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本实验在电镜下观察了毛冬青甲素对实验性心衰家兔心肌超微结构的影响及心肌细胞中线粒体琥珀酸脱氢酶量的改变。结果显示:对照组心肌细胞核染色质集聚,核膜肿胀;胞浆基质呈现片状水肿空白区;肌原纤维排列紊乱,带区不清或断裂,溶解;线粒体肿胀,外膜破裂或基质致密,嵴突模糊;糖原颗粒减少,肌质网扩张或破裂;心肌细胞线粒体琥珀酸脱氢酶活性产物完全消失,或仅少许点片状分布于线粒体的外膜上,而用药组心肌细胞超微结构的改变仅表现为线粒体肿胀与基质密度下降,与正常组仅有轻度差异。而用药组心肌琥珀酸脱氢酶活性物质明显多于对照组,与正常组相近。实验结果提示,毛冬青甲素能提高心肌细胞对缺血(缺氧)的耐受能力,其对缺血状态心肌细胞线粒体中琥珀酸脱氢酶缺失的缓解作用,可能是该药对心肌保护作用的机理之一。
In this experiment, we observed the effect of hollycine on myocardial ultrastructure of rabbits with experimental heart failure and the changes of mitochondrial succinate dehydrogenase in myocardial cells under electron microscope. The results showed that in the control group, the nuclear chromatin accumulated and the nuclear membrane swelled; the cytoplasmic matrix showed a flaky edema; the myofibril was arranged disorderly, the band was unclear or broken and dissolved; the mitochondria was swollen, the outer membrane was ruptured or the matrix was dense, Condylar obscure; reduced glycogen granules, expanded or ruptured sarcoplasmic reticulum; myocardial mitochondrial succinate dehydrogenase activity products completely disappeared, or only a few patches distributed on the mitochondrial adventitia, while the drug group myocardial cell ultramicro Structural changes only showed mitochondrial swelling and decreased matrix density, with only mild differences from the normal group. The active substance of myocardium succinate dehydrogenase in the medication group was significantly more than that in the control group, which was similar to the normal group. The experimental results suggest that Maodongqingsu A can improve the tolerance of myocardial cells to ischemia (hypoxia), and its alleviation effect on the loss of succinate dehydrogenase in mitochondria of ischemic myocardial cells may be the protection of the drug against myocardial ischemia. One of the mechanisms of action.