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应用镧离子示踪法于透射电镜下观察了缺血再灌注兔心肌细胞质膜渗透性的改变及其钙通道阻滞剂对它的影响。正常心肌中镧离子存在于细胞外间隙;缺血30min时超微结构改变呈可逆性,镧进入细胞并粘附于线粒体膜外面;再灌注后超微结构损伤呈不可逆性,镧进入线粒体内;再灌注前给以异搏停,再灌注损伤明显改善,线粒体内镧颗粒消失;缺血前给以异搏停,细胞膜和超微结构保存较好,细胞内镧基本消失。实验提示缺血再灌注心肌细胞中,细胞膜渗透性改变先于细胞的不可逆性损伤,而细胞膜渗透性改变又早于细胞器膜,无论是在缺血前还是于再灌注前给以导搏停,对质膜结构和功能均有一定的保护作用。
The changes of plasma membrane permeability of myocardial cells in ischemia-reperfusion rabbits and the effects of calcium channel blockers on it were observed by transmission electron microscopy using lanthanum ion tracer method. In the normal myocardium, lanthanum ions existed in the extracellular space. The changes of ultrastructure were reversible after ischemia for 30 min. Lanthanum entered the cells and adhered to the outside of the mitochondrial membrane. After reperfusion, the ultrastructure damage was irreversible and lanthanum entered the mitochondria. Before reperfusion to verapamil, reperfusion injury was significantly improved, mitochondrial lanthanum particles disappear; ischemic pre-given verapamil, cell membrane and ultrastructure preservation is better, intracellular lanthanum basically disappeared. Experiments suggest that ischemia-reperfusion myocardial cells, cell membrane permeability changes before irreversible cell damage, and cell membrane permeability changes earlier than the organelle membrane, either in the pre-ischemia or before reperfusion to guide stroke stop, The plasma membrane structure and function have a certain protective effect.