摘要
本实验采用细胞化学方法结合EDX微区分析及生化测试方法,从细胞水平研究了大鼠肾近曲小管上皮细胞内钙含量在缺血-再灌流损伤过程中的改变情况,并探讨了其机理。结果表明:缺血1h,可致细胞内钙含量增高,质膜Ca2+-ATPase活性下降;膜通透性无明显变化。再灌流期,细胞内钙含量持续增高;质膜Ca2+-ATPase活性在再灌流早期(2~4h)基本恢复至正常,在再灌流晚期(12~24h)下降;再灌流期膜通透性逐渐增大。肾小管上皮细胞内钙含量增加在缺血期、再灌流早期及晚期某机制并不相同。
In present experiment, we used cytochemical methods, EDX microanalysis and biochemical analysis technique to evaluate the changes of calcium content in rat renal proximal tubule cells during ischemia and reperfusion period. By the end of 1h ischemia,intra-cellular calcium increased. The activity of plasma membrane Ca2 -ATPase decreased. The membrane permeability showed no evident change. During reperfusion period, intracellular calcium increased continuously. The activity of plasma membrane Ca2+-ATPase increased near to the normal level during early reperfusion period (2 ~ 4h ), and decreased during later reperfusion period (12 ~ 24h ).The membrane permeability increased gradually during reperfusion period. The mechanisms of intracellular calcium increase during ischemia,early and later reperfusion period were different.
出处
《基础医学与临床》
CSCD
1997年第1期50-53,共4页
Basic and Clinical Medicine