Lactic acidosis: current concepts.
Lactic acidosis is now a widely recognized disorder in clinical medicine. Experimental studies during the past decade demonstrate an important role of lactate disposal mechanisms in the pathogenesis of lactic acidosis. Such factors as decreased cardiovascular reserve, inadequate liver perfusion and alterations in liver intracellular pH appear to limit the normally large capacity of the liver to dispose of lactic acid. The continued high mortality of this disorder has led to a re-examination of the conventional, empirical treatment of lactic acidosis with sodium bicarbonate. Available data suggest that alkali may cause or exacerbate the conditions of excessive lactate production, decreased cardiac reserve and inadequate hepatic lactate disposal which exist in this disorder. In contrast, dichloroacetate therapy shows strikingly beneficial results, at least in early experimental studies.
D000138:Acidosis / Q000503:physiopathology* / Q000628:therapy; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D003920:Diabetes Mellitus / Q000503:physiopathology; D003999:Dichloroacetic Acid / Q000627:therapeutic use; D005943:Gluconeogenesis; D006019:Glycolysis; D006321:Heart / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007773:Lactates / Q000378:metabolism*; D008099:Liver / Q000098:blood supply / Q000378:metabolism; D008954:Models, Biological; D010629:Phenformin / Q000009:adverse effects; D012039:Regional Blood Flow
D001639:Bicarbonates; D007773:Lactates; D003999:Dichloroacetic Acid; D010629:Phenformin