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采用动物缺血－再灌注模型，结扎兔冠状动脉左前降支（LAD）造成急性心肌梗塞（AMI）。实验组经过5min缺血，10min再灌注后持续缺血60min，3h再灌注；对照组直接造成60min缺血，3h再灌注。心肌梗塞范围由1％三苯四氮唑兰（TTC）染色确定，并以梗塞范围占缺血范围重量的百分比表示。结果：实验组梗死心肌明显少于对照组（P＜0.01）；实验组发生室性心律失常率明显低于对照组（P＜0．05）；实验组再灌注后血小板表面α－颗粒膜蛋白（GMP－140）分子数明显少于对照组（P＜0．05）。表明：预适应（Preconditioning，PC）具有心肌保护作用。
Animal model of ischemia - reperfusion was used to ligate the left anterior descending artery (LAD) of rabbit to cause acute myocardial infarction (AMI). The experimental group after 5min ischemia, 10min reperfusion after ischemia for 60min, 3h reperfusion; control group caused by 60min ischemia, 3h reperfusion. Myocardial infarct size was determined by 1% triphenyltetrazolium (TTC) staining and expressed as a percentage of the infarct area to the weight of the ischemic area. Results: The myocardial infarction in the experimental group was significantly less than that in the control group (P <0.01). The incidence of ventricular arrhythmia in the experimental group was significantly lower than that in the control group (P <0.05). The level of α-granular membrane protein (GMP-140) molecules was significantly less than the control group (P <0.05). Show: Preconditioning (PC) has a cardioprotective effect.