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目的探讨缺血后处理对心肌肥厚大鼠离体心脏缺血再灌注损伤的影响及其信号机制。方法通过腹主动脉结扎建立大鼠心肌肥厚模型,用Landendorff装置建立心肌肥厚大鼠离体心脏缺血再灌注模型。观察缺血后处理对心肌肥厚大鼠离体缺血再灌注心脏左心室收缩压,冠状动脉流量,肌酸磷酸激酶和乳酸脱氢酶释放,心肌梗死范围,心肌组织中蛋白激酶B/Akt(Akt)、糖原合成酶激酶-3β(GSK-3β)磷酸化的影响。结果与缺血再灌注对照组相比,缺血后处理组心脏左心室收缩压、冠状动脉流量显著高,冠状动脉循环流出液中肌酸磷酸激酶、乳酸脱氢酶含量低,心肌梗死范围减小,心肌组织中磷酸化Akt(Ser473)、磷酸化GSK-3β(Ser9)水平高,磷脂酰肌醇-3激酶(PI3K)抑制剂渥曼青霉素(wortmannin)能够抑制缺血后处理所致的磷酸化Akt(Ser473)、磷酸化GSK-3β(Ser9)水平升高,但只能部分消除缺血后处理的心脏保护效应。结论缺血后处理能够减轻心肌肥厚大鼠离体心脏缺血再灌注损伤,P13K/Akt/GSK-3β信号途径参与介导缺血后处理对离体缺血再灌注肥厚心肌的保护作用。
Objective To investigate the effect of ischemic postconditioning on myocardial ischemia-reperfusion injury in isolated rat hearts and its signaling mechanism. Methods The rat model of cardiac hypertrophy was established by ligation of abdominal aorta and the model of isolated heart ischemia-reperfusion in rats was established by Landendorff apparatus. The effects of ischemic postconditioning on left ventricular systolic pressure, coronary flow, release of creatine phosphokinase and lactate dehydrogenase, myocardial infarct size, and protein kinase B / Akt Akt), glycogen synthase kinase-3 beta (GSK-3 beta) phosphorylation. Results Compared with the ischemia-reperfusion control group, the left ventricular systolic pressure and coronary flow were significantly increased in the ischemic postconditioning group. The content of creatine phosphokinase and lactate dehydrogenase in the coronary circulation was lower and the range of myocardial infarction Small, myocardial tissue phosphorylated Akt (Ser473), phosphorylated GSK-3β (Ser9) high level, phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin can inhibit ischemic postconditioning Phosphorylated Akt (Ser473), phosphorylated GSK-3β (Ser9) levels increased, but only partially eliminated the cardioprotective effect of ischemic postconditioning. CONCLUSION: Ischemic postconditioning can reduce myocardial ischemia-reperfusion injury in vitro in isolated hypertrophic rats. The protective effect of P13K / Akt / GSK-3β signaling pathway on the hypertrophic myocardium after ischemia / reperfusion injury is mediated by ischemic postconditioning.