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本实验运用光镜、电镜、酶组化、钙组化和心肌及血清MDA水平测定观察2个月内心肌冠状动脉结扎后心肌梗塞的动态病理变化。主要发现为早期的心肌纤维坏死和晚期的修复。电镜改变出现早,几乎累及所有细胞器;晚期的修复主要为不完全再生,并见少量心肌细胞再生及成纤维细胞间的“连接”结构。梗塞后各种酶活性迅速被抑制,提示能量代谢的耗竭。心肌MDA于结扎后24h内升高,提示心肌缺血确可使自由基引发的LPO反应增强,此可能是心肌缺血后不可逆性膜损伤的机制之一。
In this experiment, the dynamic pathological changes of myocardial infarction after coronary artery ligation within 2 months were observed by light microscope, electron microscope, enzyme histochemistry, calcium group and myocardial MDA level. The main findings were early myocardial fibrosis and advanced repair. Electron microscopy changes appear early, involving almost all organelles; late repair mainly incomplete regeneration, and see a small amount of myocardial cell regeneration and fibroblasts “connection” structure. Various enzyme activities were rapidly inhibited after infarction, suggesting depletion of energy metabolism. Myocardial MDA increased within 24 hours after ligation, suggesting that myocardial ischemia can indeed lead to free radical-induced LPO response, which may be one of the mechanisms of irreversible membrane damage after myocardial ischemia.