Division of Cardiothoracic Surgery, Cardiovascular Research Center, Warren Alpert Medical School, Brown University, Providence, RI (A.D.L., N.Y.E., Y.L., J.F., T.A.B., N.W.K., F.W.S.); and Cardiology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (R.J.L.).
Circulation. 2013 Sep 10;128(11 Suppl 1):S136-43. doi: 10.1161/CIRCULATIONAHA.112.000207.
Moderate alcohol consumption is known to be cardioprotective compared with either heavy drinking or complete abstinence. We assessed the hypothesis that ethanol supplementation would improve myocardial function in the setting of chronic ischemia.
Sixteen male Yorkshire swine underwent placement of an ameroid constrictor into the left circumflex artery to induce chronic myocardial ischemia. Postoperatively, animals were supplemented with either 90 mL of ethanol (EtOH) daily (50%/V, EtOH) or 80 g of sucrose of equal caloric value (SUC), serving as controls. Seven weeks after ameroid placement, arteriolar density (1.74 ± 0.210% versus 3.11 ± 0.368% area of arterioles per low-powered field in sucrose (SUC) versus EtOH; P=0.004), myocardial perfusion (ratio of blood flow to the at-risk myocardium compared with the normal ventricle during demand pacing was 0.585 ± 0.107 versus 1.08 ± 0.138 for SUC versus EtOH; P=0.014), and microvascular reactivity were significantly increased in ethanol-treated animals compared with controls in the at-risk myocardium. Analysis of vascular endothelial growth factor and NOTCH pathway signaling suggested proneovascular and proliferative activity in the ischemic area. The average peak blood alcohol level in the treatment group was 40 ± 4 mg/dL, consistent with levels of moderate drinking in humans.
Ethanol supplementation increased arteriolar density and significantly improved myocardial perfusion and endothelium-dependent vasorelaxation in chronically ischemic myocardium. These findings suggest that, at moderate doses, ethanol directly promotes vasculogenesis and improves microvascular function, resulting in significant improvements in myocardial perfusion in the setting of chronic ischemia.
与重度饮酒或完全戒酒相比，适量饮酒对心脏有保护作用。我们评估了这样一个假设，即乙醇补充剂会改善慢性缺血情况下的心肌功能。
16 只雄性约克夏猪接受了左回旋动脉的 ameroid 缩窄器放置，以诱导慢性心肌缺血。手术后，动物每天补充 90 毫升乙醇（50%/V，乙醇）或 80 克等热量蔗糖（SUC），作为对照。在 ameroid 放置后 7 周，小动脉密度（1.74 ± 0.210%相对于蔗糖（SUC）中的小动脉面积的 3.11 ± 0.368%；P=0.004）、心肌灌注（需求起搏时与正常心室相比，风险心肌的血流与血流比为 0.585 ± 0.107 相对于 SUC 与 EtOH 的 1.08 ± 0.138；P=0.014）以及微血管反应性在乙醇治疗组与对照组的风险心肌中均显著增加。血管内皮生长因子和 NOTCH 通路信号分析表明，缺血区存在促血管生成和增殖活性。治疗组的平均峰值血醇水平为 40 ± 4 mg/dL，与人类适度饮酒的水平一致。
乙醇补充剂增加了小动脉密度，并显著改善了慢性缺血心肌的心肌灌注和内皮依赖性血管舒张。这些发现表明，在适度剂量下，乙醇直接促进血管生成并改善微血管功能，从而在慢性缺血情况下显著改善心肌灌注。
