Effect of alcohol on the heart and cardiac metabolism

In this report the disturbances in biochemistry of the heart muscle exposed to alcohol are delineated. All elements of cellular substructures are affected. In plasma membranes, (Na+ + K+)-activated ATPase (EC 3.6.1.3) is inhibited. Mitochondrial damage consists in diminished respiratory function and calcium uptake and binding. High-energy phosphates remain intact. Alcohol also affects the malate-aspartate shuttle. Acetaldehyde, a metabolite of ethanol, has a direct effect on myocardial protein synthesis through microsomal inhibition; however, the development of cardiac hypertrophy is not affected. Malfunction of sarcoplasmic reticulum is evidenced by disturbances in calcium binding and uptake. Effects of ethanol on the contractile machinery are deficiencies in the turnover rate of chemical into mechanical energy (diminished Vmax), and in the number of cross-bridges formed (P0). It increases stiffness of series elastic elements. There is diminished fatty acid oxidation with increased esterification. The involvement of CoA synthetase (EC 6.2.1.1), palmityl-carnitine transferase (EC 2.3.1.7), and pyruvate dehydrogenase complex in disturbed fatty acid oxidation is not certain. The role of catalase in myocardial ethanol oxidation was examined. Ethanol activates myocardial catalase-H2O2 complex (EC 1.11.1.6). The biochemical basis of fetal alcohol syndrome is low hepatic alcohol dehydrogenase (EC 1.1.1.1) activity during fetal life.