缺血后处置缓解离体大鼠心肌缺血/再灌注损伤  

Ischemic postconditioning alleviates myocardial ischemia/reperfusion injury in rats in vitro

作　　者：马立权[1] 王红霞[1] 油红捷[1] 邱笑违[1] 王晓燕[1] 芦玲巧[1] 郑少鹏[1] 张立克[1] 

机构地区：[1]首都医科大学病理生理学教研室,北京100069

出　　处：《基础医学与临床》2007年第3期259-262,共4页Basic and Clinical Medicine

基　　金：北京市自然科学基金(7062007);北京市教育委员会科技发展计划基金(KM200510025009)

摘　　要：目的观察缺血后处置对大鼠心肌缺血/再灌注损伤的影响,并初步探讨其作用机制。方法复制离体大鼠心肌缺血/再灌注损伤模型及缺血后处置模型。记录±dp/dtmax和LVEDP。用比色法检测灌流液中乳酸脱氢酶(LDH)、丙二醛(MDA)水平及超氧化物歧化酶(SOD)活性,Western blot方法检测心脏eNOS及ERK1/2的表达,RT-PCR方法测定心脏细胞色素P4502J3(CYP2J3)mRNA表达。结果与缺血/再灌注组(IR)相比,缺血后处置组(IPo)±dp/dtmax均增高(P<0.01),而LVEDP、LDH降低(P<0.05);IR组MDA水平高于对照组(CON)及IPo组(P<0.01),SOD活性低于IPo组(P<0.01);IR组大鼠心肌eNOS及磷酸化ERK1/2的表达均高于CON组和IPo组;IPo组大鼠心脏CYP2J3 mRNA的表达明显高于CON组和IR组。结论缺血后处置可能通过提高再灌注心肌SOD活性,增加氧自由基清除,而改善缺血/再灌注引起的心功能障碍及细胞损伤;CYP2J3/EET系统有可能参与其保护作用。Objective Observing the effects of ischemic postconditioning on ischemia/reperfusion injury in rat heart and reseaerching the mechanisms elementarily. Methods The wistar rat hearts were put in the Langendorff equipment, and the myocardial ischemia/reperfusion and the ischemic postconditioning model in vitro were made. Observing the changes of maximal rate of the pressure increase and decrease （dp/dtmax） , and left ventricular end diastolic press（LVEDP） of heart. Colorimetry method was used to assay the lactate dehydrogenase （LDH） of fluid, methy lnedioxyamphetamine （MDA） and superoxide dismutase （SOD） activity of cardiac muscle ; Western blotting method was used to detect endothelial nitric oxide synthase （eNOS） and phosphorylated extracellular-regulated kinases （ERK1/2） expression;RT-PCR was used to test CYP2J3 mRNA expression of heart. Results Compared with group IR, the value of ＋ dp/dtmax was increased （P〈0.01）, LVEDP and LDH level was decreased （P〈0. 05） in group IPo in reperfusion stage. The content of MDA in group IR was higher than that in group CON and IPo（P 〈0. 01）. The activity of SOD in group IR was lower than that of IPo（P 〈0. 01）, but it was almost equal to control group. The expression of eNOS and phosphorylated ERK1/2 in group IR was higher not only than that of control group but also than that of IPo group. The CYP2J3 mRNA expression of heart in group IPo was evidently higher than that of group CON and IR. Conclusion Ischemic postconditioning can improve the myocardial dysfunction and cell injury caused by ischemia/reperfusion in rat heart in vitro, maybe through activation of SOD and increasing elimination of oxygen-derived free radicals. CYP2J3/EET system may function in protective effection.

关 键 词：缺血后处置 缺血/再灌注损伤 心脏 一氧化氮合酶 细胞色素P450表氧化酶 

分 类 号：R541[医药卫生—心血管疾病]