目的:探讨延迟缺血预处理对急性心梗大鼠远期的心肌保护及其促进血管再生的作用。方法:分别制作4组大鼠模型。处理组:缺血预处理(IPC)后24h结扎冠脉建立急性心梗大鼠模型;对照组:开胸后只穿线未进行IPC,24h后结扎冠脉建立急性心梗大鼠模型;IPC组:只进行IPC不结扎冠脉;假手术组:既不进行IPC操作也不结扎冠脉。对前2组模型建立3d、7d和14d后免疫组化法检测梗死边缘区毛细血管新生、动脉再生。14d后评价心功能,测量心梗面积;对IPC组和假手术组采用免疫组化法检测缺血区心肌血管内皮生长因子(VEGF)表达。结果:处理组IPC后24h缺血区心肌可见到毛细血管新生,梗死3d、7d和14d后梗死边缘区心肌毛细血管密度和小动脉密度较对照组显著增加。处理组大鼠短轴缩短率较对照组显著升高,心梗面积减少。IPC组缺血区心肌VEGF表达较假手术组显著升高。结论:延迟缺血预处理改善心梗后远期心功能,减少心梗面积,增加梗死边缘区毛细血管新生和小动脉再生,至少部分与IPC后VEGF表达增加有关。 Objective: To investigate the long-term myocardial protection and its effect on angiogenesis induced by delayed ischemic preconditioning in acute myocardial infarction rats. Methods: Four groups of rats were made respectively. The rats in the treatment group were subjected to coronary artery ligation 24h after ischemia preconditioning (IPC), and the rats in the control group were given IPC only after threading the thoracotomy. The rats in the IPC group : Only IPC without coronary artery occlusion; sham operation group: neither IPC nor coronary artery ligation. The first two groups of models were established 3d, 7d and 14d after immunohistochemical detection of peripheral capillary zone angiogenesis, arterial regeneration. After 14 days, the cardiac function was evaluated and the area of ​​myocardial infarction was measured. The expression of vascular endothelial growth factor (VEGF) in ischemic myocardium was detected by immunohistochemistry in IPC group and sham operation group. Results: Capillary neovascularization was observed 24h after ischemic injury in IPC group. The myocardial capillary density and arteriolar density in the infarct border area were significantly increased at 3d, 7d and 14d after infarction. The short axis shortening rate of rats in treatment group was significantly higher than that in control group, and the area of ​​myocardial infarction was decreased. The expression of VEGF in ischemic myocardium in IPC group was significantly higher than that in sham operation group. CONCLUSION: Delayed ischemic preconditioning can improve long-term cardiac function, reduce infarct size, increase capillary angiogenesis and arteriolar regeneration in infarct border areas, at least partly related to the increased VEGF expression after IPC.