Vilahur Gemma, Casani Laura, Mendieta Guiomar, Lamuela-Raventos Rosa M, Estruch Ramon, Badimon Lina
Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Barcelona, Spain.
Eur J Clin Invest. 2014 Dec;44(12):1177-88. doi: 10.1111/eci.12352.
There is controversy regarding the effect of alcohol beverage intake in vascular vasodilatory function in peripheral arteries. The effects of beer intake in coronary vasodilation remain unknown. We investigated whether regular beer intake (alcohol and alcohol-free) protects against hypercholesterolaemia-induced coronary endothelial dysfunction and the mechanisms behind this effect.
Pigs were fed 10 days: (i) a Western-type hypercholesterolaemic diet (WD); (ii) WD+low-dose beer (12·5 g alcohol/day); (iii) WD+moderate-dose beer (25 g alcohol/day); or (iv) WD+moderate-dose alcohol-free-beer (0·0 g alcohol/day). Coronary responses to endothelium-dependent vasoactive drugs (acetylcholine: receptor mediated; calcium ionophore-A23189: nonreceptor mediated), endothelium-independent vasoactive drug (SNP) and L-NMMA (NOS-antagonist) were evaluated in the LAD coronary artery by flow Doppler. Coronary Akt/eNOS activation, MCP-1 expression, oxidative DNA damage and superoxide production were assessed. Lipid profile, lipoproteins resistance to oxidation and urinary isoxanthohumol concentration were evaluated.
Alcoholic and nonalcoholic beer intake prevented WD-induced impairment of receptor- and non-receptor-operated endothelial-dependent coronary vasodilation. All animals displayed a similar vasodilatory response to SNP and L-NMMA blunted all endothelial-dependent vasorelaxation responses. Haemodynamic parameters remained unchanged. Coronary arteries showed lower DNA damage and increased Akt/eNOS axis activation in beer-fed animals. Animals taking beer showed HDL with higher antioxidant capacity, higher LDL resistance to oxidation and increased isoxanthohumol levels. Weight, lipids levels, liver enzymes and MCP-1 expression were not affected by beer intake.
Non-alcoholic-related beer components protect against hyperlipemia-induced coronary endothelial dysfunction by counteracting vascular oxidative damage and preserving the Akt/eNOS pathway. Light-to-moderate beer consumption prevents and/or reduces the endothelial dysfunction associated with cardiovascular risk factors.
关于酒精饮料摄入对外周动脉血管舒张功能的影响存在争议。啤酒摄入对冠状动脉舒张的影响尚不清楚。我们研究了定期饮用啤酒（含酒精和不含酒精）是否能预防高胆固醇血症诱导的冠状动脉内皮功能障碍及其背后的机制。
猪被喂食10天：（i）西式高胆固醇饮食（WD）；（ii）WD+低剂量啤酒（12.5克酒精/天）；（iii）WD+中剂量啤酒（25克酒精/天）；或（iv）WD+中剂量无酒精啤酒（0.0克酒精/天）。通过血流多普勒评估左前降支冠状动脉对内皮依赖性血管活性药物（乙酰胆碱：受体介导；钙离子载体A23189：非受体介导）、内皮非依赖性血管活性药物（SNP）和L-NMMA（一氧化氮合酶拮抗剂）的反应。评估冠状动脉Akt/eNOS激活、MCP-1表达、氧化性DNA损伤和超氧化物产生。评估血脂谱、脂蛋白抗氧化能力和尿异黄腐醇浓度。
含酒精和不含酒精的啤酒摄入可预防WD诱导的受体和非受体介导的内皮依赖性冠状动脉舒张功能受损。所有动物对SNP表现出相似的血管舒张反应，而L-NMMA使所有内皮依赖性血管舒张反应减弱。血流动力学参数保持不变。在饮用啤酒的动物中，冠状动脉显示出较低的DNA损伤和增加的Akt/eNOS轴激活。饮用啤酒的动物显示高密度脂蛋白具有更高的抗氧化能力、更高的低密度脂蛋白抗氧化能力和增加的异黄腐醇水平。体重、血脂水平、肝酶和MCP-1表达不受啤酒摄入的影响。
与酒精无关的啤酒成分通过抵消血管氧化损伤和维持Akt/eNOS途径来预防高脂血症诱导的冠状动脉内皮功能障碍。轻度至中度饮用啤酒可预防和/或减少与心血管危险因素相关的内皮功能障碍。
