[Metabolic alkalosis. Compensation mechanisms in the light of new experimental data].
Changes in arterial blood and erythrocyte acid-base and electrolyte balance in the course of acute alkalinisation caused by bicarbonate loading showed that extracellular alkalosis has no significant effect on the concentration of intraerythrocyte bicarbonate concentration, though a marked increase in pH and electrolyte balance within the red cell is apparent. Erythrocyte alkalinisation may thus be seen as essentially due to the escape of H+ ions, while the entry of Na+ ions is the main device by which the law of electroneutrality is respected. The literature suggests that lactic acid offers a source of H+ ions for destruction of bicarbonate, whereas the diffusion of the ion lactate within the cell is compensated by the release of Cl-. In addition, the data now reported indicate that the red cell is a sufficiently valid model for the study of phenomena occurring within the intracellular compartment when a state of extracellular alkalinisation in created.
D000368:Aged; D000471:Alkalosis / Q000097:blood*; D001639:Bicarbonates / Q000097:blood; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D006400:Hematocrit; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D014882:Water-Electrolyte Balance
D001639:Bicarbonates; D010100:Oxygen
In tema di alcalosi metabolica. Il problema dei meccanismi di compenso alla luce di muovi dati sperimentali