Zilkens Renate R, Rich Lisa, Burke Valerie, Beilin Lawrence J, Watts Gerald F, Puddey Ian B
Department of Medicine, University of Western Australia and Western Australian Heart Research Institute, Royal Perth Hospital, Perth, WA 6847, Australia.
J Hypertens. 2003 Jan;21(1):97-103. doi: 10.1097/00004872-200301000-00019.
Regular light consumption of alcohol appears to reduce the risk of cardiovascular disease, whereas in heavier drinkers the opposite effect is seen. This biphasic relationship could partly be due to contrasting actions of low and high alcohol intake on endothelial function.
To determine whether reducing alcohol intake in moderate-to-heavy drinkers (40-110 g/day) would improve conduit artery endothelial function as assessed by post-ischaemic brachial artery flow-mediated dilatation (FMD).
In a two-way cross-over study, 16 healthy men either substituted their usual alcohol intake with a 0.9% alcohol beer or maintained their usual alcohol intake during sequential 4-week periods. At the end of each period of FMD and glyceryl trinitrate-induced brachial artery dilatation, blood pressure, plasma lipids, homocysteine and biomarkers of alcohol consumption (gamma-glutamyl transpeptidase) and endothelial function (E-selectin, von Willebrand factor, endothelin-1) were assessed.
The participants reduced their alcohol intake from 72.4 to 7.9 g/day. This self-reported reduction in alcohol intake was corroborated by significant decreases in gamma-glutamyl transpeptidase (24%). The decrease in alcohol intake resulted in reductions in total cholesterol (5%), high-density lipoprotein cholesterol (17%), homocysteine (9%) and systolic and diastolic blood pressure [5 mmHg (P = 0.01) and 4 mmHg (P = 0.003), respectively]. There was no effect of alcohol on FMD (6.23 +/- 0.75% compared with 6.24 +/- 0.71%, P = NS), glyceryl trinitrate-induced vasodilatation, E-selectin, endothelin-1 and von Willebrand factor.
Substantial reduction in alcohol intake in healthy moderate-to-heavy drinkers does not improve endothelial function as measured by post-ischaemic flow-mediated dilatation of the brachial artery or biomarkers of endothelial function.
规律适量饮酒似乎可降低心血管疾病风险，而重度饮酒者则出现相反效果。这种双相关系部分可能归因于低酒精摄入量和高酒精摄入量对内皮功能的不同作用。
确定减少中度至重度饮酒者（40 - 110克/天）的酒精摄入量是否会改善通过缺血后肱动脉血流介导的血管舒张（FMD）评估的 conduit 动脉内皮功能。
在一项双向交叉研究中，16名健康男性在连续4周期间，要么用0.9%酒精啤酒替代其通常的酒精摄入量，要么维持其通常的酒精摄入量。在每个FMD和硝酸甘油诱导的肱动脉舒张期结束时，评估血压、血脂、同型半胱氨酸以及酒精摄入生物标志物（γ-谷氨酰转肽酶）和内皮功能生物标志物（E-选择素、血管性血友病因子、内皮素-1）。
参与者将酒精摄入量从72.4克/天降至7.9克/天。γ-谷氨酰转肽酶显著降低（24%）证实了这种自我报告的酒精摄入量减少。酒精摄入量的减少导致总胆固醇降低（5%）、高密度脂蛋白胆固醇降低（17%）、同型半胱氨酸降低（9%）以及收缩压和舒张压分别降低[5 mmHg（P = 0.01）和4 mmHg（P = 0.003）]。酒精对FMD（6.23±0.75%对比6.24±0.71%，P =无显著差异）、硝酸甘油诱导的血管舒张、E-选择素、内皮素-1和血管性血友病因子无影响。
健康的中度至重度饮酒者大量减少酒精摄入量并不能改善通过缺血后肱动脉血流介导的血管舒张或内皮功能生物标志物所测量的内皮功能。
