【摘要】 目的探讨缺血预处理（ＩＰＣ）在肝缺血再灌注（Ｉ／Ｒ）损伤中的作用及腺苷在此过程中的作用机制．方法采用大鼠原位肝Ｉ／Ｒ模型，缺血前舌静脉注射腺苷（ａｄｅｎｏｓｉｎｅ，１００ｍｇ／ｋｇ），或硫苯茶碱（ＳＰＴ，１０ｍｇ／ｋｇ），观察血ＡＬＴ，ＡＳＴ及肝组织ＬＰＯ，ＧＳＨＰｘ和ＳＯＤ变化．结果ＩＰＣ降低了血ＡＬＴ，ＡＳＴ及肝组织自由基水平（ＡＬＴ，ｎｍｏｌ／ｓ，７８３±２００ｖｓ２８０１±２１７；ＡＳＴ，ｎｍｏｌ／ｓ，１６６７±３３３ｖｓ３１３４±６００；ＬＰＯ，μｍｏｌ／ｇ，０４５±０１１ｖｓ０６１±０１３；ＧＳＨＰｘ，ＫＥＵ／ｇ，２２２±０３０ｖｓ１５６±０２５，Ｐ＜００１）．施加腺苷后，血ＡＬＴ，ＡＳＴ及肝组织自由基水平较Ｉ／Ｒ组明显下降，呈现出类似ＩＰＣ的保护作用（ＡＬＴ，ｎｍｏｌ／ｓ，１１１７±１８３ｖｓ２８０１±２１７；ＡＳＴ，ｎｍｏｌ／ｓ，２１６７±２８３ｖｓ３１３４±６００；ＬＰＯ，μｍｏｌ／ｇ，０４６±０１１ｖｓ０６１±０１３；ＧＳＨＰｘ，ＫＥＵ／ｇ，２３４±０３５ｖｓ１５６±０２５；Ｐ＜００１）．当施加腺苷受体的阻滞剂ＳＰＴ后，ＩＰＣ的保护作用被消除（Ａ?更多还原

【Abstract】 AIM To investigate the effects of ischemic preconditioning (IPC) on hepatic ischemia/ reperfusion (I/ R) in vivo , as well as the implication of adenosine in this process. METHODS The rat model of in situ hepatic I/ R injury was intravenously injected with adenosine (100 mg/ kg) or 8 p sulfophenyl theophylline (10 mg/ kg) before hepatic ischemia and reperfusion. RESULTS IPC prevented the increases in serum ALT, AST activities and level of hepatic oxygen free radicals (ALT, nmol/ s , 783±200 vs 2801±217; AST, nmol/ s , 1667±333 vs 3134±600; LPO, μmol/ g , 0 45±0 11 vs 0 61±0 13; GSH Px, KEU/ g , 2 22±0 30 vs 1 56±0 25, P <0 01). Pretreatment with adenosine simulated the effect of IPC (ALT, nmol/ s , 1117±183 vs 2801±217; AST, nmol/ s , 2167±283 vs 3134±600; LPO, μmol/ g , 0 46±0 11 vs 0 61±0 13;GSH Px, KEU/ g , 2 34±0 35 vs 1 56±0 25; P <0 01). However, inhibition of adenosine abolished the protective effect (ALT, nmol/ s , 2501±250 vs 2801±217; AST, nmol/ s , 3084±583 vs 3134±600; LPO, μmol/ g , 0 59±0 13 vs 0 61±0 13;GSH Px, KEU/ g , 1 59±0 24 vs 1 56±0 25; P >0 05). CONCLUSION Adenosine plays a protective role in hepatic IPC and its mechanism may be inactivated oxygen free radicals.更多还原