title: Effects of ethanol metabolites on intermediary metabolism in heart muscle.
abstract: Isolated rat hearts were perfused by the Langendorff procedure to study the metabolic effects of ethanol, acetaldehyde and acetate on the myocardium. Ethanol caused a slight decrease in the work output of the heart and concomitant changes in the oxygen consumption and cellular redox state. A low-Km (1 microM) acetaldehyde dehydrogenase activity was found in rat heart mitochondria, but an acetaldehyde concentration of 50 microM or higher was necessary to reduce tissue NAD+ in the isolated perfused heart. One hundred microM or higher concentrations of acetaldehyde caused an increase in the work output of the heart, with a concomitant oxidation of NADH. Acetaldehyde at a 50 microM concentration did not affect myocardial lipid metabolism. Acetate caused a reduction of mitochondrial NAD+, an increase in the coronary flow and an increase in the O2 consumption of the perfused heart. Practically all of the oxygen consumption could be accounted for by acetate oxidation. A 2 mM concentration of acetate inhibited the oxidation of oleate by 35% and stimulated oleate incorporation into myocardial lipids by 90%; therefore, it appears that the acute metabolic derangements of the heart muscle during ethanol metabolism in vivo are probably mainly caused by acetate.
mesh_terms: D000079:Acetaldehyde / Q000378:metabolism / Q000494:pharmacology*; D000085:Acetates / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D002310:Cardiomyopathy, Alcoholic / Q000378:metabolism*; D000431:Ethanol / Q000378:metabolism / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000085:Acetates; D005227:Fatty Acids; D014280:Triglycerides; D009243:NAD; D000431:Ethanol; D000079:Acetaldehyde