Effect of acid-base status on plasma phosphorus response to lactate.
The mechanism(s) underlying the hyperphosphatemia of lactic acidosis is uncertain. We assessed the interacting influence of the acid anion and acid-base status on plasma phosphorus concentration by administering lactic acid alone, lactic acid plus sodium bicarbonate, sodium bicarbonate alone, and sodium lactate alone to four different groups of dogs. The findings of (1) no increase in plasma phosphorus concentration with lactic acid plus sodium bicarbonate versus a marked increment with lactic acid alone, and (2) no difference in the plasma phosphorus response to sodium lactate versus sodium bicarbonate indicate that acidemia is necessary for the expression of lactate-induced hyperphosphatemia. The apparent greater propensity for marked hyperphosphatemia in lactic acidosis than in other types of metabolic acidosis remains unexplained, but conceivably might relate to differences in intracellular pH and in the rate of glycolysis.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000378:metabolism; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs; D005260:Female; D006400:Hematocrit; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000494:pharmacology*; D019344:Lactic Acid; D010758:Phosphorus / Q000097:blood*; D013997:Time Factors
D001639:Bicarbonates; D007773:Lactates; D002245:Carbon Dioxide; D010758:Phosphorus; D019344:Lactic Acid