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缺血预处理对大鼠肝脏缺血再灌注损伤保护作用机制的研究
引用本文:吴刚,杨蕾,刘永锋,程颖,赵宁,何三光.缺血预处理对大鼠肝脏缺血再灌注损伤保护作用机制的研究[J].中华肝胆外科杂志,2003,9(4):221-224.
作者姓名:吴刚  杨蕾  刘永锋  程颖  赵宁  何三光
作者单位:110001,沈阳市,中国医科大学第一临床学院普外一科
摘    要:目的 探讨缺血预处理 (IPC)保护作用的发生机制。方法 建立大鼠部分肝脏热缺血再灌注模型。IPC采用肝脏缺血 10min ,再灌注 10min。结果 IPC后肝组织中腺苷和NO水平明显升高 ,与对照组相比差异显著 (P <0 0 1) ,但IPC前应用腺苷A2 受体拮抗剂后NO的升高被抑制 (P<0 0 1)。缺血再灌注 (I/R) 2h后血清中TNF α、AST、ALT、LDH及W/D水平和假手术组相比明显增加 ,而IL 10含量降低 (P <0 0 1) ;IPC、I/R前加入腺苷、IPC前应用腺苷A1受体拮抗剂显著地降低TNF α释放和AST、ALT、LDH及W /D水平 ,提高IL 10含量 ,与I/R组相比差异显著 (P <0 0 1) ;但IPC前应用腺苷A2 受体拮抗剂 (IPC +A2 antag)和NO合成酶抑制剂NAME并没有能像IPC组那样有效降低TNF α、AST、ALT、LDH及W /D的水平 ,提高IL 10的含量 (P <0 0 1) ;而IPC前给IPC+A2 antag组提供NO前体精氨酸又获得和IPC组同样的结果 (P >0 0 5 )。结论 IPC引起细胞外腺苷水平升高 ,腺苷A2 受体活化 ,介导了NO合成增加 ,最终通过抑制效应器TNF α的释放、增加IL 10的合成来实现对缺血组织的保护作用。

关 键 词:缺血预处理  大鼠  肝脏缺血  再灌注损伤  保护作用
修稿时间:2002年3月25日

Protective effects of ischemic preconditioning on liver injury induced by hepatic ischemia-reperfusion in rats
WU Gang,YANG Lei,LIU Yongfeng,et al..Protective effects of ischemic preconditioning on liver injury induced by hepatic ischemia-reperfusion in rats[J].Chinese Journal of Hepatobiliary Surgery,2003,9(4):221-224.
Authors:WU Gang  YANG Lei  LIU Yongfeng  
Institution:WU Gang,YANG Lei,LIU Yongfeng,et al. 1st Department of General Surgery,the First Affiliated Hospital,China Medical University,Shenyang 110001,P. R. China
Abstract:ObjectiveTo investigate the molecular mechanism of classic ischemic preconditioning (IPC) to induce ischemic tolerance. MethodsAfter the models of sham-operation and partial hepatic ischemia were established in rats, IPC was performed with a 10-min ischemia followed by a 10-min reperfusion. ResultsA significant increase in adenosine and NO production was found immediately after the hepatic IPC as compared with the control group (P<0.01). This increase in NO content was markedly prevented by the administration of adenosine A_2 receptor antagonist to the IPC group (P<0.01). An obvious decrease in release of TNF-a and an increase in production of IL-10 were found in IPC group at the 2nd h after reperfusion (P<0.01). The levels of AST, ALT, LDH and W/D were significantly lower in IPC group than in I/R group (P<0.01). The values of these parameters were remarkably decreased by administration of adenosine in the I/R group (P<0.01). Pretreatment with adenosine A_1 receptor antagonist resulted in increase of TNF-a, AST, ALT, LDH and W/D levels but decrease of IL-10. However, pretreatment with adenosine A_2 receptor antagonist and NAME abolished the protective effects of IPC. The administration of NO precursor to the IPC+A_2 antagonist group prevented the injurious effect of A_2 receptor antagonist on hepatic IPC, leading to the same results as those observed in the IPC group. ConclusionsAn elevated adenosine extracellular concentration induces the activation of adenosine A_2 receptor, which, in turn, by induction of NO synthesis and subsequent prevention of TNF-a liberation and promotion of IL-10 production, confers cytoprotection to ischemic tissue.
Keywords:Reperfusion injury  Ischemic preconditioning  Adenosine  Nitric oxide  Cytokine
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