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目的:研究阿魏酸钠(SF)对离体大鼠心脏急性缺氧/复氧(A/R)损伤的药理性预适应延迟保护作用及其与缓激肽的关系。方法:6组Wistar大鼠分别为对照(Cont)组、A/R组、缺氧预适应(APC)组、APC+HOE140组、SF组、SF+HOE140组。SF组、SF+HOE140组大鼠静脉注射SF10mg/kg;25h后取大鼠心脏行Langendorff逆行灌流、制作A/R损伤模型。实验结束后分别检测LVP、±dp/dtmax等心功能指标、表面心电图、CF量以及其中LDH、CPK活性、心肌组织MDA含量与GSH-Px、SOD活性、心肌梗塞面积、心肌组织超微结构改变。结果:SF预处理能显著提高大鼠心脏LVP、±dp/dtmax、CF,降低LDH、CPK活性,SOD活性、GSH-Px活性增加,MDA含量减少;大鼠心脏梗塞面积明显减少。HOE140能取消SF预处理的上述延迟保护作用。结论:SF预处理对心肌组织急性A/R损伤有明显的延迟保护作用,其机制与缓激肽系统活性增强有关。
OBJECTIVE: To study the pharmacological preconditioning delayed protective effect of sodium ferulate (SF) on acute hypoxia / reoxygenation (A / R) injury in isolated rat hearts and its relationship with bradykinin. Methods: Six Wistar rats were divided into control group, A / R group, APC group, APC + HOE140 group, SF group and SF + HOE140 group. SF and SF + HOE140 rats were injected with SF10mg / kg intravenously. After 25h, rats were subjected to Langendorff retrograde perfusion to make A / R injury model. After the experiment, LVP, ± dp / dtmax and other cardiac function indexes, surface electrocardiogram, CF, LDH, CPK activity, myocardial MDA content and GSH-Px, SOD activity, myocardial infarct size, myocardial ultrastructure were detected . Results: SF pretreatment significantly increased LVP, ± dp / dtmax, CF, LDH, CPK activity, SOD activity, GSH-Px activity and MDA content in rat heart; infarct area of rats decreased significantly. HOE140 abolishes the above described delay protection of SF pretreatment. Conclusion: SF preconditioning has significant protective effect on acute A / R injury in myocardium, and its mechanism is related to the enhancement of bradykinin system activity.