Shishov V I, Novoselova N G, Maevskiĭ E I
Farmakol Toksikol. 1977 Mar-Apr;40(2):168-73.
Evidence is given of disturbances of aerobic oxidative process in the myocardial mitochondria occurring in acute and chronic alcoholic intoxication. A single introduction of alcohol in a dose of 1 and 3 g/kg to rats and dogs produces "hypoxyform" changes in the myocardium, viz. a fall of PO2, a reduced activity of most NAD-independent enzymes, activation of succinate- and lactate-dehydrogenases in a moderate dissociation of oxidative phosphorylation reactions. The damaging effect of the alcohol persists for 24 hours after its one-time introduction. Following a 2-month long alcoholic intoxication there was seen a depressed respiratory activity of the mitochondria and of the study enzymes, except for cytochrome-C-oxidase. It is assumed that the cardiotoxic effect of alcohol is due to the damage of the energy-producing system of the mitochondria.