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目的:探讨卡维地洛抗豚鼠再灌注早期心室颤动作用及其机制。方法:利用心肌缺血再灌注损伤模型,研究卡维地洛在0·1、1·0和10·0μmo1/L3个浓度时对再灌注早期心脏去甲肾上腺素(NE)释放及心室颤动发生的影响。结果:①卡维地洛在1·0μmo1/L和10·0μmo1/L时心脏流出液中的NE含量分别为(13·390±7·011)pmol/g心脏组织和(5·004±2·598)pmol/g心脏组织,均显著低于空白对照组(38·670±13·661)pmol/g(P<0·05);②卡维地洛可明显降低再灌注早期心室颤动的发生。结论:缺血再灌注心脏释放的NE在再灌注心律失常的发生中可能起着重要作用,卡维地洛呈浓度依赖性的减少再灌注早期心脏交感神经递质NE释放的作用应是其抗再灌注心律失常心室颤动的作用机制之一。
Objective: To investigate the effect of carvedilol on guinea pig ventricular fibrillation during early reperfusion and its mechanism. Methods: Myocardial ischemia-reperfusion injury model was used to study the effects of carvedilol on the release of cardiac norepinephrine (NE) and ventricular fibrillation during early reperfusion at 0 · 1, -1 · 0 and 10 · 0μmo1 / L3 Impact. Results: (1) The contents of NE in cardiac efflux of carvedilol at 1μmol / L and 10μmol / L were (13.390 ± 7.01) pmol / g heart tissue and (5.004 ± 2) · 598) pmol / g heart tissue were significantly lower than the control group (38.670 ± 13.666 pmol / g) (P <0.05); ② Carvedilol can significantly reduce the early reperfusion ventricular fibrillation occur. CONCLUSION: The release of NE from ischemia-reperfusion myocardium may play an important role in the reperfusion arrhythmia. Carvedilol should reduce the release of NE, an early sympathetic neurotransmitter, in a dose-dependent manner Reperfusion arrhythmia ventricular fibrillation one of the mechanisms.