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缺血预处理和缺血后处理对大鼠心肌缺血再灌注时炎性反应影响的比较
引用本文:熊军,薛富善,袁玉静,王强,廖旭,李杉,王卫利,张雁鸣,刘建华.缺血预处理和缺血后处理对大鼠心肌缺血再灌注时炎性反应影响的比较[J].中华麻醉学杂志,2010,30(10).
作者姓名:熊军  薛富善  袁玉静  王强  廖旭  李杉  王卫利  张雁鸣  刘建华
摘    要:目的 比较缺血预处理和缺血后处理对大鼠心肌缺血再灌注时炎性反应的影响.方法 雄性SD大鼠40只,体重290~320 g,随机分为4组(n=10),缺血再灌注组(I/R组)、缺血预处理组(IPC组)和缺血后处理组(IPOC组)采用结扎左冠状动脉前降支30 min进行再灌注的方法制备心肌缺血再灌注模型,假手术组(S组)仅在左冠状动脉前降支下穿线.监测再灌注期间HR和MAP,并计算HR和MAP的乘积(心肌氧耗指数,RPP).分别于再灌注30和180 min时采集静脉血样,测定血清TNF-α、IL-6、高迁移率组蛋白1(HMGB1)和心肌肌钙蛋白I(cTnI)的浓度.采集完血样,取心肌组织,测定心肌梗死体积.结果 与S组比较,I/R组MAP和RPP降低,血清cTnI和炎性细胞因子浓度升高,心肌梗死体积增大(P<0.05);与I/R组比较,IPC组MAP升高,IPOC组MAP和RPP均升高,两组血清cTnI和炎性细胞因子浓度降低,心肌梗死体积缩小(P<0.05);与IPC组比较,IPOC组血清炎性细胞因子浓度升高,心肌梗死体积增大(P<0.05).结论缺血预处理减轻大鼠心肌缺血再灌注时炎性反应的作用强于缺血后处理,从而使心肌保护效应较好.

关 键 词:缺血预处理  心肌  心肌再灌注损伤  炎症  缺血后处理

Effects of ischemic preconditioning versus ischemic postconditioning on myocardial ischemia-reperfusion-induced inflammatory response in rats
XIONG Jun,XUE Fu-shan,YUAN Yu-jing,WANG Qiang,LIAO Xu,LI Shan,WANG Wei-li,ZHANG Yan-ming,LIU Jian-hua.Effects of ischemic preconditioning versus ischemic postconditioning on myocardial ischemia-reperfusion-induced inflammatory response in rats[J].Chinese Journal of Anesthesilolgy,2010,30(10).
Authors:XIONG Jun  XUE Fu-shan  YUAN Yu-jing  WANG Qiang  LIAO Xu  LI Shan  WANG Wei-li  ZHANG Yan-ming  LIU Jian-hua
Abstract:Objective To compare the effects of ischemic preconditioning versus ischemic postconditioning on myocardial ischemia-reperfusion (I/R)-induced inflammatory response in rats. Methods Forty male SD rats weighing 290-320 g were randomly divided into 4 groups ( n = 10 each): Ⅰ group sham operatin (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPC) and Ⅳ group ischemic postconditioning (group IPOC).Myocardial I/R was induced by 30 min ligation of left anterior descending branch (LAD) of coronary artery followed by reperfusion. In group IPC myocardial I/R was preceded by 3 cycles of ischemia followed by reperfusion (each lasting 5 min) while in group IPOC 3 cycles of I/R (each lasting 10 s) was started at the end of 30 min myocardial ischemia. MAP, HR and RPP ( MAP × HR) were recorded before (baseline) and at 1 and 20 min of ischemia and 60, 120 and 180 min of reperfusion. Venous blood samples were collected at 30 and 180 min of reperfusion for determination of serum concentrations of TNF-α, IL-6, high-mobility group box 1 (HMGB1) and cTnI. The animals were sacrificed at 180 min of reperfusion and the myocardial infarct size was measured. Results Myocardial I/R significantly decreased MAP and RPP and increased myocarcial infarct size, serum concentrations of TNF-α, IL-6,HMGB1 and cTnI in group I/R as compmed with group S. Ischemic pre- and postconditioning significantly increased MAP and reduced myocardial infarct size and I/R-induced increase in serum TNF-α, HMGB1 and cTnI concentrations in group Ⅲ and Ⅳ as compared with group Ⅱ (I/R). The myocardial infarct size was significantly larger and the serum concentrations of TNF-α, IL-6 and HMGB1 were significantly higher in ischemic postconditioning group than in the preconditioning group. Conclusion Ischemic preconditioning is more effective in attenuating the myocardial I/R-induced inflammatory response than the ischemic postconditioning.
Keywords:Ischemic preconditioning  myocardial  Myocardial repcrfusion injury  Inflammation  Ischemia postconditioning
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