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[目的 ]从形态学角度进一步研究钙离子在心肌细胞中的转运机制和分布规律 .[方法 ]以放射性钙离子为放射源 ,利用电子显微镜放射自显影和冷冻蚀刻 电子显微镜放射自显影方法对小鼠心肌细胞进行研究 .[结果 ]电子显微镜放射自显影实验结果显示 ,正常组的线粒体嵴完好 ,缺血对照组的线粒体肿胀 ,嵴不完整 ;腺苷三磷酸氯化酶组的线粒体较缺血对照组破坏较轻 ,嵴较完整 ;同位素标记的正常、缺血对照组、腺苷三磷酸氯化酶组中可观察到菊花状的银丝团散布于组织切片上 ,且主要分布于内质网和线粒体上 ,缺血对照组的线粒体上有较多的银丝团 .冷冻复型 电子显微镜放射自显影结果显示 ,缺血对照组细胞核膜的E片劈裂面和P片劈裂面上核孔稀少 ,分布不均匀 ;腺苷三磷酸氯化酶组质膜蛋白颗粒丰富 ,且分布均匀 ;在各组复型膜上可见到菊花状银丝团 .缺血缺氧时细胞质膜蛋白颗粒减少 ,提示做为钙通道的糖蛋白受体减少 ,而此时线粒体钙却增加 .[结论 ]钙离子的进入更多地依赖于钠、钙交换 ,而不是钙通道 .高能磷酸盐制剂改善了细胞膜的功能 ,防止了钙离子在线粒体内的聚集 .
[Objective] To further study the transport mechanism and distribution of calcium ion in cardiomyocytes from the morphological point of view. [Methods] With radioactive calcium ion as a radioactive source, using electron microscopy autoradiography and cryo-etching electron microscopy autoradiography [Results] The results of electron microscopy autoradiography showed that the mitochondrial ridges of the normal group were intact, the mitochondria in the ischemic control group were swollen, and the ridges were incomplete. The mitochondria of adenosine triphosphate chloride group were more ischemic The control group was less damaged and the ridges were more complete. Isotope-labeled normal, ischemic control group and adenosine triphosphate chloride group could be observed in the chrysanthemum-like filaments scattered on the tissue sections, and mainly distributed in the endoplasmic reticulum There were more silver filaments on the mitochondria and mitochondria in ischemic control group.Free autoradiography of cryopreserved electronic microscope showed that in the ischemic control group, the E-piece cleavage surface and P-piece cleavage surface Nuclear pore sparse, uneven distribution; adenosine triphosphate chloride plasma membrane protein-rich group of particles, and evenly distributed; in each group of compound membrane can be seen on the chrysanthemum-like group. Hypoxia plasma membrane protein particles decreased, suggesting that as the calcium channel of the glycoprotein receptor decreased, while the mitochondrial calcium increased at this time. [Conclusion] Calcium entry more dependent on sodium and calcium exchange, rather than calcium channels High energy phosphate formulations improve the function of the cell membrane and prevent the accumulation of calcium ions in the mitochondria.