors embedded in the lung tissue and pleura. This reflex appears when the lungs and pleura are stretched. The reflex arc closes at the level of the cervical and thoracic segments of the spinal cord.

The respiratory center is constantly supplied nerve impulses from proprioceptors of the respiratory muscles. During inhalation, the proprioceptors of the respiratory muscles are excited and nerve impulses from them enter the inspiratory part of the respiratory center. Under the influence of nerve impulses, the activity of inspiratory neurons is inhibited, which promotes the onset of exhalation.

Fickle reflex influences on the activity of respiratory neurons associated with arousal various extero- and interoreceptors . These include reflexes that arise from irritation of receptors in the mucous membrane of the upper respiratory tract, nasal mucosa, nasopharynx, temperature and pain receptors of the skin, proprioceptors skeletal muscles. For example, if you suddenly inhale vapors of ammonia, chlorine, sulfur dioxide, tobacco smoke and some other substances, irritation of the receptors of the mucous membrane of the nose, pharynx, and larynx occurs, which leads to a reflex spasm of the glottis, and sometimes even the muscles of the bronchi and a reflex holding of breath.

Hering and Breuer reflexes. The change in respiratory phases, i.e., the periodic activity of the respiratory center, is facilitated by signals coming from the mechanoreceptors of the lungs along the afferent fibers of the vagus nerves. After transection of the vagus nerves, which turns off these impulses, breathing in animals becomes rarer and deeper. During inhalation, inspiratory activity continues to increase at the same rate to a new, more high level(Fig. 160). This means that afferent signals coming from the lungs ensure a change from inhalation to exhalation earlier than the respiratory center, deprived of feedback from the lungs, does. After transection of the vagus nerves, the expiratory phase also lengthens. It follows that impulses from the lung receptors also contribute to the replacement of exhalation with inhalation, shortening the expiration phase.

Hering and Breuer (1868) discovered strong and constant respiratory reflexes with changes in lung volume. An increase in lung volume causes three reflex effects. First, the inflation of the lungs during inhalation can stop it prematurely. (inspiratory inhibitory reflex). Secondly, the inflation of the lungs during exhalation delays the onset of the next inhalation, lengthening the expiration phase (expiratory-facilitating reflex). Thirdly, a sufficiently strong inflation of the lungs causes a short (0.1-0.5 s) strong excitation of the inspiratory muscles, and a convulsive inhalation occurs - a “sigh” (paradoxical Head effect).

A decrease in lung volume causes an increase in inspiratory activity and a shortening of exhalation, i.e., it contributes to the onset of the next inhalation (reflex to collapse of the lungs).

Thus, the activity of the respiratory center depends on changes in lung volume. The Hering and Breuer reflexes provide the so-called volumetric feedback respiratory center with the executive apparatus of the respiratory system.

The significance of the Hering and Breuer reflexes is to regulate the ratio of depth and frequency of breathing depending on the condition of the lungs. With preserved vagus nerves, hyperpyoe, caused by hypercapnia or hypoxia, is manifested by an increase in both the depth and frequency of breathing. After turning off the vagus nerves, breathing does not increase; ventilation of the lungs gradually increases only due to an increase in the depth of breathing. As a result, the maximum value of pulmonary ventilation is reduced by approximately half. Thus, signals from lung receptors provide an increase in respiratory rate during hyperpnea, which occurs during hypercapnia and hypoxia.

In an adult, unlike animals, the significance of the Hering and Breuer reflexes is regulation of calm breathing not much. Temporary blockade of the vagus nerves local anesthetics is not accompanied by a significant change in the frequency and depth of breathing. However, the increase in respiratory rate during hyperpnea in humans, as well as in animals, is ensured by the Hering and Breuer reflexes: this increase is turned off by blockade of the vagus nerves.

Hering and Breuer reflexes are well expressed in newborns. These reflexes play important role in shortening the respiratory phases, especially exhalations. Magnitude


Hering and Breuer reflexes decrease in the first days and weeks after birth. The lungs contain numerous endings of afferent nerve fibers. Three groups of lung receptors are known: pulmonary stretch receptors, irritant receptors and juxtaalveolar capillary receptors (j-receptors). There are no specialized chemoreceptors for carbon dioxide and oxygen.

Lung stretch receptors. Excitation of these receptors occurs or increases with increasing lung volume. The frequency of action potentials in stretch receptor afferent fibers increases with inhalation and decreases with exhalation. The deeper the inhalation, the greater the frequency of impulses sent by stretch receptors to the respiratory center. Lung stretch receptors have different thresholds. Approximately half of the receptors are also excited during exhalation, in some of them rare impulses occur even with complete collapse of the lungs, but during inhalation the frequency of impulses in them increases sharply (low threshold receptors). Other receptors are excited only during inhalation, when lung volume increases beyond the functional residual capacity (high threshold receptors). With a prolonged, many seconds, increase in lung volume, the frequency of receptor discharges decreases very slowly (receptors are characterized slow adaptation). The frequency of discharges of lung stretch receptors decreases with increasing carbon dioxide content in the lumen of the airways.

There are about 1000 stretch receptors in each lung. They are located mainly in the smooth muscles of the walls of the airways - from the trachea to the small bronchi. There are no such receptors in the alveoli and pleura.

Increasing lung volume stimulates stretch receptors indirectly. Their immediate irritant is internal tension the walls of the airways, depending on the pressure difference on both sides of their walls. As lung volume increases, elastic traction of the lungs increases. The alveoli tending to collapse stretch the walls of the bronchi in the radial direction. Therefore, the excitation of stretch receptors depends not only on the volume of the lungs, but also on the elastic properties of the lung tissue, on its extensibility. Excitation of receptors in the extrapulmonary airways (trachea and large bronchi) located in the chest cavity is determined mainly by negative pressure in pleural cavity, although it also depends on the degree of contraction of the smooth muscles of their walls.

Irritation of lung stretch receptors causes inspiratory inhibitory reflex of Hering and Breuer. Most of the afferent fibers from the lung stretch receptors are sent to the dorsal respiratory nucleus of the medulla oblongata, the activity of the inspiratory neurons of which changes unequally. About 60% of inspiratory neurons are inhibited under these conditions. They behave in accordance with the manifestation of the inspiratory inhibitory reflex of Hering and Breuer. Such neurons are designated as lex. The remaining inspiratory neurons, on the contrary, are excited when the stretch receptors are stimulated (1p neurons). Probably, neurons 1(3) represent an intermediate authority through which neutrons 1a and inspiratory activity in general are inhibited. It is assumed that they are part of the mechanism for turning off inhalation.

Hering reflex (H.E. Hering, 1866-1948, German physiologist)

slowing of the pulse when holding the breath at the stage of deep inspiration; if in a sitting position this deceleration exceeds 6 beats per minute, then it indicates increased excitability of the vagus nerve.


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

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