论文部分内容阅读
目的:观察银杏酮酯(GBE50)对大鼠离体心肌缺血再灌注(L/R)损伤的影响及其作用机制。方法:65只SD大鼠随机分为模型组,GBE50低、中、高剂量组,丹参组和地尔硫卓组。进行Langendorff离体心脏灌流,各组均平衡灌注15 min,停灌造成全心缺血30 min,再复灌40 min。观察药物对各组大鼠心律失常,心肌组织与冠脉流出液SOD活性、MDA含量以及心肌组织LDH含量的影响。结果:GBE50能够降低室颤的发生率,部分缩短室颤的持续时间。GBE50用药组心肌组织和冠脉流出液中SOD活性明显高于模型组(P<0.05,P<0.01),心肌MDA、LDH含量显著低于模型组(P<0.05,P<0.01)。结论:GBE50可明显减少I/R引起的心律失常,减轻心肌损伤,其作用机制可能与抑制氧化应激,减少自由基生成有关。
Objective: To observe the effect of GBE50 on myocardial ischemia / reperfusion (L / R) injury in rats and its mechanism. Methods: Sixty-five SD rats were randomly divided into model group, GBE50 low, medium and high dose groups, Salvia miltiorrhiza group and diltiazem group. Langendorff perfusion was performed in vitro. The rats in each group were infused with equilibration for 15 min. The animals were sacrificed for 30 min after ischemia and reperfusion for 40 min. The effects of drugs on cardiac arrhythmia, myocardial SOD activity, MDA content and LDH content in myocardium were observed. Results: GBE50 reduced the incidence of ventricular fibrillation and partially shortened the duration of ventricular fibrillation. The activity of SOD in myocardial tissue and coronary effluent of GBE50 treatment group was significantly higher than that of model group (P <0.05, P <0.01), and the content of MDA and LDH in myocardium was significantly lower than that of model group (P <0.05, P <0.01). CONCLUSION: GBE50 can significantly reduce the arrhythmia induced by I / R and relieve myocardial injury. Its mechanism may be related to the inhibition of oxidative stress and the reduction of free radical production.