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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,GSHPx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,045±011vs061±013;GSHPx,KEU/g,222±030vs156±025,P<001).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,046±011vs061±013;GSHPx,KEU/g,234±035vs156±025;P<001).当施加腺苷受体的阻滞剂SPT后,IPC的保护作用被消除(A?
Objective To investigate the role of ischemic preconditioning (IPC) in hepatic ischemia-reperfusion (I / R) injury and the role of adenosine in this process. Methods The rat model of orthotopic liver I / R was used to observe the changes of ALT, AST and hepatic LPO after injection of adenosine (100 mg / kg) or thiophanophylline (SPT, 10 mg / kg) , GSH Px and SOD changes. Results IPC reduced the levels of ALT, AST and liver tissue free radicals (ALT, nmol / s, 783 ± 200 vs 2801 ± 217; AST, nmol / s, 1667 ± 333 vs 3144 ± 600; LPO, 11vs061 ± 013; GSHPx, KEU / g, 222 ± 030vs156 ± 025, P <001). After administration of adenosine, the levels of ALT, AST and free radical in liver tissue decreased significantly compared with those in I / R group, showing protective effects similar to IPC (ALT, nmol / s, 1117 ± 183 vs 2801 ± 217; AST, nmol / s, 2167 ± 283vs3134 ± 600; LPO, μmol / g, 046 ± 011vs061 ± 013; GSHPx, KEU / g, 234 ± 035vs156 ± 025; P <0 01). The protective effect of IPC was abolished when adenosine receptor blocker SPT was applied (A?