Effects of acute administration of Ethanol on experimental Arrhythmia

Many studies have shown that the relationship between alcohol consumption and most cardiovascular diseases is U-shaped, with nondrinkers and heavier drinkers having higher risks than moderate drinkers. However, the association between cardiac arrhythmias and acute alcohol consumption is not well understood. We set up several experimental arrhythmia animal models to examine the effects of acute administration of ethanol on arrhythmia. The results showed 0.4 g/kg, 0.8 g/kg and 1.6 g/kg ethanol consumption obviously delayed the onset time of atrial fibrillation (AF) (P < 0.05 or P < 0.01) and increased the survival rates on acetylcholine-CaCl ₂ -induced AF in mice. 0.4 g/kg, 0.8 g/kg and 1.6 g/kg ethanol consumption significantly delayed the onset time of ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) (P < 0.01), and 0.4 g/kg and 0.8 g/kg ethanol consumption increased the survival rates on CaCl ₂ -induced arrhythmia in rats. 0.4 g/kg ethanol essentially increased the cumulative dosage of aconitine required to CA (P < 0.05), and 0.8 g/kg, 1.6 g/kg ethanol reduced the cumulative aconitine dosage to induce VT, VF and CA (P < 0.05 or P < 0.01) on aconitine-induced arrhythmia in rats. 0.4 g/kg, 0.8 g/kg and 1.6 g/kg ethanol consumption remarkably increased the cumulative dosage of deslanoside to induce ventricualr premature contraction (VPC) (P < 0.01) on deslanoside-induced arrhythmia in guinea pigs. Collectively, our results indicate that low concentrations of ethanol had anti-arrhythmic effects on experimental arrhythmia, and high concentrations of ethanol may aggravated the occurrence of experimental arrhythmia.