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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 this study, cytochemical methods combined with EDX microanalysis and biochemical test methods were used to study the change of intracellular calcium content in renal proximal tubule epithelial cells during ischemia-reperfusion injury at the cellular level and to explore its mechanism . The results showed that: ischemia 1h, increased intracellular calcium content, plasma membrane Ca2 + -ATPase activity decreased; membrane permeability did not change significantly. At the period of reperfusion, the content of intracellular calcium continued to increase. The plasma membrane Ca2 + -ATPase activity returned to normal in the early reperfusion period (2-4 h) and decreased in the late stage of reperfusion (12-24 h) Increase. Increased calcium content in tubular epithelial cells during ischemia, early and late reperfusion a mechanism is not the same.