再灌注早期渐增灌注压力对缺血再灌注心肌保护作用的实验研究  

The study of cardioprotective effects of reperfusion initial period increasing perfusion pressure on isolated rat heart suffering from ischemia and reperfusion

作　　者：李庆志[1] 李欣[2] 祝沪军[1] 郭德庆[1] 

机构地区：[1]大庆油田总医院心胸外科,163001 [2]大庆油田总医院超声心动室,163001

出　　处：《中国实用医药》2011年第8期50-52,共3页China Practical Medicine

摘　　要：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 discussion after myocardial ischemia reperfusion when whether perfusion pressure increasing with standard myocardial ischemia post-processing same myocardial protection to and its mechanism. Methods Observed for slow rise perfusion pressure after myocardial ischemic reperfusion coronary outflow fluid cTnI levels and coronary flow, myocardial ultrastructure of change and influence of P-Akt expression. Results Continued slow pressor group can promote effectively the ischemia-reperfusion heart coronary flow recovery, coronary outflow cTnI levels decrease in liquid, P-Akt high expression, and electron microscopic observation shows cells also reduce damage ultrastructure.Conclusion Continue to slow rise perfusion pressure vitro ischemia-reperfusion heart protective, PI3K/Akt/GSK-3βpathways are probably the myocardial protection of signaling pathways that one.

关 键 词：缺血再灌注损伤 渐增再灌注压力 缺血后处理 P-AKT 

分 类 号：R541[医药卫生—心血管疾病]