β-受体阻滞剂促大鼠缺血心肌血管新生的实验研究

Experimental study of myocardial angiogenesis of infarcted rats promoted by beta-receptor blocker

目的：评价β-受体阻滞剂是否有促进缺血心肌血管新生的作用并探讨其发生机制。 方法：将急性心肌梗塞1周后的大鼠分别用美托洛尔灌胃1～3周，用免疫组织化学法检测缺血心肌中毛细血管内皮细胞及VEGF，并计数毛细血管密度，同时观察心率的变化。 结果：服用美托洛尔后的大鼠缺血心肌中毛细血管密度和VEGF蛋白表达明显增加；用美托洛尔后心率下降显著的心肌梗塞大鼠，其缺血心肌中毛细血管密度和VEGF表达又显著高于心率下降不明显的大鼠。 结论：β-受体阻滞剂可以促进缺血心肌毛细血管新生，该作用可能是由窦性心动缓触发的内源性VEGF分泌增加所致。

Objective: We studied expression of Vascular endothelial growth factor (VEGF) and angiogenesis in ischemic myocardium from a group of rats with acute myocardial infarction (AMI) after taking metoprolol---- a beta-receptor blocker, in order to determine if beta-receptor blocker can promote myocardial angiogenesis in rat s with AMI and reveal the mechanism. Methods: The infarcted rats received last metoprolol administration for 1-3 weeks. Vascular endothelial cells and VEGF protein in ischemic myocardium were detected by immunohisto-chemical technique. Capillary density and heart rate were detected too. Results: Capillary density and expression of VEGF protein were higher in ischemic myocardium of rats with metoprolol treatment than in ischemic myocardium of rats in control group. Capillary density and expression of VEGF significantly increased in ischemic myocardium with reduction of heart rate in comparison with no reduction of heart rate in rats with metoprolol treatment. Conclusion: Beta-receptor blocker may promote capillary angiogenesis in ischemic myocardium of rats. It suggests that VEGF plays a key role in the angiogenic response that occurs with chronic bradycardia.