DEMONSTRATION OF DISSIMILAR ACUTE HEMODYNAMIC-EFFECTS OF ETHANOL AND ACETALDEHYDE

Summary: 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 <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<0.02, whereas end-diastolic volume (P <0.005), myocardial oxygen consumption (P <0.05) and coronary blood flow (P <0.005) had increased. Higher ethanol levels exaggerated these changes when peak arterial acetaldehyde was 20.2 ±4 (μmol·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·min-1 (P<0.01), coronary sinus oxygen saturation from 46±4 to 55±3% (P<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<0.001). High dosage of acetaldehyde to a level of 129 ±23 μmol·litre-1 produced elevation of cardiac output (P<0.001), ejection fraction (P<0.01), coronary blood flow (P<0.02), whereas systemic resistance (P <0.001), heart rate (P <0.05) and myocardial oxygen consumption (P <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.