Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA.
J Mol Cell Cardiol. 2012 Jan;52(1):93-104. doi: 10.1016/j.yjmcc.2011.10.011. Epub 2011 Oct 23.
While ethanol intake at high levels (3-4 or more drinks), either in acute (occasional binge drinking) or chronic (daily) settings, increases the risk for myocardial infarction and stroke, an inverse relationship between regular consumption of alcoholic beverages at light to moderate levels (1-2 drinks per day) and cardiovascular risk has been consistently noted in a large number of epidemiologic studies. Although initially attributed to polyphenolic antioxidants in red wine, subsequent work has established that the ethanol component contributes to the beneficial effects associated with moderate intake of alcoholic beverages regardless of type (red versus white wine, beer, spirits). Concerns have been raised with regard to interpretation of epidemiologic evidence for this association including heterogeneity of the reference groups examined in many studies, different lifestyles of moderate drinkers versus abstainers, and favorable risk profiles in moderate drinkers. However, better controlled epidemiologic studies and especially work conducted in animal models and cell culture systems have substantiated this association and clearly established a cause and effect relationship between alcohol consumption and reductions in tissue injury induced by ischemia/reperfusion (I/R), respectively. The aims of this review are to summarize the epidemiologic evidence supporting the effectiveness of ethanol ingestion in reducing the likelihood of adverse cardiovascular events such as myocardial infarction and ischemic stroke, even in patients with co-existing risk factors, to discuss the ideal quantities, drinking patterns, and types of alcoholic beverages that confer protective effects in the cardiovascular system, and to review the findings of recent experimental studies directed at uncovering the mechanisms that underlie the cardiovascular protective effects of antecedent ethanol ingestion. Mechanistic interrogation of the signaling pathways invoked by antecedent ethanol ingestion may point the way towards development of new therapeutic approaches that mimic the powerful protective effects of socially relevant alcohol intake to limit I/R injury, but minimize the negative psychosocial impact and pathologic outcomes that also accompany consumption of ethanol.
虽然高剂量（3-4 或更多饮料）的乙醇摄入，无论是急性（偶尔酗酒）还是慢性（每日）摄入，都会增加心肌梗死和中风的风险，但大量流行病学研究一致指出，轻至中度（每天 1-2 饮料）的规律饮酒与心血管风险之间呈反比关系。虽然最初归因于红葡萄酒中的多酚抗氧化剂，但随后的研究已经确定，无论酒精类型（红葡萄酒与白葡萄酒、啤酒、烈酒）如何，乙醇成分都有助于与适度饮酒相关的有益效果。关于这种关联的流行病学证据的解释存在一些担忧，包括许多研究中检查的参考组的异质性、适度饮酒者与戒酒者的不同生活方式，以及适度饮酒者的有利风险特征。然而，更好控制的流行病学研究，特别是在动物模型和细胞培养系统中进行的研究，证实了这种关联，并明确确立了饮酒与缺血/再灌注（I/R）引起的组织损伤减少之间的因果关系。本综述的目的是总结支持乙醇摄入可降低不良心血管事件（如心肌梗死和缺血性中风）发生可能性的流行病学证据，即使在伴有共存危险因素的患者中也是如此，讨论在心血管系统中具有保护作用的理想数量、饮酒模式和类型的酒精饮料，并回顾最近旨在揭示先前乙醇摄入的心血管保护作用的机制的实验研究结果。对先前乙醇摄入引起的信号通路的机制探究可能为开发新的治疗方法指明方向，这些方法模仿社交相关的饮酒对限制 I/R 损伤的强大保护作用，但最大限度地减少了与乙醇消耗相关的负面心理社会影响和病理后果。
