[Energy metabolism disorders in the myocardium due to alcoholic intoxication].

Energy metabolism was studied in rat myocardial mitochondria by estimation of respiratory enzymes activity and content of the Krebs cycle substrates under conditions of acute and chronic intoxication with ethyl alcohol. In the acute intoxication mitochondrial redox enzymes were inhibited (glutamate- and malate dehydrogenases, NADH cytochrome C oxidoreductase and cytochrome C oxidase), succinate- and lactate dehydrogenases were activated; at the same time, contents of pyruvate, succinate, and alpha-ketoglutarate were elevated and the content of oxalacetic acid was decreased. Prolonged administration of alcohol (within 2 months) caused an intensification of glycolysis and an increase in NADH cytochrome C oxidoreductase pathway with preferable oxidation of succinate and activation of cytochrome C oxidase; the phenomenon appears to be an adaptation to chronic "alcohol hypoxia". Discontinuation of alcohol administration led to deficiency of native substrates in myocardium (primarily, oxalacetic and succinic acids) due to decrease in NAD reduction via alcohol dehydrogenase reaction and to increase in oxidation of NAD-dependent endogenous substrates.