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为探讨纳洛酮（NAL）对肾脏缺血再灌注损伤中的保护作用，利用大鼠肾脏缺血再灌注致急性缺血性肾功能衰竭（肾衰）模型，观察NAL对肾缺血再灌注后血中丙二醛（MDA）、超氧化物歧化酶（SOD）及肾组织中Na+、K+－ATP酶和Ca2+－ATP酶的影响，并观察组织病理学变化。结果缺血60min再灌注后，血MDA含量明显升高，SOD活力明显降低，肾组织Na+、K+－ATP酶和Ca2+－ATP酶活力均显著降低。用NAL（Ⅰ组为2mg／kg，Ⅱ组为4mg／kg）后，MDA显著下降，SOD和Na+、K+－ATP酶及Ca2+－ATP酶均明显升高，且有量效关系。组织病理学检查显示应用NAL后肾小管上皮细胞的损伤明显减轻，NAL－Ⅱ组明显好于NAL－Ⅰ组。认为NAL对急性缺血性肾衰有一定的保护作用。
To investigate the protective effect of naloxone on renal ischemia-reperfusion injury, the model of acute ischemic renal failure (renal failure) induced by renal ischemia-reperfusion in rats was used to observe the effect of NAL on renal ischemia-reperfusion (MDA), superoxide dismutase (SOD) and Na +, K + -ATPase and Ca2 + -ATPase in renal tissue were detected by enzyme-linked immunosorbent assay (ELISA) and histopathological changes were observed. Results After reperfusion for 60 minutes, the content of MDA in blood increased significantly, the activity of SOD decreased significantly, and the activity of Na +, K + -ATPase and Ca2 + -ATP in kidney decreased significantly. With NAL (Ⅰ group 2mg / kg, Ⅱ group 4mg / kg), MDA decreased significantly, SOD and Na +, K + -ATPase and Ca2 + -ATP enzyme were significantly increased, and a dose-effect relationship. Histopathological examination showed that the injury of renal tubular epithelial cells was significantly reduced after NAL application, and NAL-Ⅱ group was significantly better than NAL-Ⅰ group. That NAL has a protective effect on acute ischemic renal failure.