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Buffer systems of blood

Blood plays a crucial role in maintaining the acid-base balance, the change of which can lead to pathological conditions or death of the organism. Therefore, in the body, there are special systems that prevent change in pH of the blood and other body fluids in the formation of acidic and alkaline substances or high water inflow. This is the role of individual physiological systems (respiratory, excretory) and buffer systems. The latter are very fast (within seconds), respond to changes in the concentration of H + and OH- in aqueous solutions and are urgent regulators of acid-base status in the tissues of the body.

Buffer systems are mixtures of a weak acid and its soluble salts, two salts, or proteins that are able to prevent the change of pH of body fluids. Effect of buffer systems is directed to binding excess H+ or OH- in the environment and the maintenance of constant pH. Weakly dissociated substances or water are formed under the influence of the buffer system. The main buffer systems of blood are bicarbonate, protein (hemoglobin) and phosphate. There are also the acetate and ammonium buffer systems.

Bicarbonate buffer system is powerful and very manageable system of the blood and extracellular fluid. It accounts for about 10% of the total buffer capacity of the blood. Bicarbonate system is a conjugate acid-base pair consisting of a molecule of carbonic acid H2CO3, acting as a proton donor, and bicarbonate ion HCO3- performing the role of a proton acceptor:

2 + 223+ + 3-

The true concentration of undissociated 23 molecules in the blood is low and is directly dependent on the concentration of dissolved CO2. At normal blood pH (7,4), the concentration of bicarbonate ions HCO3- in plasma exceeds the CO2 concentration in about 20 times. Bicarbonate buffer system is functioning as an effective regulator of pH = 7,4. The mechanism of action of this system is characterized by the secretion of relatively large amounts of blood acidic substances. Protons H + react with bicarbonate ions HCO3-. This leads to the formation of weakly dissociated 23. The following decrease in the concentration of 23 is achieved as a result of the accelerated release of CO2 through the lungs as a result of hyperventilation. If the amount of bases in the blood is increased, they interact with weak carbonic acid; and bicarbonate ions and water are formed. This does not occur to any appreciable changes in pH. In addition, to maintain normal relations between the components of the buffer system in this case, the physiological mechanisms of regulation of acid-base balance are involved. There is retention of a certain amount of CO2 in the blood plasma as a result of lungs hypoventilation. Bicarbonate system is closely connected to hemoglobin system.

Phosphate buffer system is a conjugate acid-base pair consisting of an ion 24- (proton donor, acts as acid) and ion 42- (proton acceptor plays the role of salt). Phosphate buffer system is only 1% of the buffer capacity of blood. In other tissues, this system is one of the key. Phosphate buffer system is capable to influence on pH changes from 6,1 to 7,7 and can provide a capacity of intracellular fluid, the pH of which is within the limits of 6,9-7,4. In the blood, the maximum capacity of phosphate buffer is near 7.2. Organic phosphates also have buffer properties, but their buffer capacity is weaker than the inorganic phosphate buffer.



Protein buffer system is less important for maintaining acid-base balance in blood plasma than the other buffers. Proteins form a buffer system due to the presence of acid-base groups in the molecules of proteins: a protein-+ (acid, proton donor) and protein (conjugate base, the acceptor of protons). The protein buffer system of blood plasma is effective in the pH range of 7,2-7,4.

Hemoglobin buffer system is the most powerful buffer system of blood, accounting for 75% of the buffer capacity. Participation of hemoglobin in the regulation of blood pH is due to its role in the transport of oxygen and carbon dioxide. At oxygen saturation hemoglobin become more stronger acid (b2). Hemoglobin, giving oxygen, turns into a very weak organic acid (b).

Hemoglobin buffer system consists of non-ionized hemoglobin b (a weak organic acid, proton donor) and potassium salt of hemoglobin b (conjugate base, the acceptor of protons). In the same way oxyhemoglobin buffer system can be considered. The system of hemoglobin and oxyhemoglobin are exist as a coherent whole. Buffering properties of hemoglobin are due to the ability of acid reacting compounds interact with potassium salt of hemoglobin:

KHb + 23 =>3 + b.

This ensures maintaining of blood pH within physiologically acceptable values, despite the flow of large amounts of CO2 and other metabolic products of acidic nature in venous blood. Hemoglobin (b), entering into the capillaries of the lungs, is converted into oxyhemoglobin (b2), which leads to an acidification of the blood, the displacement of 23 from bicarbonate and a decrease in alkali reserve of blood.

Respiratory function of the blood. An important function of blood is its ability to carry oxygen to the tissues and CO2 from the tissues to the lungs. Agent performing this function is hemoglobin. Hemoglobin is able to absorb O2 at relatively high concentration of it in the air and can easily give it at lower partial pressure of O2:

b + 2 ↔ b.

Therefore, blood in the pulmonary capillary is saturated with O2, while in tissue capillaries, where the partial pressure of its greatly decreased, there is a reverse process - the return of blood oxygen to the tissues.

Forming in tissues during oxidative processes CO2 is subjected to removal from the body. Ensuring of such gas exchange is carried out by several body systems.

The most important are: external, or pulmonary, respiration, providing directed diffusion of gases through alveolar-capillary walls in the lungs and gas exchange between outside air and blood; respiratory function of blood, depending on the capacity of plasma to dissolve and the ability of hemoglobin reversibly bind oxygen and carbon dioxide; transport function of the cardiovascular system (blood flow), ensuring the transfer of blood gases from the lungs to the tissues and back; function of enzyme systems, providing the exchange of gases between the blood and tissue cells, i.e., tissue respiration.

The diffusion of gases of blood realizes through the cells membranes in a concentration gradient. Due to this process in the alveoli of the lungs at the end of inspiration there is the alignment of the partial pressures of gases in alveolar air and blood. Exchange with atmospheric air during expiration and inspiration again leads to differences in the concentration of gases in alveolar air and blood, and therefore the diffusion of oxygen into the blood and carbon dioxide from the blood occure.

Most of the O2 and CO2 is transferred into the bound with hemoglobin in the form of HbO2 and HbCO2 molecules. The maximum amount of oxygen, bounding by blood at full saturation of hemoglobin with oxygen, is called oxygen capacity of blood. Normally, its value varies between 16,0-24,0% vol. and depends on the content of hemoglobin in the blood, 1 g of which can bind 1,34 ml of oxygen (Hüfner number).

The binding of oxygen by hemoglobin is reversible process, dependent on oxygen partial pressure in the blood, as well as other factors, such as the pH of the blood.

CO2 produced in the tissues, passes into the blood capillaries, and then diffuses into the erythrocytes, where under the influence of carbonic anhydrase turns into carbonic acid which dissociates into H+ and 3-. 3- ions partly diffuse into the blood plasma, forming sodium bicarbonate. It enters to the lungs with the blood flow (as 3- ions contained in red blood cells) and forms CO2, which diffuses into the alveoli. About 80% of the total amount of CO2 is transferred from tissues to the lungs in the form of bicarbonate, 10% - in the form of freely dissolved carbon dioxide and 10% - in the form of carboxyhemoglobin. Carboxyhemoglobin dissociates in the pulmonary capillaries on hemoglobin and free CO2 that is removed with the expired air. Release of CO2 from the complex with hemoglobin contributes the transformation of the latter in oxyhemoglobin, which, having expressed acidic properties is able to convert bicarbonate into carbonic acid, which dissociates to form molecules of water and CO2.

With low blood saturation by oxygen hypoxemiais developed, which is accompanied by development of hypoxia, i.e., insufficient supply of oxygen to tissues. Severe forms of hypoxemia can cause complete cessation of oxygen supply to tissues, whereas anoxia is developed, in these cases loss of consciousness occurs, which can result in death.

Pathology of the gas exchange is associated with infringement of transport of gases between the lungs and body cells and observed at a decrease of the gas capacity of the blood due to insufficiency or changes of hemoglobin, and manifested in the form of anemic hypoxia. In anemia oxygen capacity of blood is decreased in proportion to the decrease of concentration of hemoglobin. Decreasing of hemoglobin concentration in anemia limits the transport of carbon dioxide from the tissues to the lungs in the form of carboxyhemoglobin.

Violation of oxygen transport by blood also occurs in the pathology of hemoglobin, such as sickle cell anemia, inactivation of hemoglobin molecules by converting it to methemoglobin, for example, in cases of poisoning by nitrates (methemoglobinemia) or carboxyhemoglobin (CO poisoning).

Disturbances of gas exchange by reducing the volume velocity of blood flow in capillaries occur in heart failure, circulatory failure (including the collapse, shock), local disturbances - during vasospasm, and others. When there is blood stagnation the concentration of reduced hemoglobin is increased. In heart failure, this phenomenon is especially expressed in the capillaries of the distant from the heart parts of the body, where blood flow is slowed down more that clinically is manifesteded by acrocyanosis. Primary disturbance of gas exchange at the cellular level is mainly observed during influence of poisons that block the respiratory enzymes. As a result, cells lose the ability to utilize oxygen, and acute tissue hypoxia is developed, which leads to structural disorganization of the subcellular and cellular elements, up to necrosis. Vitamin deficiency, such as lack of vitamins B2, PP, which are coenzymes of respiratory enzymes, can lead to disruption of cellular respiration.

 


Date: 2016-04-22; view: 1738


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