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目的 :探讨预处置对缺血再灌注损伤肝脏的防护及其机制。方法 :随机将家兔分为对照组、缺血再灌注组和预处置组 ,复制肝缺血再灌注损伤 (HIRI)模型 ,观察反复 3次缺血 5min再灌注 5min(预处置 )后再缺血 45min再灌注 45min ,对血浆、肝组织一氧化氮 (NO)和丙二醛 (MDA)水平、谷丙转氨酶 (ALT)值及肝细胞形态学改变的影响。结果 :肝缺血再灌注期间 ,预处置组血浆及肝组织NO水平明显高于缺血再灌注组 (P <0 0 5 ) ;而MDA水平和血浆ALT均显著低于缺血再灌注组 (P <0 0 5和P <0 0 1) ;且与仅行游离、不阻断肝血流的对照组比较均无明显差异 ;肝细胞形态学异常改变也明显减轻。结论 :预处置可通过提高体内NO水平及降低体内氧自由基水平而减轻HIRI。
Objective: To investigate the protective effect of preconditioning on the liver of ischemia-reperfusion injury and its mechanism. Methods: Rabbits were randomly divided into control group, ischemia reperfusion group and preconditioning group. The model of liver ischemia reperfusion injury (HIRI) was duplicated. The rats were sacrificed 3 minutes after reperfusion for 5 minutes Blood 45min 45min reperfusion for plasma and liver tissue of nitric oxide (NO) and malondialdehyde (MDA) levels, alanine aminotransferase (ALT) and liver cell morphological changes. Results: During the period of hepatic ischemia / reperfusion, the level of NO in plasma and liver tissue in preconditioning group was significantly higher than that in ischemia / reperfusion group (P <0.05), but MDA level and ALT in plasma were significantly lower than those in ischemia / reperfusion group P <0 05 and P 0 01). There was no significant difference between the control group and the control group which only had free and did not block the hepatic blood flow. The change of morphological abnormality of hepatocytes was also significantly reduced. Conclusion: Pretreatment can reduce HIRI by increasing NO level in the body and reducing the level of oxygen free radicals in the body.