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Role of the lungs in AAB regulation

Free ions [H⁺] are not released with the lungs, however, strong acids, with the help of Na bicarbonate, are converted into a weak carbonic acid that dissociates down to C0₂ and H₂0:

C0₂ is a specific stimulator of respiratory center, dyspnea and hyperven­tilation arise and excessive amounts of C0₂ are eliminated with the lungs.

In excessive accumulation of alkaline products an increased need arises in H₂C0₃ that is spent for neutralization of these alkalies.

When the supplies of H₂C0₃ are reduced and [C0₂] concentration decreases the intensity of the respiratory center stimulation lowers: a hypoventilation arises that leads to a preservation of C0₂ in the organism and replenishment of H₂C0₃ reserves in blood.

When ventilation worsens and gas diffusion decreases, C0₂ is accumulated in blood and at the expense of this an excess of [H⁺] ions is accumulated in blood.

pH decreases. A resultant acidosis is called as gaseous or respiratory since it is associated with accumulation of volatile acids.

In hyperventilation caused by stimulation of respiratory center (in CCC1, intracerebral bleeding) a primary dyspnea develops. The same condition may develop in improperly chosen parameters of APV.

C0₂ is eliminated excessively and a respiratory alkalosis develops.

In the norm PC0₂ = 40 mm Hg.

When PC0₂ is less than the norm, a respiratory alkalosis arises, and if C0₂ is more than the norm — a respiratory acidosis results.

The state associated with an excessive accumulation of nonvolatile acids or alkalies is called metabolic acidosis or alkalosis.

Role of kidnevs in AAB maintenance lies in elimination of hydrogen ions from the blood with acidic properties and bicarbonate from the blood with alkaline properties.

Hydrogen ions are excreted with the urine, and Na⁺ enters the cells of tubules from the urine where it binds with HC0₃^_ forming Na bicarbonate, the latter enters the blood alkalizing it.

The kidneys can excrete H⁺ and reabsorb Na⁺ and bicarbonate at the expense of ammoniogenesis. Ammonia (NH₃) is formed as a result of deamination of amino acids and easily diffuse through the membrane into tubular urine where it binds with hydrogen ions forming ammonium (NH^) that is not able to pass through a cellular membrane. In the urine ammonium binds with CI" ions and in the form of ammonium chloride is excreted with the urine. Na⁺, freed from CI", passes into the cells of renal tubules, binds with HC0₃" and then enters the blood.

Reabsorption of bicarbonate also exists. In this case the cells of renal tubules absorb Na⁺ from the urine in exchange for H⁺. Hydrogen ion enters the urine where binding with bicarbonate it forms H₂C0₃ that dissociates at once to C0₂ and H₂0. Almost all carbon dioxide diffuses into blood.

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