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为探讨急性心肌损害对心肌肌球蛋白磷酸化系统的影响，选择对于心肌有特异性损害作用的异丙基肾上腺素（ＩＳＰ），造成大鼠实验性心肌损害的动物模型，动态观察心肌损害时肌球蛋白磷酸化系统的变化规律。研究结果表明，低剂量ＩＳＰ导致心肌匀浆中肌球蛋白轻链激酶（ＭＬＣＫ）和肌动球蛋白ＡＴＰ酶的活性下降，但心肌组织病理切片基本正常；高剂量注射ＩＳＰ，ＭＬＣＫ和ＡＴＰ酶活性显著下降，与正常对照组和低剂量组相比，差异十分显著（Ｐ＜０．０１）。在病理形态学上大鼠心肌组织有多处较大的坏死灶。提示，在未发生明显的病理性变化前，心肌细胞内就已发生了一系列的代谢紊乱，如酶活性下降，心肌细胞的收缩功能发生改变；当心肌组织出现病理形态学改变时，细胞内酶活性显著下降，表明已由可逆性损害发展到不可逆的心肌坏死。
To investigate the effect of acute myocardial damage on myocardial myosin phosphorylation system, select the isoproterenol (ISP) that has specific damage to the myocardium, an animal model of experimental myocardial damage in rats, to dynamically observe myocardial damage Myosin phosphorylation system changes. The results showed that low-dose ISP caused myocardial myosin light chain kinase (MLCK) and actomyosin ATPase activity decreased, but myocardial histopathology was normal; high-dose injection of ISP, MLCK and ATPase activity (P <0.01). Compared with normal control group and low dose group, the difference was significant (P <0.01). Pathological morphology of myocardial tissue in many large necrosis. Tip, in the absence of significant pathological changes, myocardial cells have occurred within a series of metabolic disorders, such as decreased enzyme activity, myocardial contractile function changes; when myocardial tissue pathological changes, intracellular Significantly decreased enzymatic activity indicates that irreversible myocardial necrosis has been developed from reversible lesions.