title: Effects of acute administration of ethanol on experimental arrhythmia.
abstract: 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.
authors.affiliation: Department of Pharmacology, Xi'an Jiaotong University Xi'an, Shaanxi, People's Republic of China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Gao
authors.forename: Peng
authors.initials: P
authors.lastname: Li
authors.forename: Li-Xia
authors.initials: LX
authors.lastname: Ma
authors.forename: Ke-Xin
authors.initials: KX
authors.lastname: Du
authors.forename: Xing-Hui
authors.initials: XH
authors.lastname: Wang
authors.forename: Meng-Jie
authors.initials: MJ
authors.lastname: Tang
authors.forename: Hui-Kang
authors.initials: HK
authors.lastname: He
authors.forename: Xiao-Jiang
authors.initials: XJ
authors.lastname: Yu
authors.forename: Wei-Jin
authors.initials: WJ
authors.lastname: Zang
authors.forename: Hao
authors.initials: H
authors.lastname: Hu
mesh_terms: D000109:Acetylcholine / Q000633:toxicity; D000157:Aconitine / Q000633:toxicity; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000188:drug therapy* / Q000401:mortality; D001281:Atrial Fibrillation / Q000139:chemically induced / Q000188:drug therapy / Q000401:mortality; D002122:Calcium Chloride / Q000633:toxicity; D002316:Cardiotonic Agents / Q000633:toxicity; D002492:Central Nervous System Depressants / Q000097:blood / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000633:toxicity; D003892:Deslanoside / Q000633:toxicity; D004195:Disease Models, Animal; D004347:Drug Interactions; D000431:Ethanol / Q000097:blood / Q000494:pharmacology*; D006168:Guinea Pigs; D006323:Heart Arrest / Q000139:chemically induced / Q000401:mortality / Q000503:physiopathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D017180:Tachycardia, Ventricular / Q000139:chemically induced / Q000188:drug therapy / Q000401:mortality; D014693:Ventricular Fibrillation / Q000139:chemically induced / Q000188:drug therapy / Q000401:mortality; D061585:Voltage-Gated Sodium Channel Agonists / Q000633:toxicity
chemical_list: D002316:Cardiotonic Agents; D002492:Central Nervous System Depressants; D018679:Cholinergic Agonists; D061585:Voltage-Gated Sodium Channel Agonists; D000431:Ethanol; D002122:Calcium Chloride; D000109:Acetylcholine; D000157:Aconitine; D003892:Deslanoside