卡托普利对老年大鼠肾缺血/再灌注损伤的影响

目的 探讨卡托普利（CAP）对老年大鼠急性缺血／再灌注损伤的保护机制。方法 将60只老年大鼠（20-22月龄）随机等分为假手术组（A组）、缺血／再灌注组（B组）和CAP治疗组（C组，预先两周喂服卡托普利）。检测各组在急性缺血1h、再灌注1h及24h，肾组织匀浆中的超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量变化，并观察肾组织形态学改变。结果 与A组对比，B、C组中肾组织的SOD活性显著下降，MDA的含量明显增高。C组在再灌注期肾皮质中的MDA浓度明显低于B组（P〈0.01），SOD活性明显高于B组（P〈0．01）。B组电镜可见明显急性肾小管损伤和坏死，而C组肾小管损伤轻微。结论 老年大鼠缺血／再灌注损伤中，氧自由基参与了肾脏的损伤过程。卡托普利可以降低MDA含量，增加SOD活性．通过抑制氧自由基的产生．减轻脂盾过氧化反应．对肾脏有保护作用。

Effect of captopril on the aged rats with renal ischemia-reperfusion injury

Objective To evaluate the protective effect of captopril (CAP) on acute ischemia-reperfusion injury in the aged rats. Methods 60 aged rats were randomly divided into sham operation group (A, n=20), ischemia -reperfusion (I/R) group (B, n=20), and CAP-group (C, n=20). CAP was fed by ig to the rats two weeks before renal ischemia-reperfusion in advance. After 1h renal ischemia, 1 h and 24 h renal ischemia-reperfusion, the content of malonyldialdehyde (MDA) and activity of superoxide dismutase (SOD) were detected in the homogenate of renal tissue. The kidney specimens were examined by using electron microscope. Results In group C and group B, the SOD activity in renal tissue reduced significantly and MDA level increased significantly, compared with group A. In group C, renal cortex MDA concentration after reperfusion was significantly decreased (P<0.01), SOD activity increased significantly (P<0.01), compared with group B. Under electron microscope, renal pathology was associated wih acute injury and necrosis was observed in group B, meanwhile, it was obviously alleviated in group C.Conclusions In ischemia-reperfusion injury the oxygen free radicals (OFR) can cause renal injury; CAP can decrease the level of MDA, increase the activation of SOD by inhibiting the generation of OFR, elevating the ability of anti-lipid peroxidation reaction.