Department of Legal Medicine, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Alcohol Clin Exp Res. 2010 Feb;34 Suppl 1:S45-53. doi: 10.1111/j.1530-0277.2008.00851.x. Epub 2009 Dec 16.
Pathologists examining victims of sudden unexpected death encounter alcoholics more often than expected; alcohol may play a role in sudden arrhythmic death. Here we determine whether a pattern of alcohol consumption, chronic ethanol intake, and withdrawal increases the incidence of malignant ventricular arrhythmia and modulates susceptibility to the arrhythmogenic potential of sympathetic stimulation from an epinephrine test in rats.
Male Wistar rats were treated with a continuous ethanol liquid diet for 7 weeks, and then subjected to 1-day withdrawal or 21-day abstinence. Ventricular ectopy was evaluated by 24-hour electrocardiographic telemetry recording; whole-body sympathetic activation, cardiac sympathovagal balance, and susceptibility to ventricular arrhythmia induced by sympathetic stimulation were evaluated based on blood noradrenalin metabolite concentrations, heart rate variability, and a 3-step epinephrine test.
Ventricular arrhythmia and related death were observed only in rats at 1 day of withdrawal, but not in nonalcoholic, continuous ethanol intake or 21-day abstinence rats. One-day withdrawal after a 7-week continuous ethanol regimen elevated circulating noradrenalin metabolite levels and induced cardiac sympathovagal imbalance. Deaths related to the epinephrine test and ventricular arrhythmia induced by low doses of epinephrine were observed only in 1-day withdrawal rats. However, all anomalies were normalized by 21-day abstinence.
Abrupt termination of a 7-week continuous ethanol regimen is sufficient to enhance the whole-body sympathetic activation and cardiac sympathovagal imbalance that contribute to ventricular arrhythmia and sudden death in alcoholic rats. Those providing medical care for alcoholics, including in cases of legal imprisonment, should be aware of the possibility of enhanced susceptibility to sudden arrhythmic death due to the abrupt termination of a chronic ethanol regimen.
检查猝然意外死亡受害者的病理学家比预期更常遇到酗酒者；酒精可能在心律失常性猝死中发挥作用。在此，我们确定是否存在一种饮酒模式、慢性乙醇摄入和戒断会增加恶性室性心律失常的发生率，并调节大鼠肾上腺素试验中交感刺激的致心律失常易感性。
雄性 Wistar 大鼠接受 7 周的连续乙醇液体饮食治疗，然后进行 1 天戒断或 21 天戒断。通过 24 小时心电图遥测记录评估室性异位；通过全身体交感神经激活、心脏交感神经迷走神经平衡以及对交感刺激诱导的室性心律失常的易感性评估，根据血液去甲肾上腺素代谢物浓度、心率变异性和 3 步肾上腺素试验进行评估。
仅在 1 天戒断的大鼠中观察到室性心律失常和相关死亡，但在非酒精性、连续乙醇摄入或 21 天戒断的大鼠中未观察到。7 周连续乙醇方案后 1 天戒断会升高循环去甲肾上腺素代谢物水平并引起心脏交感神经迷走神经失衡。仅在 1 天戒断的大鼠中观察到与肾上腺素试验相关的死亡和低剂量肾上腺素诱导的室性心律失常。然而，所有异常在 21 天戒断后均恢复正常。
突然终止 7 周的连续乙醇方案足以增强全身交感神经激活和心脏交感神经迷走神经失衡，导致酒精性大鼠的室性心律失常和猝死。为酗酒者提供医疗服务的人员，包括在法律监禁的情况下，应意识到由于慢性乙醇方案的突然终止，突然发生心律失常性死亡的易感性增强的可能性。
