短QT间期综合征发生室性心律失常机制探讨  

Study of the mechanism of ventricular arrhythmias in the short QT duration syndrome

作　　者：阮磊[1] 张存泰[1] 全小庆[1] 魏勇[2] 李连东[1] 蔡少艾[1] 周清[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院综合科,武汉430030 [2]上海市松江区中心医院

出　　处：《临床心血管病杂志》2009年第10期773-777,共5页Journal of Clinical Cardiology

基　　金：国家自然科学基金资助项目(No:30770879)

摘　　要：目的:探讨吡那地尔(pinacidil)建立的短QT间期综合征模型致室性心律失常的机制,并观察缝隙连接激动剂抗心律失常肽(AAP10)对该模型电生理参数的影响。方法:利用pinacidil灌注家兔楔形心肌块建立短QT间期综合征模型。将20只新西兰长耳白兔随机分成pinacidil组和AAP10组,每组10只。pinacidil组灌流10μmol/L的pinacidil,AAP10组灌流AAP10500nmol/l和pinacidil10μmol/L的混合液,同步记录灌流前后内外膜动作电位和容积心电图,观察灌流前后QT间期,跨室壁离散度(TDR),程序性刺激观察心肌组织不应期和室性心律失常的诱发情况。结果:灌流pinacidil后,QT间期从(291±19)ms缩到(232±19)ms(P<0.05),TDR从(44±12)ms减少到(22±7)ms(P<0.05),而不应期从(164±8)ms减少到(112±14)ms(P<0.05),室性心律失常发生率从0/10增加至8/10(P<0.05)。AAP10组和pinacidil组的TDR、QT间期、不应期及室性心律失常的诱发率无显著差别。结论:TDR减小和不应期的缩短可能是pinacidil建立的短QT间期模型致室性心律失常的基础,AAP10对pinacidil诱导的短QT间期综合征模型电不稳定性无明显影响。Objective：To study the mechanism of electrical instability of short QT syndrome modle induce by pinacid and the effect of gap junction agonist AAP 10 to the modle. Methods：To establish short QT syndrome mo- die by arterially perfuse pinacidil in rabbit left ventricular wedge preparations. 20 New-Zealand rabbits were fell in- to pinacidil group and AAP 10 group randomly , every group 10 rabbits, the pinacidil group perfused 10 μmol/L pinacidil and the AAP 10 group perfused pinacidil 10 μmol/L and AAP 10 500 nmol/L raised liquor. Transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded. To observe the change of TDR （transmural dispersion of repolarization）, QT interval and refractory period ,and the induction of ventricular tachycardia （VT） or fibrillation （VF）. Results： At a basic cycle length of 1 000 ms, pinacidil （10 mol/L） abbreviated the QT interval from （291±19） ms to （232±19）ms （P〈0.05）. The transmural dispersion of repolarization （TDR） decrease from （44±12） ms to （22±7） ms （P〈0.05）, refractory period decrease from （164±8） ms to （112±14）ms （P〈0.05） and stimulation applied to the endocardium induced a polymorphic VT （pVT） in 8 of 10 wedge preparations （P〈0.05）. There are no signally different in QT interval , TDR refractory period and the induce of VT after addition of AAP 10. Conclusions：The decrease of TDR and refractory period pos- sible is the ventricular arrhythmia mechanism of the short QT interval modle estabished by pinacidil . and there are no signally influence in short QT interval modle established by pinacidl caused by AAP 10.

关 键 词：心律失常 心室 心动过速 电生理 缝隙连接 

分 类 号：R541.7[医药卫生—心血管疾病]