摘要
目的:研究传统降血脂药物阿托伐他汀(Atorvastatin,Ator)对SD大鼠缺血/复灌(I/R)诱导的心肌电生理影响及其机制。方法:采用Langendorff大鼠离体心脏灌流方法,结扎冠状动脉左前降支30 min后释放复制局部缺血/复灌模型,测定Ator对心肌缺血/复灌前后的心室电生理学参数:舒张期兴奋阈(DET),有效不应期(ERP)和室颤阈(VFT)的影响。结果:与对照组相比,中浓度Ator明显延长离体大鼠心脏的ERP,低、中、高浓度Ator均明显抑制了缺血/复灌诱导的DET、ERP和VFT的下降,而L-NAME取消了这些由Ator介导的心肌电生理学效应。结论:阿托伐他汀减轻了缺血/复灌引起的心肌电生理改变,其机制可能与激活一氧化氮通路,延长ERP、提高DET和VFT以增强心肌电生理稳定性有关。
Objective: To investigate the myocardial electrophysiological effect and its underlying mechanisms of atorvastatin(Ator) on isolated rat hearts injured by ischemia/reperfusion(I/R).Methods: Isolated SD rat hearts were mounted on Langendorff system,and a local I/R was induced by ligation(30 min) and release(15 min) of the left anterior descending artery.During the reperfusion period,the effect of Ator on diastolic excitation threshold(DET),effective refractory period(ERP) and ventricular fibrillation threshold(VFT) on rat heart were measured.Results: Compared with the control group,medium concentration of Ator prolonged the ERP in normal rat hearts;low,medium and high concentration of Ator significantly inhibited the decrease of DET,ERP and VFT induced by I/R.However,pretreatment with L-NAME cancelled these cardiac electrophysiological effects of Ator.Conclusion: Ator reduced electrophysiological alteration induced by I/R in isolated rat hearts,which may be mediated by activating nitric oxide pathway to enhance the myocardial electrophysiological stability.
出处
《浙江大学学报（医学版）》
CAS
CSCD
北大核心
2010年第6期589-593,共5页
Journal of Zhejiang University(Medical Sciences)
关键词
吡咯类/药理学
心肌再灌注损伤
心肌缺血/病理生理学
心肌缺血/药物疗法
阿托伐他汀
电生理学
一氧化氮
Pyrroles/pharmacol
Myocardial reperfusion injury
Myocardial ischemia/physiopathol
Myocardial ischemia/drug ther
Atorvastatin
Myocardial ischemia/reperfusion
Electrophysiology
Nitric oxide
