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出 处:《肝脏》2002年第1期20-21,27,共3页Chinese Hepatology
摘 要:目的 探讨肝动脉缺血 (HAI)对肝脏组织损伤的影响及其机制。方法 将家兔按有无再灌注后HAI分为HAI组和对照组。在兔肝自体原位移植模型基础上 ,应用原位末端标记 (TUNEL)技术、免疫组化法和硝酸还原酶法 ,检测肝细胞凋亡指数 (AI)、bcl 2蛋白表达和肝组织中一氧化氮 (NO)生成水平。结果 HAI组再灌注后各时点肝细胞AI均高于对照组 ;bcl 2蛋白表达阳性细胞于再灌注后较灌注前增多 ,但HAI组与对照组比较 ,各时点均无明显差异 (P >0 .0 5 ) ;再灌注后NO浓度较灌注前降低 ,而且再灌注早期HAI组明显低于对照组 (P <0 .0 5 )。结论 HAI可通过进一步降低缺血再灌注后NO水平而加重肝细胞凋亡损伤 ,阻碍供肝功能的恢复 ,是移植术后供肝功能不全和并发症发生的关键因素之一。Objective To observe the effects of hepatic artery ischemia (HAI) on hepatocytic apoptosis and investigate the initial mechanism. Methods Rabbits were divided into HAI and control groups, depending on the occurrence of HAI after reperfusion. On the model of orthotopic hepatic autotransplantation in rabbits, the apoptosis index (AI) of hepatocytes was examined by the in situ end nick labelling technique(TUNEL), bcl 2 protein expression by immunohistochemistry and release of nitric oxide(NO) using nitrite/nitrate colormetric method.Results The AI of hepatocytes in HAI group during 1 to 12 h after reperfusion was higher than that of the control; The bcl 2 positive cell increased after reperfusion and there was no significant difference in all the indices between HAI and control groups( P >0.05); The concentration of NO in hepatic tissue decreased after reperfusion, moreover, it was lower in HAI group than in the control group. The difference was significant in the early stage of reperfusion( P <0.05).Conclusion HAI initiated the apoptosis of hepatocytes by reduced production of NO and impeded the recovery of hepatic function. HAI might be one of the key factors of development of posttransplant hepatic insufficiency and complications.
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