Effect of hypocapnia on intracellular pH during metabolic acidosis.
Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.
D000138:Acidosis / Q000378:metabolism*; D000472:Alkalosis, Respiratory / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000097:blood / Q000378:metabolism; D002245:Carbon Dioxide / Q000097:blood / Q000378:metabolism; D002712:Chlorides / Q000097:blood; D006863:Hydrogen-Ion Concentration; D008297:Male; D009132:Muscles / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats
D001639:Bicarbonates; D002712:Chlorides; D002245:Carbon Dioxide