External respiration and gas transport by blood. Internal respiration and transport of gases Transport of gases in the human body

Transport of oxygen by blood. Oxygen is transported by blood in two forms - dissolved and combined with hemoglobin. Arterial blood plasma contains very little a large number of physically dissolved oxygen, total

0.3 vol.%, i.e. 0.3 ml of oxygen in 100 ml of blood. The main part of the oxygen enters into a fragile connection with the hemoglobin of erythrocytes, forming oxyhemoglobin. The saturation of blood with oxygen is called oxygenation or arterialization of blood. The blood flowing from the lungs through the pulmonary veins has the same gas composition as arterial blood in the systemic circulation.

The amount of oxygen present in 100 ml of blood, provided that hemoglobin is completely converted to oxyhemoglobin, is called oxygen capacity blood. This value, in addition to the partial pressure of oxygen, depends on the hemoglobin content in the blood. It is known that 1 g of hemoglobin can bind on average 1.34 ml of oxygen. Therefore, knowing the level of hemoglobin in the blood, it is possible to calculate the oxygen capacity of the blood. Thus, in horses, with a hemoglobin content in the blood of about 14 g/100 ml, the oxygen capacity of the blood is (1.34 14) about 19 vol.%, in cattle with a hemoglobin level of 10... 12 g/100 ml - about 13 ...16 vol.%. Having recalculated the oxygen content in the total volume of blood, it turns out that its supply will only be enough for 3...4 minutes, provided that it does not come from the air.

At sea level, with corresponding fluctuations in atmospheric pressure and partial pressure of oxygen in the alveolar air, hemoglobin is almost completely saturated with oxygen. At high altitudes, where atmospheric pressure is low, the partial pressure of oxygen decreases and the oxygen capacity of the blood decreases. The oxygen content in the blood is also affected by blood temperature: with an increase in body temperature, the oxygen saturation of the blood decreases. The high content of hydrogen ions and carbon dioxide in the blood promotes the removal of oxygen from oxyhemoglobin as blood passes through the capillaries great circle blood circulation

The exchange of gases between blood and tissues occurs in the same way as the exchange of gases between blood and alveolar air - according to the laws of diffusion and osmosis. The arterial blood entering here is saturated with oxygen, its tension is 100 mmHg. Art. In tissue fluid, oxygen tension is 20...37 mm Hg. Art., and in cells that consume oxygen, its level drops to 0. Therefore, oxyhemoglobin splits off oxygen, which passes first into the tissue fluid and then into the tissue cells.

During tissue respiration, carbon dioxide is released from cells. It first dissolves in the tissue fluid and creates a voltage there of about 60...70 mm Hg. Art., which is higher than in the blood (40 mm Hg. Art.). The gradient of oxygen tension in the tissue fluid and blood causes the diffusion of carbon dioxide from the tissue fluid into the blood.

Transport of carbon dioxide in the blood. Carbon dioxide is transported in three forms: dissolved, combined with hemoglobin (carbohemoglobin) and in the form of bicarbonates.

Carbon dioxide coming from tissues dissolves slightly in blood plasma - up to 2.5 vol.%; its solubility is slightly higher than that of oxygen. From plasma, carbon dioxide penetrates into red blood cells and displaces oxygen from oxyhemoglobin. Oxyhemoglobin is converted into reduced, or reduced, hemoglobin. The enzyme 4 carbonic anhydrase present in erythrocytes accelerates the combination of carbon dioxide with water and the formation of carbonic acid - H 2 CO 3. This acid is unstable, it dissociates into H + and HCOJ.

Since the erythrocyte membrane is impermeable to H +, it remains in the erythrocytes, and HC0 3 passes into the blood plasma, where it is converted into sodium bicarbonate (NaHC0 3). Part of the carbon dioxide in red blood cells combines with hemoglobin, forming carbohemoglobin, and with potassium cations - potassium bicarbonate (KHC0 3).

In the pulmonary alveoli, where the partial pressure of carbon dioxide is lower than in the venous blood, carbon dioxide dissolved and released during the dissociation of carbohemoglobin diffuses into the alveolar air. At the same time, oxygen enters the blood and binds to reduced hemoglobin, forming oxyhemoglobin. Oxyhemoglobin, being a stronger acid than carbonic acid, displaces carbonic acid from bicarbonates and potassium ions. Carbonic acid breaks down to C0 2 and H 2 0 with the participation of carbonic anhydrase. Carbon dioxide passes from red blood cells into blood plasma and then into the alveolar air (see Fig. 7.6).

Despite the fact that the main part of carbon dioxide is present in the blood plasma in the form of sodium bicarbonate, carbon dioxide is predominantly released into the alveolar air not from the blood plasma, but from red blood cells. The fact is that only red blood cells contain carbonic anhydrase, which breaks down carbonic acid. There is no carbonic anhydrase in the blood plasma, so bicarbonates are destroyed very slowly and carbon dioxide does not have time to escape into the alveolar air (blood passes through the pulmonary capillaries in less than 1 second). Thus, carbon dioxide is in the blood in three forms: dissolved, in the form of carbohemoglobin, bicarbonates, but it is removed through the lungs only in one form - CO 2.

Not all oxygen from arterial blood enters the tissues; some of it passes into venous blood. The ratio of the volume of oxygen absorbed by tissues to its content in arterial blood is called oxygen utilization coefficient. Under conditions of physiological rest, it is about 40%. With more high level metabolism, the oxygen utilization rate increases and its level in the venous blood decreases.

Passing through the lungs, not all carbon dioxide enters the alveolar air; some of it remains in the blood and passes into the arteries.

real blood. Thus, if venous blood contains 58 vol.% carbon dioxide, then arterial blood contains 52 vol.%. The presence of a certain level of oxygen and especially carbon dioxide in arterial blood is of great importance in the processes of regulation of external respiration.

Tissue (intracellular) respiration. Tissue respiration is the process of biological oxidation in the cells and tissues of the body.

Biological oxidation occurs in mitochondria. The internal space of mitochondria is surrounded by two membranes - outer and inner. A large number of enzymes are concentrated on the inner membrane, which has a folded structure. The oxygen entering the cell is spent on the oxidation of fats, carbohydrates and proteins. At the same time, energy is released in the form most accessible to cells, primarily in the form of ATP - adenosine triphosphoric acid. Dehydrogenation reactions (hydrogen release) are of leading importance in oxidative processes.

ATP synthesis occurs during the migration of electrons from the substrate to oxygen through a chain of respiratory enzymes (flavin enzymes, cytochromes, etc.). The released energy accumulates in the form of high-energy compounds (for example, ATP), and the end products of the reactions are water and carbon dioxide.

Along with oxidative phosphorylation, oxygen can be used in some tissues by direct introduction into the oxidized substance. This oxidation is called microsomal, because it occurs in microsomes - vesicles formed by the membranes of the endoplasmic reticulum of the cell.

Tissues and organs have different needs for oxygen: the brain, especially the cerebral cortex, liver, heart, and kidneys absorb oxygen from the blood more intensively. Blood cells, skeletal muscles, and the spleen consume less oxygen at rest. During exercise, oxygen consumption increases. For example, during heavy muscular work, skeletal muscles consume 40 times more oxygen, cardiac muscle - 4 times (per 1 g of tissue).

Even within the same organ, oxygen consumption can vary dramatically. For example, in the cortical part of the kidneys it is 20 times more intense than in the brain part. This depends on the structure of the tissue, the density of distribution of blood capillaries in it, the regulation of blood flow, the oxygen utilization rate and a number of other factors. It should be remembered that the more cells consume oxygen, the more metabolic products - carbon dioxide and water - are formed.

7.4. REGULATION OF BREATHING

The main biological function of respiration is to ensure gas exchange in tissues. It is for the sake of tissue respiration that the circulatory and external respiration systems arose and improved in the process of evolution. The delivery of oxygen to tissues and the removal of hydrogen ions and carbon dioxide must precisely correspond to the needs of the tissues and the body at a certain period of their life. Participating in the implementation of these processes and their dynamic equilibrium are: complex mechanisms, including regulation of blood gas composition, regional blood circulation and tissue trophism. In this chapter we will look at how the body maintains a certain level of oxygen and carbon dioxide in the blood, that is, how the respiratory cycles, depth and frequency of breathing are regulated.

External respiration is regulated by neurohumoral mechanisms. Back in 1885, the Russian physiologist N.A. Mislavsky discovered in medulla oblongata respiratory center and proved the presence of two sections in it - the center of inhalation and the center of exhalation. Through centrifugal (efferent) pathways, the respiratory center is connected with effectors - the respiratory muscles. Afferent, or sensory, or centripetal, impulses enter the respiratory center from various extero- and interoreceptors, as well as from overlying parts of the brain. Thus, in a rather simplified form general scheme one can imagine a typical reflex arc consisting of receptors, afferent pathways, a nerve center, efferent pathways and effectors - the respiratory muscles.

Respiratory center. The respiratory center is a collection of neurons located in all parts of the central nervous system and taking one or another part in the regulation of breathing. The main part, or as they say, “core” respiratory center, is located, as Mislavsky experimentally proved, in the medulla oblongata, in the region of the reticular formation at the bottom of the fourth cerebral ventricle. Without this department, breathing is impossible, damage to the medulla oblongata inevitably leads to death due to respiratory arrest.

There is no clear morphological division between the centers of inhalation and exhalation in the medulla oblongata, but there is a distribution of functions between neurons: some neurons - inspiratory - generate action potentials that excite the inspiratory muscles, others - expiratory - excite the expiratory muscles.

In inspiratory neurons, electrical activity turns on quickly, the impulse frequency gradually increases (up to 70... 100 impulses per 1 s) and drops sharply towards the end of inspiration. This impulse causes the diaphragm to contract,

intercostal and other inspiratory muscles. “Switching off” the inspiratory neurons leads to relaxation of the inspiratory muscles and exhalation. The activity of expiratory neurons is less important during normal quiet breathing. But with increased breathing, especially with forced exhalation, expiratory neurons determine the contraction of the expiratory muscles.

The bulbar section of the respiratory center of the brain is automatic. This unique feature of the respiratory center is that its neurons can spontaneously, that is, spontaneously, without any external influences, depolarize or discharge. For the first time, spontaneous fluctuations in the electrical activity of the respiratory center were discovered by I.M. Sechenov. The nature of the automaticity of the respiratory center has not yet been clarified. It probably depends on the specific metabolism of neurons in this area of ​​the brain and the special sensitivity of inspiratory neurons to the environment and the composition of the cerebrospinal fluid. The automaticity of the respiratory center is preserved after its almost complete deafferentation, that is, after the cessation of influences from various receptors.

Thanks to automation, the respiratory center of the medulla oblongata provides rhythmic alternations of inhalation and exhalation and determines the respiratory rate under conditions of physiological rest.

The bulbar section of the respiratory center is the most resistant section of the central nervous system to the effects of narcotic drugs. Even with deep anesthesia, when there are no reflex reactions, spontaneous breathing remains. The arsenal of pharmacological drugs includes substances that selectively increase the excitability of the respiratory center - lobelia, cititon, which act on the respiratory center reflexively, through receptors in the sinocarotid zone.

I.P. Pavlov said that the respiratory center, which was previously thought to be the size of a pinhead, has grown unusually: it went down into the spinal cord and rose up to the cerebral cortex.

What role do other parts of the respiratory center play? The spinal cord contains neurons (motoneurons) that innervate the respiratory muscles (Fig. 7.7). Excitation to them is transmitted from inspiratory and expiratory neurons of the medulla oblongata along descending pathways lying in the white matter spinal cord. Unlike the boulevard center, spinal cord motor neurons do not have automaticity. Therefore, after transection of the spinal cord immediately behind the medulla oblongata, breathing stops, since the respiratory muscles do not receive the command to contract. If the spinal cord is cut at the level of the 4th...5th cervical vertebra, then independent

Rice. 7.7. Scheme of organization of the central respiratory regulation apparatus

breathing is maintained due to contractions of the diaphragm, because the center of the phrenic nerve is located in the 3...5-M cervical segments of the spinal cord.

Above the medulla oblongata, adjacent to it, is the pons, in which the “pneumotaxic center” is located. It does not have automaticity, but thanks to continuous activity it ensures periodic respiratory activity.

central center, increases the rate of development of inspiratory and expiratory impulses in the neurons of the medulla oblongata.

Midbrain It has great importance in the regulation of striated muscle tone. Therefore, when various muscles contract, afferent impulses from them enter the midbrain, which changes the nature of breathing according to the muscle load. The midbrain is also responsible for coordinating breathing with the acts of swallowing, vomiting and regurgitation. During swallowing, breathing is held during the exhalation phase, the epiglottis closes the entrance to the larynx. When vomiting or regurgitating gases, an “idle inhalation” occurs - inhalation with the larynx closed. At the same time, intrapleural pressure is greatly reduced, which promotes the flow of contents from the stomach into the thoracic part of the esophagus.

The hypothalamus is a part of the diencephalon. The importance of the hypothalamus in the regulation of breathing lies in the fact that it contains centers that control all types of metabolism (protein, fat, carbohydrate, mineral), and a heat regulation center. Therefore, increased metabolism and increased body temperature lead to increased breathing. For example, when body temperature rises, breathing becomes more frequent, which increases heat transfer along with exhaled air and protects the body from overheating (thermal shortness of breath).

The hypothalamus takes part in changing the nature of the breath
Hania with painful stimuli, with various behavioral
certain acts (feeding, sniffing, mating, etc.). By
past the regulation of the frequency and depth of breathing by the hypothalamus through
the autonomic nervous system regulates the lumen of the bronchioles,
collapse of non-functioning alveoli, degree of expansion
pulmonary vessels, permeability of the pulmonary epithelium and walls
capillaries. /

The importance of the cerebral cortex in the regulation of breathing is multifaceted. The cortex contains the central sections of all analyzers that provide information about external influences, and about the state of the internal environment of the body. Therefore, the most subtle adaptation of breathing to the immediate needs of the body is carried out with the obligatory participation of the higher departments nervous system.

Special meaning has a cerebral cortex during muscular work. It is known that increased breathing begins a few seconds before the start of work, immediately after the command “get ready.” A similar phenomenon is observed in sports horses along with tachycardia. The reason for such “anticipatory” reactions in people and animals is conditioned reflexes developed as a result of repeated training. Only the influence of the cerebral cortex can explain voluntary, volitional changes in the rhythm, frequency and depth of breathing. A person can voluntarily hold his breath for a few seconds or increase

his. The role of the cortex in changing the breathing pattern during vocalization, diving, and sniffing is undoubted.

So, the respiratory center is involved in the regulation of external respiration. The nucleus of this center, located in the medulla oblongata, sends rhythmic impulses through the spinal cord to the respiratory muscles. The boulevard section of the respiratory center itself is under constant influence from the overlying sections of the central nervous system and various receptors - pulmonary, vascular, muscle, etc.

The importance of lung receptors in the regulation of breathing. IN the lungs have three groups of receptors: stretch and contraction; irritant; juxtacapillary.

Stretch receptors are located between the smooth muscles in the airways - around the trachea, bronchi and bronchioles, and are absent in the alveoli and pleura. Stretching the lungs during inhalation causes excitation of mechanoreceptors. The resulting action potentials are transmitted along the centripetal fibers of the vagus nerve to the medulla oblongata. Towards the end of inspiration, the impulse frequency increases from 30 to 100 impulses per 1 s and becomes pessimal, causing inhibition of the inspiratory center. Exhalation begins. Receptors for lung collapse have not been sufficiently studied. Perhaps, with quiet breathing, their significance is small.

Reflexes from the mechanoreceptors of the lungs are named after the scientists who discovered them - Hering-Breuer reflexes. The purpose of these reflexes is as follows: to inform the respiratory center about the state of the lungs, their filling with air and, in accordance with this, regulate the sequence of inhalation and exhalation, limit excessive stretching of the lungs when inhaling or collapse of the lungs when exhaling. In newborns, reflexes from the mechanoreceptors of the lungs play an important role; with age their importance decreases.

Thus, the importance of the vagus nerve in the regulation of breathing lies in the transmission of afferent impulses from the mechanoreceptors of the lungs to the respiratory center. In animals, after transection of the vagus, information from the lungs does not reach the medulla oblongata, so breathing becomes slow, with a short inhalation and a very long exhalation (Fig. 7.8). When the vagus is irritated, breathing is held, depending on what phase of the respiratory

cycle, irritation acts. If irritation occurs during inhalation, then inhalation stops prematurely and is replaced by exhalation, and if it coincides with the exhalation phase, then, on the contrary, exhalation is replaced by inhalation (Fig. 7.9).

Irritant receptors are located in the epithelial and subepithelial layers of all airways. They become irritated when dust, toxic gases enter the airways, as well as when there are sufficiently large changes in lung volume. Some of the irritant receptors are excited during normal inhalations and exhalations. Reflexes from irritant receptors are protective in nature - sneezing, coughing, deep breathing (“sigh”). The centers of these reflexes are located in the medulla oblongata.

Juxtacapillary receptors (juxta - around) are located near the capillaries of the pulmonary circulation. In function, they are similar to collapse receptors; for them, the irritant is an increase in the interstitial space of the lungs, for example, during edema. Irritation of juxtacapillary receptors causes shortness of breath. It is possible that with intense muscular work, blood pressure in the pulmonary vessels increases, this increases the volume of interstitial fluid and stimulates the activity of juxtacapillary receptors. The irritant of pulmonary receptors can be histamine, synthesized in basophils and mast cells. There are quite a lot of these cells in the lungs, and when allergic diseases they release histamine in such quantities that it leads to swelling and shortness of breath.

The importance of respiratory muscle receptors. The respiratory muscles have stretch receptors - muscle spindles, tendon receptors. The density of their placement is especially high in the intercostal muscles and muscles of the abdominal walls. Mechanoreceptors of the respiratory muscles are excited when they contract or stretch during inhalation or exhalation. According to principle feedback they regulate the excitation of spinal cord motor neurons depending on their initial length and the resistance they encounter.

Tea when contracting. Severe irritation of mechanoreceptors chest(for example, when it is compressed) causes inhibition of the inspiratory activity of the respiratory center.

The importance of chemoreceptors in the regulation of respiration. The gas composition of arterial blood is extremely important in the regulation of external respiration. The biological expediency of this is quite understandable, since the exchange of gases between blood and tissues depends on the content of oxygen and carbon dioxide in arterial blood. Frederick's (1890) experiments with cross-circulation have long become classics, when arterial blood from one dog entered the blood of another, and venous blood from the head of the second dog entered the venous blood of the first dog (Fig. 7.10). If you compress the trachea and thereby stop the breathing of the first dog, then its blood with insufficient oxygen and excess carbon dioxide washes the brain of the second dog. The respiratory center of the second dog increases breathing (hyper-pnea), and the concentration of carbon dioxide in its blood decreases and breathing slows down until it stops (apnea).

Thanks to Frederick's experiments, it became obvious that the respiratory center is sensitive to the level of gases in the arterial blood. The increased concentration of carbon dioxide (hypercapnia) and hydrogen ions in the blood causes increased respiration, as a result of which carbon dioxide is released with exhaled air and its concentration in the blood is restored. A decrease in the level of carbon dioxide in the blood (hypocapnia), on the contrary, causes a decrease in breathing or a stop until the concentration of carbon dioxide in the blood reaches a normal value again (normocapnia).

The concentration of oxygen in the blood also affects the excitability of the respiratory center, but to a lesser extent than carbon dioxide. This is due to the fact that with normal fluctuations in atmospheric pressure, even at altitudes up to 2000 m above sea level, almost all hemoglobin is converted into oxyhemoglobin, therefore the partial pressure of oxygen in arterial blood is always higher than in tissue fluid, and tissues receive, in any case case in

state of physiological rest, enough oxygen. With a significant decrease in the partial pressure of oxygen in the air, the oxygen content in the blood (hypoxemia) and tissues (hypoxia) decreases, as a result of which the excitability of the respiratory center increases and breathing becomes more frequent.

Decrease in acid concentration Fig. 7.10. Cross circulation of blood in the blood (hypoxemia) MO-

It can also occur due to more intensive consumption of its tissues. In this case, oxygen deficiency may develop, which, in turn, will cause increased external respiration. When the oxygen content in the blood increases, for example, when inhaling a gas mixture with a high oxygen content or when being in a pressure chamber under high atmospheric pressure, ventilation of the lungs decreases due to depression of the respiratory center.

We examined separately the value of oxygen and carbon dioxide content in arterial blood, i.e. analytically. However, in reality, both gases affect the respiratory center simultaneously. It has been established that hypoxia increases the sensitivity of the respiratory center to increased levels of carbon dioxide, and increased breathing under these conditions is an integral reaction of the respiratory center in response to changes in the gas composition of the blood. Thus, during physical work, more oxygen enters the muscles from the inflowing blood, the oxygen utilization rate increases, and its concentration in the blood decreases. At the same time, as a result of increased metabolism, more carbon dioxide and organic acids enter the blood from the muscles.

The role of vascular chemoreceptors during the first breath of a newborn is great. A decrease in oxygen content in the blood and an increase in carbon dioxide during childbirth, especially after clamping the umbilical cord, is the main irritant of the respiratory center, which causes the first breath.

If you voluntarily increase your breathing as much as possible within 1 minute and thereby cause hyperventilation of the lungs, then the respiratory pause between exhalation and subsequent inhalation will noticeably lengthen. Short-term apnea may occur - breathing stops for 1...2 minutes. Without previous hyperventilation, you can hold your breath only for 20...30 s. Such hyperventilation of the lungs followed by apnea is caused by divers - pearl or sponge hunters. After long training, they remain under water for up to 4...5 minutes.

Let's try to understand the mechanisms of apnea after shortness of breath. Since during normal quiet breathing the blood is 95% saturated with oxygen, increased breathing does not lead to a significant increase in the concentration of oxygen in the blood. Hyperventilation has a noticeable effect on the carbon dioxide content - the level of carbon dioxide decreases first in the alveolar air and then in the blood. Consequently, apnea after hyperventilation is associated with a decrease in the concentration of carbon dioxide in the blood. Breathing will resume when sufficient, or threshold, levels of carbon dioxide have again accumulated in the blood.

If you hold your breath for 20...30 seconds, then an uncontrollable urge to sigh and make several deep breathing movements sets in. Consequently, the delay leads to hyperpnea - increased

breathing. This is also due to the accumulation of carbon dioxide in the blood, since in 20...30 s the oxygen concentration in the blood will decrease slightly, and carbon dioxide constantly enters the blood from the tissues.

So, carbon dioxide is the main humoral irritant of the respiratory center. A change in its concentration in the blood leads to changes in the frequency and depth of breathing that restore a constant level of carbon dioxide in the blood. When the level of carbon dioxide in the blood increases, the respiratory center is stimulated and breathing increases; when it decreases, the frequency and depth of breathing decreases. This is why the mouth-to-mouth method of artificial respiration is so effective, and carbon dioxide must be added to gas mixtures for artificial respiration.

Where are the sensors or receptors that detect the concentration of gases in the blood? They are located where careful control over the gas composition of the internal environment of the body is necessary. Such areas are the vascular reflexogenic zones of the carotid sinus and aorta, as well as the central reflexogenic zones in the medulla oblongata.

The sinocarotid zone, or carotid sinus zone, is particularly important in monitoring blood gases and pH. It is located in the branching area carotid arteries into external and internal branches, from where arterial blood is sent to the brain. The threshold concentration of oxygen, carbon dioxide and hydrogen ions for the receptors of the sinocarotid zone corresponds to their level in the blood under normal conditions at rest. A slight excitation occurs in individual receptors with rare deep breathing when the concentration of gases in the blood begins to change slightly. The more the gas composition of the blood changes, the higher the frequency of impulses occurs in the chemoreceptors, stimulating the respiratory center.

Changes in respiratory movements occur not only with irritation of the chemoreceptors of the aorta or carotid sinus. Irritation of the baro- or pressoreceptors located here when blood pressure increases usually leads to a slowdown in breathing, and when blood pressure decreases, to an increase in it. However, when physical activity An increase in blood pressure does not lead to respiratory depression or depressor reflexes.

Central (medullary) chemoreceptors in the medulla oblongata are sensitive to the level of carbon dioxide in the cerebrospinal fluid. If arterial chemoreceptors regulate the gas composition of arterial blood, then central chemoreceptors keep under control the gas and acid-base homeostasis of the fluid washing the brain, the most vulnerable tissue of the body. Chemoreceptors sensitive to

changes in pH, carbon dioxide and oxygen are also present in the venous vessels and in various tissues of the body. However, their significance lies not in the regulation of external respiration, but in changing the regional, or local, blood flow.

Of great interest are the mechanisms of changes in breathing during physical work: with heavy loads, the frequency and strength of respiratory movements increase, which leads to hyperventilation of the lungs. What causes this? Increased tissue respiration in the muscles leads to the accumulation of lactic acid up to 10...200 mg/100 ml of blood (instead of 15...24 normally) and a lack of oxygen for oxidative processes. This condition is called oxygen debt. Lactic acid, being a stronger acid than carbonic acid, displaces carbon dioxide from blood bicarbonates, resulting in hypercapnia, which increases the excitability of the respiratory center.

Further, during muscular work, various receptors are excited: proprioceptors of muscles and tendons, mechanoreceptors of the lungs and airways, chemoreceptors of vascular reflexogenic zones, heart receptors, etc. From these and other receptors, afferent impulses also reach the respiratory center. During muscular work, the tone of the sympathetic nervous system increases, the content of catecholamines in the blood increases, which stimulate the respiratory center both reflexively and directly. During muscle work, heat production increases, which also leads to increased breathing (thermal shortness of breath).

Irritation of various exteroceptors leads to the formation of conditioned reflexes. The environment in which work is usually performed (racetrack, landscape, bridling, appearance of the rider, and time of day) is a complex pattern of stimulation that prepares the horse for subsequent work. Along with various behavioral acts, the animal’s heart function increases in advance, blood pressure rises, breathing changes, and other vegetative changes occur.

At the beginning of work, energy is supplied to the muscles through anaerobic processes. In the future, this turns out to be insufficient and then a new stationary state (“second wind”) arises, in which ventilation of the lungs, systolic and cardiac output, and blood flow in working muscles increase.

Thus, the regulation of respiration includes two mechanisms: regulation of external respiration, aimed at ensuring optimal oxygen and carbon dioxide content in the blood, i.e. adequate to tissue metabolism, and regulation of blood circulation, creating best conditions exchange of gases between blood and tissues.

In the regulation of inhalation and exhalation, the automation of the respiratory center and afferent impulses from the mechanoreceptors of the lungs and respiratory muscles are of greater importance, and in the regulation of the frequency and depth of breathing - the gas composition of the blood, cerebrospinal fluid and afferent impulses from chemoreceptors blood vessels, tissues and medullary (bulbar) chemoreceptors.

When studying external respiration, the following concepts are used:

Alveolar air– contained in the alveoli after normal exhalation;

Exhaled air– the first portions of exhaled air are a mixture of alveolar air and dead space air.

Air composition in %

As a result of gas exchange between blood and alveolar air, venous blood is converted into arterial blood.

Factors determining the diffusion of gases in the lungs.

I Alveolar-capillary gradient.

II Ratio of ventilation to perfusion.

III Perfusion path length.

IV Diffusion capacity of gases.

V Diffusion area.

1) The difference between partial pressure and voltage.

Partial pressure is the part of the pressure of a mixture of gases that falls on the share of one gas.

Partial pressure depends on:

b) on the value of total pressure: Calculated using the following formula.

For example O 2 in atmospheric air

100% gas – 760mm Hg. Art.

x = 159 mm Hg. Art. in atmospheric air.

When calculating the partial pressure of gas in the alveolar air, it is necessary to take into account the pressure of water vapor located there = 47 mm Hg. Art.

Gas partial voltage is the force with which a gas dissolved in a liquid tends to leave it. Typically, a dynamic equilibrium is established between the gas in the liquid and above the liquid.

In the pulmonary circulation, O 2 goes into the venous blood from the lungs, and CO 2 from the blood into the lungs.

The driving force is the alveolar-capillary gradient.

For O 2 AKG = 60 mm Hg. Art., for CO 2 – 6 mm Hg. Art. Those. The diffusion properties of CO2 are higher than those of O2.

2) Ratio of ventilation to perfusion= MAV/MOK = 4 – 6 / 4.5 – 5 = 0.8 – 1.1 – normal.

Ventilation and perfusion of the lungs must be consistent with each other. However, the distribution of blood flow throughout the lungs in humans is not uniform. Depends on the position of the body and changes under the influence of gravity. In a vertical position, the Q value of blood flow per unit volume of tissue decreases almost linearly from bottom to top and the apices of the lungs are less supplied with blood. Lying down, blood flow in the apex increases, but does not change at the base. However, when lying on your back, the blood flow in the posterior parts of the lungs is higher than in the anterior ones.

During work, the blood flow is approximately the same in all departments.

The vertical position also affects ventilation. Its intensity increases from top to bottom (as does blood flow).

However, HPEs are not uniform across departments.

Mechanisms that adapt blood flow to ventilation are vasomotor and bronchomotor reactions to changes in the gas composition of alveolar air.

Vasoconstriction with a decrease in pO 2 in the alveoli, or PCO 2.

Bronchoconstriction at ↓ РСО 2 in alveolar air.

HPO is affected by:

a) uneven ventilation of the lungs in different positions of the body in space;

b) the nature of pulmonary blood flow depending on the position of the body and the activity of the body;

c) blood flow speed

3) Path length.

CO 2; O 2 pass along the path: alveolar wall + intercellular space + basement membrane of the capillary + endothelium of the capillary + plasma layer + erythrocyte membrane. Increased path length – deterioration of blood oxygenation – inverse relationship.

5) Diffusion area– depends on the surface of the alveoli and capillaries through which diffusion occurs (direct relationship).

Let's consider the process of gas exchange in the lungs. In the lungs, gas exchange occurs between the air entering the alveoli and the blood flowing through the capillaries (Fig. 11). Intense gas exchange between the air of the alveoli and the blood is facilitated by the small thickness of the so-called air-blood barrier. This barrier between air and blood is formed by the wall of the alveoli and the wall of the blood capillary. The thickness of the barrier is about 2.5 microns. The walls of the alveoli are built of single-layer squamous epithelium (alveolocytes), covered from the inside, from the lumen of the alveoli, with a thin film of phospholipid, proteins and glycoproteins - surfactant, secreted by type 2 pneumocytes. Surfactant prevents alveoli from sticking together during exhalation and reduces surface tension at the air-liquid interface. It also prevents fluid from the blood from leaking into the alveoli. By “lubricating” the alveoli from the inside, the surfactant protects the lung tissue from penetration through air-blood barrier microorganisms, dust particles, etc. The alveoli are intertwined with a dense network of blood capillaries, which greatly increases the area over which gas exchange occurs between air and blood.

In the inhaled air - in the alveoli, the concentration (partial pressure) of oxygen is much higher (100 mm Hg) than in the venous blood (40 mm Hg) flowing through the pulmonary capillaries. Therefore, oxygen easily leaves the alveoli into the blood, where it quickly combines with the hemoglobin of red blood cells. At the same time, carbon dioxide, the concentration of which in the venous blood of the capillaries is high (47 mm Hg), diffuses

Fig. 11. Diagram of the exchange of gases between the blood and air of the alveoli: 1 - lumen of the alveoli, 2 - wall of the alveoli, 3 - wall of the blood capillary, 4 - lumen of the capillary, 5 - red blood cell in the lumen of the capillary.

The arrows show the path of oxygen (O 2), carbon dioxide (CO 2) through the aerohematic barrier between blood and air

into the alveoli, where the partial pressure of CO 2 is much lower (40 mm Hg). Carbon dioxide is removed from the alveoli of the lung with exhaled air.

Thus, the difference in pressure (or rather, tension) of oxygen and carbon dioxide in the alveolar air, in arterial and venous blood allows oxygen to diffuse from the alveoli into the blood, and carbon dioxide from the blood into the alveoli.

In the body, gas exchange of O 2 and CO 2 through the alveolar-capillary membrane, as mentioned above, occurs through diffusion. Diffusion of O 2 and CO 2 through the airborne barrier depends on the following factors: ventilation of the respiratory tract; mixing and diffusion of gases in the alveolar ducts and alveoli; mixing and diffusion of gases through the airborne barrier, the membrane of erythrocytes and the plasma of alveolar capillaries; chemical reaction gases with various components of blood, and finally from blood perfusion of the pulmonary capillaries.

Diffusion of gases through the alveolar-capillary membrane of the lungs occurs in two stages. At the first stage, the diffusion transfer of gases occurs along a concentration gradient through a thin aerohematic barrier, at the second stage, gases are bound in the blood of the pulmonary capillaries, the volume of which is 80-150 ml, with a thickness of the blood layer in the capillaries of only 5-8 microns and a blood flow velocity of about 0 .1 mm/s. After overcoming the airborne barrier, the gases diffuse through the blood plasma into the red blood cells.

A significant obstacle to O2 diffusion is the erythrocyte membrane. Blood plasma practically does not interfere with the diffusion of gases, in contrast to the alveolar-capillary membrane and the membrane of erythrocytes.

The general laws of the diffusion process can be expressed in accordance with Fick's law by the following formula:

M/t = ∆P/X ∙C ∙ K ∙ α,

where M is the amount of gas, t is time, M/t is the diffusion rate, ∆P is the difference in the partial pressure of gas at two points, X is the distance between these points, C is the gas exchange surface, K is the diffusion coefficient, α is the gas solubility coefficient .

In the lungs, ∆P is the gas pressure gradient in the alveoli and in the blood of the pulmonary capillaries. The permeability of the alveolar-capillary membrane is directly proportional to the contact area between functioning alveoli and capillaries (C), diffusion and solubility coefficients (K and α).

The anatomical and physiological structure of the lungs creates extremely favorable conditions for gas exchange: the respiratory zone of each lung contains about 300 million alveoli and approximately the same number of capillaries, has an area of ​​40-140 m2, with a thickness of the air-hematic barrier of only 0.3-1.2 microns.

Features of gas diffusion through the airborne barrier are quantitatively characterized through the diffusion capacity of the lungs.

For O2, the diffusion capacity of the lungs is the volume of gas transferred from the alveoli to the blood per minute with an alveolar-capillary gas pressure gradient of 1 mm Hg. Art. According to Fick's law, the diffusion capacity of the airborne barrier membrane is inversely proportional to its thickness and molecular weight of the gas and directly proportional to the area of ​​the membrane and, in particular, to the solubility coefficient of O 2 and CO 2 in the liquid layer of the alveolar-capillary membrane.

Oxygen transport occurs in physically dissolved and chemically bound form. Physical processes, i.e., gas dissolution, cannot provide the body’s demands for 0 2 . It is estimated that physically dissolved O 2 can support normal O 2 consumption in the body (250 ml/min) if the minute volume of blood circulation is approximately 83 L/min at rest. The most optimal mechanism is the transport of O2 in a chemically bound form.

According to Fick's law, O2 gas exchange between alveolar air and blood occurs due to the presence of an O2 concentration gradient between these media. In the alveoli of the lungs, the partial pressure of O 2 is 13.3 kPa, or 100 mm Hg. Art., and in the venous blood flowing to the lungs the partial tension of O 2 is approximately 5.3 kPa, or 40 mm Hg. Art. The pressure of gases in water or in the tissues of the body is designated by the term “gas tension” and is designated by the symbols Po 2, Pco 2. O 2 gradient on the alveolar-capillary membrane, equal to an average of 60 mm Hg. Art., is one of the most important, but not the only, according to Fick’s law, factors in the initial stage of diffusion of this gas from the alveoli into the blood.

O2 transport begins in the capillaries of the lungs after its chemical binding to hemoglobin.

Hemoglobin (Hb) is capable of selectively binding O 2 and forming oxyhemoglobin (HbO 2) in an area of ​​high O 2 concentration in the lungs and releasing molecular O 2 in an area of ​​low O 2 content in tissues. In this case, the properties of hemoglobin do not change and it can perform its function for a long time.

Due to the special property of hemoglobin to combine with oxygen and carbon dioxide, the blood is able to absorb these gases in significant quantities. 100 ml of arterial blood contains up to 20 ml of oxygen and up to 52 ml of carbon dioxide. One hemoglobin molecule is capable of attaching four oxygen molecules to itself, forming the unstable compound oxyhemoglobin. It is known that 1 ml of hemoglobin binds 1.34 ml of oxygen. 100 ml of blood contains 15 g of hemoglobin.

The dependence of the degree of oxygenation of hemoglobin on the partial pressure of oxygen in the alveolar air is graphically represented

Fig. 12. Whole blood oxyhemoglobin dissociation curve.

A - the effect of changes in blood pH on the affinity of hemoglobin for oxygen; B - the effect of temperature changes on the affinity of hemoglobin for oxygen. Curves 1-6 correspond to temperatures of 0,10,20,30,38 and 43 degrees C.

in the form of an oxyhemoglobin dissociation curve, or saturation curve (Fig. 12). The plateau of the dissociation curve is characteristic of oxygenated (saturated) arterial blood, and the steep descending part of the curve is characteristic of venous, or desaturated, tissue blood.

The affinity of oxygen for hemoglobin is influenced by various metabolic factors, which is expressed as a shift of the dissociation curve to the left or right. The affinity of hemoglobin for oxygen is regulated by the most important factors of tissue metabolism: PO 2, pH, temperature and intracellular concentration of 2,3-diphosphoglycerate. The pH value and CO 2 content in any part of the body naturally change the affinity of hemoglobin for O 2: a decrease in blood pH causes a shift of the dissociation curve, respectively, to the right (the affinity of hemoglobin for 0 2 decreases), and an increase in blood pH causes a shift of the dissociation curve to the left (the affinity of hemoglobin for O 2 increases). O 2) (Fig. 12, A). For example, the pH in red blood cells is 0.2 units lower than in blood plasma. In tissues, due to the increased CO 2 content, the pH is also lower than in blood plasma. The effect of pH on the oxyhemoglobin dissociation curve is called the “Bohr effect”.

An increase in temperature reduces the affinity of hemoglobin for O 2. In working muscles, an increase in temperature promotes the release of 0 2 . A decrease in tissue temperature or 2,3-diphosphoglycerate content causes a shift to the left in the oxyhemoglobin dissociation curve (Fig. 12, B).

Metabolic factors are the main regulators of the binding of O 2 to hemoglobin in the capillaries of the lungs, when the level of O 2, pH and CO 2 in the blood increases the affinity of hemoglobin for O 2 along the pulmonary capillaries. Under the conditions of body tissues, these same metabolic factors reduce the affinity of hemoglobin for O2 and promote the transition of oxyhemoglobin to its reduced form - deoxyhemoglobin. As a result, O 2 flows along a concentration gradient from the blood of tissue capillaries to the body tissues.

Carbon monoxide (II) - CO, is able to combine with the iron atom of hemoglobin, changing its properties and reaction with O 2. The very high affinity of CO for hemoglobin (200 times higher than that of O 2) blocks one or more iron atoms in the heme molecule, changing the affinity of hemoglobin for O 2.

The oxygen capacity of the blood refers to the amount of O 2 that is bound by the blood until hemoglobin is completely saturated. With a hemoglobin content in the blood of 8.7 mmol/l, the oxygen capacity of the blood is 0.19 ml O 2 in 1 ml of blood (temperature O ° C and barometric pressure 760 mm Hg or 101.3 kPa). Size oxygen capacity blood determines the amount of hemoglobin, 1 g of which binds 1.36-1.34 ml O 2. Human blood contains about 700-800 g of hemoglobin and can thus bind almost 1 liter 0 2.

Hemoglobin in red blood cells can combine with other gases. For example, hemoglobin combines with carbon monoxide, which is formed during incomplete combustion of coal or other fuel, 150-300 times faster than with oxygen. In this case, a fairly strong compound, carboxyhemoglobin, is formed. Therefore, even with a low content of carbon monoxide (CO) in the air, hemoglobin combines not with oxygen, but with carbon monoxide. At the same time, the supply of oxygen to the body and its transport to cells and tissues are disrupted and stopped. A person under these conditions suffocates and may die due to lack of oxygen supply to the body tissues.

Insufficient oxygen supply to tissues (hypoxia) can occur when there is a lack of oxygen in the inhaled air, for example in the mountains. A decrease in hemoglobin content in the blood - anemia - occurs when the blood cannot carry oxygen (in case of carbon monoxide poisoning).

When breathing stops or stops, suffocation (asphyxia) develops. This condition can happen due to drowning or other unexpected circumstances, if foreign body into the respiratory tract (talking while eating), with swelling vocal cords in connection with the disease. Food particles can be removed from respiratory tract reflex cough (cough impulse), resulting from irritation of the mucous membrane of the respiratory tract, primarily the larynx.

In case of respiratory arrest (drowning, electric shock, gas poisoning), when the heart is still beating, artificial respiration is performed using special devices, and in their absence, mouth-to-mouth, mouth-to-nose, or by compressing the chest.

In the tissues of the body, as a result of continuous metabolism and intense oxidative processes, oxygen is consumed and carbon dioxide is formed. When blood enters the tissues of the body, hemoglobin gives oxygen to cells and tissues. Carbon dioxide formed during metabolism passes (diffuses) from tissues into the blood and joins hemoglobin. In this case, a fragile compound - carbhemoglobin - is formed. The rapid combination of hemoglobin with carbon dioxide is facilitated by the enzyme carbonic anhydrase found in red blood cells.

The supply of CO 2 in the lungs from the blood to the alveoli is ensured from the following sources: 1) from CO 2 dissolved in the blood plasma (5-10%); 2) from hydrocarbonates (80-90%); 3) from carbamine compounds of erythrocytes (5-15%), which are capable of dissociating.

For CO 2, the solubility coefficient in the membranes of the air-hematic barrier is greater than for O 2, and averages 0.231 mmol/l ∙ Pa, therefore CO 2 diffuses faster than O 2. This position is true only for the diffusion of molecular CO 2. Most of the CO 2 is transported in the body in a bound state in the form of bicarbonates and carbamine compounds, which increases the CO 2 exchange time spent on the dissociation of these compounds.

In venous blood flowing to the capillaries of the lungs, the CO 2 tension averages 46 mm Hg. Art. (6.1 kPa), and in the alveolar air the partial pressure of CO 2 is on average 40 mm Hg. Art. (5.3 kPa), which ensures the diffusion of CO 2 from the blood plasma into the alveoli of the lungs along a concentration gradient.

The capillary endothelium is permeable only to molecular CO 2 as a polar molecule (O = C = O). Molecular CO 2 physically dissolved in the blood plasma diffuses from the blood into the alveoli. In addition, CO 2 diffuses into the alveoli of the lungs, which is released from the carbamine compounds of erythrocytes due to the oxidation reaction of hemoglobin in the capillaries of the lung, as well as from bicarbonates of the blood plasma as a result of their rapid dissociation with using the enzyme carbonic anhydrase contained in red blood cells.

Molecular CO 2 passes the air-hematic barrier and then enters the alveoli.

Normally, after 1 s, the concentrations of CO 2 on the alveolar-capillary membrane are equalized, so in half the time of capillary blood flow, a complete exchange of CO 2 occurs through the air-hematic barrier. In reality, equilibrium occurs somewhat more slowly. This is due to the fact that the transfer of CO 2, like O 2, is limited by the perfusion rate of the lung capillaries.

The process of removing CO 2 from the blood into the alveoli of the lung is less limited than blood oxygenation. This is due to the fact that molecular CO 2 penetrates biological membranes more easily than O 2 . For this reason, it easily penetrates from tissues into the blood. In addition, carbonic anhydrase promotes the formation of bicarbonate. Poisons that limit O2 transport (such as CO, methemoglobin-forming substances - nitrites, methylene blue, ferrocyanides, etc.) do not affect CO2 transport. Carbonic anhydrase blockers, for example Diacarb, which are often used in clinical practice or for the prevention of mountain or altitude sickness, never completely disrupt the formation of molecular CO 2. Finally, tissues have a large buffer capacity, but are not protected from O 2 deficiency. For this reason, disruption of O 2 transport occurs in the body much more often and faster than disruption of CO 2 gas exchange. However, in some diseases, high CO 2 levels and acidosis can cause death.

Measurement of O 2 and CO 2 voltage in arterial or mixed venous blood is carried out using polarographic methods using a very small amount of blood. The amount of gases in the blood is measured after they have been completely removed from the blood sample taken for analysis.

Such studies are performed using manometric devices such as the Van-Slyke apparatus, or a hemoalkarimeter (0.5-2.0 ml of blood is required) or on a Holander micromanometer (about 50 μl of blood is required).

And about . Today you will learn about how gases are transported in our blood.

Blood is the carrier of oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs. In a free (dissolved) state, such a small amount of these gases is transferred that they can safely be neglected when assessing the body's needs. For simplicity, we will further assume that the main amount of oxygen and carbon dioxide is transported in a bound state.

Oxygen transport

Oxygen is transported in the form of oxyhemoglobin. Oxyhemoglobin is a complex of hemoglobin and molecular oxygen.

Hemoglobin is found in red blood cells - red blood cells. Under a microscope, red blood cells look like a slightly flattened donut, in which they forgot to pierce the hole all the way. This unusual shape allows red blood cells to interact with the surrounding blood over a larger area than spherical cells (remember, of bodies with equal volume, a ball has the minimum area). And in addition, the red blood cell is capable of curling into a tube, squeezing into a narrow capillary and reaching the most remote corners of the body.

Only 0.3 ml of oxygen dissolves in 100 ml of blood at body temperature. Oxygen, dissolving in the blood plasma of the capillaries of the pulmonary circulation, diffuses into red blood cells and is immediately bound by hemoglobin, forming oxyhemoglobin, in which oxygen is 190 ml/l. The rate of oxygen binding is high - the absorption time of diffused oxygen is measured in thousandths of a second. In the capillaries of the alveoli with appropriate ventilation and blood supply, almost all the hemoglobin of the incoming blood is converted into oxyhemoglobin. But the very rate of diffusion of gases “back and forth” is much slower than the rate of binding of gases. this implies second practical conclusion: In order for gas exchange to proceed successfully, the air must “receive pauses”, during which the concentration of gases in the alveolar air and inflowing blood manages to equalize, that is there must be a pause between inhalation and exhalation .

Remember this!
The conversion of reduced (oxygen-free) hemoglobin (deoxyhemoglobin) into oxidized (oxygen-containing) hemoglobin (oxyhemoglobin) depends on the dissolved oxygen content in the liquid part of the blood plasma. Moreover, the mechanisms for assimilation of dissolved oxygen are very effective.

For example, an increase to a height of 2 km above sea level is accompanied by a decrease atmospheric pressure from 760 to 600 mm Hg. Art., partial pressure of oxygen in the alveolar air from 105 to 70 mm Hg. Art., and the content of oxyhemoglobin decreases only by 3%. And, despite the decrease in atmospheric pressure, the tissues continue to be successfully supplied with oxygen.

In tissues that require a lot of oxygen for normal functioning (working muscles, liver, kidneys, glandular tissues), oxyhemoglobin “gives up” oxygen very actively, sometimes almost completely. In tissues in which the intensity of oxidative processes is low (for example, in adipose tissue), most of the oxyhemoglobin does not “give up” molecular oxygen - level dissociation oxyhemoglobin is low. The transition of tissues from a resting state to an active state (muscle contraction, gland secretion) automatically creates conditions for increasing the dissociation of oxyhemoglobin and increasing the supply of oxygen to tissues.

The ability of hemoglobin to “hold” oxygen ( affinity of hemoglobin for oxygen) decreases with increasing concentrations of carbon dioxide and hydrogen ions. An increase in temperature has a similar effect on the dissociation of oxyhemoglobin.

From here it becomes easy to understand how natural processes are interconnected and balanced relative to each other. Changes in the ability of oxyhemoglobin to retain oxygen are of great importance for ensuring the supply of oxygen to tissues. In tissues in which metabolic processes occur intensively, the concentration of carbon dioxide and hydrogen ions increases, and the temperature rises. This accelerates and facilitates the release of oxygen by hemoglobin and facilitates the course of metabolic processes.

Skeletal muscle fibers contain myoglobin, which is similar to hemoglobin. It has a very high affinity for oxygen. Having “grabbed” an oxygen molecule, it will no longer release it into the blood.

The amount of oxygen in the blood

The maximum amount of oxygen that can bind blood when hemoglobin is completely saturated with oxygen is called blood oxygen capacity. The oxygen capacity of the blood depends on the hemoglobin content in it.

In arterial blood, the oxygen content is only slightly (3-4%) lower than the oxygen capacity of the blood. Under normal conditions, 1 liter of arterial blood contains 180-200 ml of oxygen. Even in cases where, under experimental conditions, a person breathes pure oxygen, its amount in arterial blood practically corresponds to the oxygen capacity. Compared to breathing with atmospheric air, the amount of oxygen transferred increases slightly (by 3-4%).

Venous blood at rest contains about 120 ml/l of oxygen. Thus, as blood flows through tissue capillaries, it does not give off all its oxygen.

The portion of oxygen absorbed by tissues from arterial blood is called oxygen utilization coefficient. To calculate it, divide the difference in oxygen content in arterial and venous blood by the oxygen content in arterial blood and multiply by 100.

For example:
(200-120): 200 x 100 = 40%.

At rest, the body's oxygen utilization rate ranges from 30 to 40%. With intense muscular work, it increases to 50-60%.

Read about it in the next article.

Material prepared by: Atamovich

Blood is the carrier of oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs. Only a small amount of these gases is transported in a free (dissolved) state. The main amount of oxygen and carbon dioxide is transported in a bound state.

Oxygen transport. Oxygen, dissolving in the blood plasma of the capillaries of the pulmonary circulation, diffuses into red blood cells and immediately binds to hemoglobin, forming oxyhemoglobin. The rate of oxygen binding is high: the half-saturation time of hemoglobin with oxygen is about 3 ms. One gram of hemoglobin binds 1.34 ml of oxygen; in 100 ml of blood there are 16 g of hemoglobin and, therefore, 19.0 ml of oxygen. This value is called blood oxygen capacity (BOC).

The conversion of hemoglobin to oxyhemoglobin is determined by the dissolved oxygen tension. Graphically, this dependence is expressed by the oxyhemoglobin dissociation curve (Fig. 6.3).

The figure shows that even at a low partial pressure of oxygen (40 mm Hg), 75-80% of hemoglobin is bound to it.

At a pressure of 80-90 mm Hg. Art. hemoglobin is almost completely saturated with oxygen.

Rice. 6.3.

The dissociation curve has a 5-shape and consists of two parts - steep and sloping. The sloping part of the curve, corresponding to high (more than 60 mm Hg) oxygen tensions, indicates that under these conditions the content of oxyhemoglobin only weakly depends on the oxygen tension and its partial pressure in the inhaled and alveolar air. The upper sloping part of the dissociation curve reflects the ability of hemoglobin to bind large amounts of oxygen, despite a moderate decrease in its partial pressure in the inspired air. Under these conditions, the tissues are sufficiently supplied with oxygen (saturation point).

The steep part of the dissociation curve corresponds to the oxygen tension normal for body tissues (35 mmHg and below). In tissues that absorb a lot of oxygen (working muscles, liver, kidneys), oxyhemoglobin dissociates into to a greater extent, sometimes almost completely. In tissues in which the intensity of oxidative processes is low, most of the oxyhemoglobin does not dissociate.

The property of hemoglobin - it is easily saturated with oxygen even at low pressures and easily releases it - is very important. Due to the easy release of oxygen by hemoglobin with a decrease in its partial pressure, an uninterrupted supply of oxygen is ensured to tissues in which, due to the constant consumption of oxygen, its partial pressure is zero.

The breakdown of oxyhemoglobin into hemoglobin and oxygen increases with increasing body temperature (Fig. 6.4).

Rice. 6.4.

A - depending on the reaction of the environment (pH); B - on temperature; B - on salt content; G - on the carbon dioxide content. The abscissa axis is the partial pressure of oxygen (in mmHg), the ordinate axis is the degree of saturation (in%)

The dissociation of oxyhemoglobin depends on the reaction of the blood plasma environment. With increasing blood acidity, the dissociation of oxyhemoglobin increases (Fig. 6.4, A).

The binding of hemoglobin with oxygen in water occurs quickly, but its complete saturation is not achieved, just as the complete release of oxygen does not occur when its partial pressure decreases. More complete saturation of hemoglobin with oxygen and its complete release with a decrease in oxygen tension occur in salt solutions and in blood plasma (see Fig. 6.4, B).

The carbon dioxide content in the blood is of particular importance in the binding of hemoglobin to oxygen: the higher its content in the blood, the less hemoglobin binds to oxygen and the faster the dissociation of oxyhemoglobin occurs. In Fig. Figure 6.4, D shows the dissociation curves of oxyhemoglobin at different levels of carbon dioxide in the blood. The ability of hemoglobin to combine with oxygen decreases especially sharply at a carbon dioxide pressure of 46 mm Hg. Art., i.e. at a value corresponding to the carbon dioxide tension in the venous blood. The effect of carbon dioxide on the dissociation of oxyhemoglobin is very important for the transport of gases in the lungs and tissues.

The tissues contain large amounts of carbon dioxide and other acidic breakdown products formed as a result of metabolism. Passing into the arterial blood of tissue capillaries, they contribute to a more rapid breakdown of oxyhemoglobin and the release of oxygen to tissues.

In the lungs, as carbon dioxide is released from the venous blood into the alveolar air and the carbon dioxide content in the blood decreases, the ability of hemoglobin to combine with oxygen increases. This ensures the conversion of venous blood into arterial blood.

Transport of carbon dioxide. Three forms of carbon dioxide transport are known:

• physically dissolved gas - 5-10%, or 2.5 ml/100 ml of blood;
• chemically bound in bicarbonates: in plasma NaHC0 3, in erythrocytes KHC0 3 - 80-90%, i.e. 51 ml/100 ml blood;
• chemically bound in carbamine compounds of hemoglobin - 5-15%, or 4.5 ml/100 ml of blood.

Carbon dioxide is continuously produced in cells and diffuses into the blood of tissue capillaries. In red blood cells it combines with water to form carbonic acid. This process is catalyzed (accelerated 20,000 times) by the enzyme carbonic anhydrase. Carbonic anhydrase is found in erythrocytes; it is not found in blood plasma. Therefore, carbon dioxide hydration occurs almost exclusively in red blood cells. Depending on the tension of carbon dioxide, carbonic anhydrase is catalyzed with the formation of carbonic acid and its splitting into carbon dioxide and water (in the capillaries of the lungs).

Some carbon dioxide molecules combine with hemoglobin in red blood cells, forming carbohemoglobin.

Thanks to these binding processes, the carbon dioxide tension in erythrocytes is low. Therefore, more and more new amounts of carbon dioxide diffuse into the red blood cells. The concentration of HC0 3 - ions formed during the dissociation of carbonic acid salts in erythrocytes increases. The erythrocyte membrane is highly permeable to anions. Therefore, some of the HC0 3 - ions pass into the blood plasma. Instead of HC0 3 - ions, C1 _ ions enter the red blood cells from the plasma, the negative charges of which are balanced by K + ions. The amount of sodium bicarbonate (NaHC0 3 -) increases in the blood plasma.

The accumulation of ions inside erythrocytes is accompanied by an increase in osmotic pressure in them. Therefore, the volume of red blood cells in the capillaries of the systemic circulation increases slightly.

To bind most of the carbon dioxide, the properties of hemoglobin as an acid are extremely important. Oxyhemoglobin has a dissociation constant 70 times greater than deoxyhemoglobin. Oxyhemoglobin is a stronger acid than carbonic acid, and deoxyhemoglobin is a weaker acid. Therefore, in arterial blood, oxyhemoglobin, which has displaced K + ions from bicarbonates, is transported in the form of the KHbO 2 salt. In tissue capillaries, KH0 2 gives up oxygen and turns into KHH. From it, carbonic acid, being stronger, displaces K + ions:

Thus, the conversion of oxyhemoglobin to hemoglobin is accompanied by an increase in the blood's ability to bind carbon dioxide. This phenomenon is called Haldane effect. Hemoglobin serves as a source of cations (K +) necessary for the binding of carbonic acid in the form of bicarbonates.

So, in the red blood cells of tissue capillaries an additional amount of potassium bicarbonate is formed, as well as carbohemoglobin, and the amount of sodium bicarbonate increases in the blood plasma. In this form, carbon dioxide is transferred to the lungs.

In the capillaries of the pulmonary circulation, the carbon dioxide tension decreases. C0 2 is split off from carbohemoglobin. At the same time, oxyhemoglobin is formed and its dissociation increases. Oxyhemoglobin displaces potassium from bicarbonates. Carbonic acid in red blood cells (in the presence of carbonic anhydrase) quickly decomposes into water and carbon dioxide. HC03 ions enter erythrocytes, and SG ions enter the blood plasma, where the amount of sodium bicarbonate decreases. Carbon dioxide diffuses into the alveolar air. All these processes are shown schematically in Fig. 6.5.

Rice. 6.5.

• See: Human Physiology / Ed. A. Kositsky.
• See: Leontyeva N.N., Marinova K.V. Decree. op.