缺血预处理对大鼠肝缺血再灌注损伤的保护

Ischemic preconditioning protects liver from ischemiareperfusion injury in rats

目的反复短时间缺血可保护组织免受随之而来的长时间缺血性损伤，这种现象称之为缺血预处理（ＩＰＣ）．现探讨ＩＰＣ在肝脏缺血再灌注（Ｉ／Ｒ）损伤中的作用及机制．方法采用大鼠肝脏原位Ｉ／Ｒ模型，术前腹腔注射Ｌ精氨酸（ＬＡｒｇ）２５０ｍｇ·ｋｇ－１或Ｌ硝基精氨酸（ＬＮＮＡ）１５ｍｇ·ｋｇ－１，分别观察血一氧化氮（ＮＯ），ＡＬＴ，ＡＳＴ；肝组织ＮＯ，脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）及肝组织病理损伤．结果肝组织ＬＰＯ含量（多少ｖｓ多少）、血清ＡＬＴ（多少ｖｓ多少）、ＡＳＴ（多少ｖｓ多少）活性明显低于Ｉ／Ｒ组，ＩＰＣ显著改善了由Ｉ／Ｒ引起的肝脏损伤．这种保护作用完全被ＮＯ供体（ＬＡｒｇ）或ＮＯ合酶抑制剂（ＬＮＮＡ）消除．同时，各组之间血、肝ＮＯ含量无显著差异．结论ＩＰＣ对肝脏Ｉ／Ｒ损伤呈现出明显的保护作用，其机理是灭活了氧自由基．ＮＯ在肝脏ＩＰＣ中似乎无明显作用．

IM Short periods of ischemia can protect tissues against the effects of subsequent prolonged period of ischemia, which is called ischemic preconditioning(IPC). To investigate the action of IPC protection on hepatic ischemiareperfusion(I/R) injury and its mechanism in rats. METHODS With in situ hepatic I/R injury model, the rats were intraperitoneally injected with Larginine (LArg) 250mg·kg-1 or NGnitroLarginine (LNNA) 15mg·kg-1 before operation. Nitric oxide (NO) content, ALT, AST activities in serum, NO and LPO contents and SOD activity in liver tissues, hepatic pathology were observed and assayed. RESULTS LPO content in hepatic tissues and serum ALT, AST activities were significantly lower than those in the I/R group. These protective effects were completely abolished by administration of NO donor (LArg) or NO synthase inhibitor (LNNA). Serum had hepatic NO contents had no changes in each group. CONCLUSION IPC protects liver from I/R injury. The mechanism may be inactivation of the oxygen free radicals, and it is unlikely that NO is involved in hepatic ischemic preconditioning.