Effects of ethanol metabolites on intermediary metabolism in heart muscle.
Pharmacol Biochem Behav
; 18 Suppl 1: 279-83, 1983.
Article
em En
| MEDLINE
| ID: mdl-6634841
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Cardiomiopatia Alcoólica
/
Etanol
/
Acetaldeído
/
Acetatos
/
Miocárdio
Limite:
Animals
Idioma:
En
Revista:
Pharmacol Biochem Behav
Ano de publicação:
1983
Tipo de documento:
Article