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用新西兰大白兔制作急性肾缺血及再灌流损伤模型，观察肾组织细胞内三磷酸肌醇（ＩＰ３）、细胞内总钙及胞浆游离钙（［Ｃａ（２＋）］ｉ）浓度变化。结果显示，缺血组与对照组的ＩＰ３浓度（±ｓ）分别为（４３０．３±４６．８）、（２９７．９±５４．３）ｍｉｎ（－１），［ｃａ（２＋）］ｉ浓度分别为（２１２．５±４３．５）、（１０６．１±１５．５）ｎｍｏｌ／Ｌ，前者较后者均显著性升高（均为Ｐ＜０．０１），总钙浓度分别为（３９８．６±３２．３）、（３８５．０±３２．４）μｍｏｌ／Ｌ，两组无显著性差异（Ｐ＞０．０５）。再灌流６０ｍｉｎ后ＩＰ３浓度为（７７６．０±６８．０）ｍｉｎ（－１）、［Ｃａ（２＋）］ｉ浓度为（４１２．１±４７．３）ｎｍｏｌ／Ｌ、总钙浓度为（４４７．１±４２．５）μｍｏｌ／Ｌ，较对照组和缺血组均显著性增加（Ｐ＜０．０１）。提示，细胞内ＩＰ３对急性肾缺血及再灌流损伤中肾组织细胞内钙超负荷的形成具有重要作用。
Acute renal ischemia / reperfusion injury model was made in New Zealand white rabbits. The changes of intracellular total inositol triphosphate (IP3), intracellular total calcium and cytoplasmic free calcium ([Ca (2 +)] i were observed. The results showed that IP3 concentrations in ischemic group and control group were (430.3 ± 46.8), (297.9 ± 54.3) min (-1), [ca (2 +)] i (212.5 ± 43.5) and (106.1 ± 15.5) nmol / L, respectively. The former was significantly higher than the latter (all P <0.01), and the total calcium concentrations were (398.6 ± 32.3) and (385 ± 32.4) μmol / L, respectively. There was no significant difference between the two groups (P> 0.05). The IP3 concentration was (776.0 ± 68.0) min (-1) at 60 min after reperfusion, the concentration of [Ca (2 +)] i was (412.1 ± 47.3) nmol / L and the total calcium concentration was (447 .1 ± 42.5) μmol / L, which was significantly higher than that of the control group and the ischemia group (P <0.01). These results suggest that intracellular IP3 plays an important role in the formation of intracellular calcium overload in acute renal ischemia and reperfusion injury.