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目的探讨心肌缺血后再灌注时渐增灌注压力是否具有与标准心肌缺血后处理相同的心肌保护用以及其机制。方法观察持续缓慢升高灌注压力对缺血再灌注后心肌的冠脉流出液中cTnI含量及冠脉流量、心肌细胞超微结构变化的影响以及P-Akt的表达。结果持续缓慢升压组能有效促进缺血再灌注心脏的冠脉流量恢复,冠脉流出液中cTnI含量减少,P-Akt高表达,同时电镜观察显示细胞超微损伤亦减轻。结论持续缓慢升高灌注压力对离体缺血再灌注心脏具有保护作用,PI3K/Akt/GSK-3β通路可能是其心肌保护作用的信号传导通路之一。
Objective To investigate whether myocardial perfusion with increasing myocardial perfusion pressure after myocardial ischemia has the same myocardial protection as myocardial ischemia and its mechanism. Methods The effect of continuous and slowly increasing perfusion pressure on cTnI, coronary flow and myocardial ultrastructure in myocardial effusion after ischemia-reperfusion was observed and the expression of P-Akt was observed. The results of continuous slow pressure group can effectively promote myocardial ischemia and reperfusion of coronary flow recovery, cTnI content in coronary effluent decreased, P-Akt high expression, while electron microscopy showed that cell ultrastructure damage also reduced. CONCLUSION: Continuous and slowly increasing perfusion pressure has a protective effect on isolated ischemia-reperfusion heart. PI3K / Akt / GSK-3β pathway may be one of the signal transduction pathways for cardioprotection.