RESUMO
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-CaCl2-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 CaCl2-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.
Assuntos
Arritmias Cardíacas/induzido quimicamente , Arritmias Cardíacas/tratamento farmacológico , Depressores do Sistema Nervoso Central/farmacologia , Etanol/farmacologia , Acetilcolina/toxicidade , Aconitina/toxicidade , Animais , Arritmias Cardíacas/mortalidade , Fibrilação Atrial/induzido quimicamente , Fibrilação Atrial/tratamento farmacológico , Fibrilação Atrial/mortalidade , Cloreto de Cálcio/toxicidade , Cardiotônicos/toxicidade , Depressores do Sistema Nervoso Central/sangue , Agonistas Colinérgicos/toxicidade , Deslanosídeo/toxicidade , Modelos Animais de Doenças , Interações Medicamentosas , Etanol/sangue , Cobaias , Parada Cardíaca/induzido quimicamente , Parada Cardíaca/mortalidade , Parada Cardíaca/fisiopatologia , Masculino , Camundongos , Camundongos Endogâmicos ICR , Ratos , Ratos Sprague-Dawley , Fatores de Risco , Taquicardia Ventricular/induzido quimicamente , Taquicardia Ventricular/tratamento farmacológico , Taquicardia Ventricular/mortalidade , Fibrilação Ventricular/induzido quimicamente , Fibrilação Ventricular/tratamento farmacológico , Fibrilação Ventricular/mortalidade , Agonistas do Canal de Sódio Disparado por Voltagem/toxicidadeRESUMO
Functional ablation of the cerebral cortex by cortical spreading depression (CSD) significantly increased the dose of desacetyl lanatoside C required to induce A-V block and ventricular fibrillation. To examine the role of the posterior hypothalamus in the increased resistance of decorticated rats to arrhythmia induced by toxic doses of desacetyl lanatoside C, four groups of animals were injected with this drug: group 1 rats had a craniotomy; group 2 rats had a craniotomy and functional decortication; group 3 rats had a craniotomy and a hypothalamic lesion; and group 4 rats had a craniotomy, hypothalamic lesion and functional decortication. The dose of drug required to induce A-V block and ventricular fibrillation was significantly less in group 1, than in groups 2,3 and 4, and there was no statistically significant difference between these last three groups. These results are consistent with the hypothesis that the increased resistance to arrhythmia induced by desacetyl lanatoside C in decorticated rats is mediated by the posterior hypothalamus.