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, 0.8 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-CaClâ‚‚-induced AF in mice.
Ethanol (0.4, 0.8 and 1.6 g/kg) consumption significantly delayed the onset time of
ventricular tachycardia (VT),
ventricular fibrillation (VF) and
cardiac arrest (CA) (P < 0.01), and 0.4 and 0.8 g/kg
ethanol consumption increased the survival rates on CaClâ‚‚-induced
arrhythmia in rats.
Ethanol (0.4 g/kg) 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.
Ethanol (0.4, 0.8 and 1.6 g/kg) consumption remarkably increased the cumulative dosage of
deslanoside to induce ventricualr premature contraction (P < 0.01) on
deslanoside-induced
arrhythmia in guinea pigs. Collectively, our results indicate that low concentrations of
ethanol had
anti-arrhythmic effect on experimental
arrhythmia, and high concentrations of
ethanol may aggravated the occurrence of experimental
arrhythmia.