To determine whether the acute cardiac depressant effects of ethanol could be attributed to its metabolite (acetaldehyde), either ethanol or acetaldehyde was intravenously infused into pentobarbital anaesthetised, closed-chest dogs. At a venous blood ethanol level of 199 +/- 43 (SE) mg . dl-1, ejection fraction had decreased from 35 +/- 2 to 30 +/-2%, P less than 0.05, max dP/dt/end-diastolic volume from 14.0 +/- 2.1 to 8.6 +/- 1.1 kPa . s-1 . cm-3 (105 +/- 16 to 65 +/- 8 mmHg . s-1 . cm-3), P less than 0.02, whereas end-diastolic volume (P less than 0.005), myocardial oxygen consumption (P less than 0.05) and coronary blood flow (P less than 0.005) had increased. Higher ethanol levels exaggerated these changes when peak arterial acetaldehyde was 20.2 +/- mumol . litre-1. By contrast, infusion of acetaldehyde to a peak blood level comparable with that produced by ethanol increased cardiac output from 2.4 +/- 0.2 to 2.8 +/- 0.2 litre-1 . min-1 P less than 0.01), coronary sinus oxygen saturation from 46 +/- 4 to 55 +/- 3% (P less than 0.25) and reduced systemic resistance from 8.0 +/- 0.7 to 6.3 +/- 0.5 kPa . litre-1 . min-1 (60 +/- 5 to 47 +/- 4 mmHg . litre-1 . min-1) (P less than 0.001). High dosage of acetaldehyde to a level of 129 +/- 23 mumol . litre-1 produced elevation of cardiac output (P less than 0.001), ejection fraction (P less than 0.01), coronary blood flow (P less than 0.02), whereas systemic resistance (P less than 0.001), heart rate (P less than 0.05) and myocardial oxygen consumption (P less than 0.05) decreased. Discontinuation of acetaldehyde infusion significantly reversed these changes. Max dP/dt/left ventricular end-diastolic volume and left ventricular end-diastolic volume were not significantly altered by acetaldehyde. Thus, ethanol depresses cardiac performance and increases myocardial oxygen consumption. By contrast, acetaldehyde at levels produced by ethanol metabolism improves cardiac performance, consequent to afterload reduction, and reduces myocardial oxygen consumption.
