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利用大鼠肾脏缺血再灌注致急性缺血性肾衰模型，观察纳洛酮（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。结果显示缺血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2mg．kg－1，Ⅱ组4mg．kg-1ip）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，NALⅡ组明显好于Ⅰ组。表明NAL对急性缺血性肾衰有一定的保护作用。
The model of acute ischemic renal failure induced by ischemia / reperfusion in rat kidneys was used to observe the effects of naloxone (NAL) on plasma malondialdehyde (MDA), superoxide dismutase (SOD) and renal The effects of Na +, K + -ATPase and Ca2 + -ATPase in the tissue and histopathological changes were observed. The results showed that after 60 min of ischemia, the content of MDA in blood increased significantly, the activity of SOD decreased obviously, and the activity of Na +, K + -ATPase and Ca2 + -ATP in kidney decreased significantly. After treatment with NAL (2mg.kg-1 in group I, 4mg.kg-1ip in groupⅡ), MDA was significantly decreased, SOD and Na +, K + -ATPase and Ca2 + -ATPase were significantly increased, and there was a dose-effect relationship. Histopathological examination showed that the damage of renal tubular epithelial cells was significantly reduced after NAL application, and NALⅡgroup was significantly better than that of group Ⅰ. Show that NAL has some protective effect on acute ischemic renal failure.