Mitochondrial respiration after cardiac perfusion with ethanol or acetaldehyde

Hemodynamics, energetics, and mechanics of isolated working rat hearts were studied during perfusion with Krebs-Henseleit medium containing either ethanol (24 +/- 2 mM) or acetaldehyde (74 +/- 6 microM). After 60-min perfusion with agent, mitochondria were isolated from the hearts and assayed polarographically using glutamate, alpha-keto-glutarate, pyruvate-malate, and succinate-rotenone substrates. Hemodynamic and mechanical function of the ethanol-treated hearts declined significantly more than that of control hearts during the 60-min perfusion. The acetaldehyde-perfused hearts did not differ from the controls. A 90-sec washout period reversed the ethanol-induced depression of physiologic function. Respiratory function (respiratory control ratio and Qo2) of mitochondria isolated from the ethanol- and acetaldehyde-treated hearts was slightly, though not significantly, depressed compared with control hearts. These data indicate that ethanol and acetaldehyde, at physiologically significant concentrations, have dissimilar effects on cardiac hemodynamics and mechanics: ethanol has a direct depressive effect which is reversible; acetaldehyde has no significant effect. Mitochondrial respiration is not irreversibly affected by brief exposure to ethanol or acetaldehyde at the concentrations tested.