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目的确定细胞凋亡参与心肌缺血 /再灌注损伤 ,观察凋亡相关基因 (Bcl 2、Bax和Fas)表达的变化。方法在 12只雄性家兔心脏缺血 /再灌注模型上 ,监测血流动力学、心外膜电图和心肌梗死范围。由原位末端标记法和凝胶电泳法确定心肌细胞凋亡 ;流式细胞分析法测定细胞凋亡率以及Bcl 2、Bax和Fas表达量。结果在缺血/再灌注过程中 ,心率、血压和心肌耗氧量均持续性下降 ;心外膜电图ST段在缺血期明显抬高 ,再灌注时逐渐恢复正常。心肌梗死范围占缺血心肌的 (5 7.7± 2 .0 ) %。原位末端标记法显示 ,缺血区存活心肌中有大量凋亡细胞 ,且缺血区心肌凝胶电泳上呈典型的云梯状 ,细胞凋亡率为 (11.2± 0 .4) % ,Bax和Fas表达较非缺血区增高。结论缺血 /再灌注可使心肌细胞发生凋亡 ,可能与Bax和Fas过量表达有关
Objective To determine whether apoptosis is involved in myocardial ischemia / reperfusion injury and to observe the changes of apoptosis related genes (Bcl 2, Bax and Fas). Methods The hemodynamics, epicardiogram, and myocardial infarction range were monitored in a model of cardiac ischemia / reperfusion in 12 male rabbits. Cardiomyocyte apoptosis was determined by in situ terminal labeling and gel electrophoresis. Flow cytometry was used to determine the apoptosis rate and the expression of Bcl 2, Bax and Fas. Results During the process of ischemia / reperfusion, heart rate, blood pressure and myocardial oxygen consumption decreased continuously. ST segment in epicardial electrocardiogram was significantly elevated during ischemia and gradually returned to normal after reperfusion. Myocardial infarction range of ischemic myocardium (5 7.7 ± 2.0%). In situ terminal labeling showed that there were a large number of apoptotic cells in the ischemic myocardium and the typical ladder-shaped electrophoresis on myocardial gel electrophoresis. The apoptotic rates were (11.2 ± 0.4)%, Bax and Fas expression increased compared with non-ischemic area. Conclusion Ischemia / reperfusion can induce cardiomyocyte apoptosis, which may be related to overexpression of Bax and Fas