急性心肌损害对心肌肌球蛋白磷酸化系统的影响

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。

Studies on the effect of injured myocardium on the phosphorylation of myosin

Studies on the dynamic changes of MLCK and actin myosin ATPase in myocardium injury were made.The activities of MLCK and ATPase in myocardium injured by ISP decreased,the pathological sections of myocardium were almost normal under light microscope.With the aggravation of the injury,the activies of MLCK and ATPase were much lower than those of the control and low dose groups and there were many greater necroticareas.The results suggested that before occurrence of pathological changes there was a series of metabolic disorders in cardiac cells.After changes of pathological morphology,the activities of enzymes in cells decreased significantly and the reversible damage developed irreversible myocardium necrosis.