钠通道阻断剂对模拟在体犬LQT_3跨室壁复极离散影响的实验研究  

Effects of mexiletine on transmural dispersion of repolarization of left anterior ventricular wall in canine model of long-QT Syndroml type-3 in vivo

作　　者：刘福元[1] 曾秋棠[1] 毛奕[1] 刘晓飞[1] 钱忠杰[1] 毛晓波[1] 

机构地区：[1]华中科技大学协和医院心内科华中科技大学同济医学院心血管病研究所

出　　处：《临床心血管病杂志》2006年第5期305-308,共4页Journal of Clinical Cardiology

摘　　要：目的:观察心率减慢时模拟体内长QT综合征第3型(LQT3)动作电位时程(APD)和跨室壁复极离散(TDR)的变化及钠通道阻断剂美西律对这种变化的影响,为先天性LQT3室性心律失常的防治提供实验依据。方法:采用自制电极记录犬体内左心室前壁跨室壁单相动作电位,静脉注射海葵毒素(ATX-Ⅱ)模拟LQT3,消融窦房结后改变心房起搏周长(PCL)控制心室率。结果:静脉注射ATX-Ⅱ(3μg／kg)后成功模拟出LQT3模型; PCL为500 ms和1000 ms时ATX-Ⅱ使TDR均显著性增加[分别为(20±4)ms:(41±9)ms和(39±5)ms:(83 ±10)ms,均P<0．05],但PCL为1 000 ms比500 ms时TDR的增加幅度(ATDR)更为明显[(44±13);(20± 12)ms,P<0．05],伴随起源于中层心肌细胞的早期后除极和自发性室性心动过速发生;美西律(20μg／kg)能逆转ATX-Ⅱ的这种电生理作用。结论:LQT3室性心律失常的发生呈慢心室率依赖性,美西律可能对先天性 LQT3猝死的防治有一定的作用。Objective：To investigate the changes of action potential duration（APD） and transmural dispersion of repolarization（TDR） in Canine model of long-QT syndrome type 3（LQT3 ） in vivo during bradycardia, to explore the the impact of the sodium channel block-mexiletine on this changes, and to provide experimental evidence for the prevention and treatment of ventricular arrhythemia in congenital LQT3. Methord：The monophasic action potentials（MAP） of endocardium, mid-myocardium and epicardium at the anterior ventricular wall were recorded synchronously in vivo by a self-made electrode, sea anemone toxin （ATX-Ⅱ ） was administered intravenously to mimic LQT3 model, the heart rate was controlled by altering atrium pacing cycle length（PCL） after the sinoatrial node been ablated by 40% formaldehyde. Result：The LQT3 model had been made successfully by the intravenous injection of ATX- Ⅱ （3 μg/kg）. The TDR had been increased remarkably by the ATX-Ⅱ when the PCL was both 500 ms and 1000 ms （20±4 ms vs 41±9 ms and 39±5 ms vs 83＋10 ms respectively, P〈0.05）, but the net increase of TDR（ATDR） was more remarkable when the PCL was 1000 ms compared to 500 ms （44±13 ms vs 20±12 ms, P 〈0. 05）, with the occurrence of early after depolarization（EAD） originated from mid-myocardium and spontaneity ventricular tachycardia. This electrophysiological effect of ATX-Ⅱ could be reversed by mexiletine（20 μg/kg）. Conclusion：The occurrence of ventricular tachycardia in LQT3 model is bradycardia dependent, Mexiletine is probably an effective medicine in the prevention and treatment of the sudden cardiac death of congenital LQT3.

关 键 词：心律失常 长QT综合征 心脏电生理学 美西律 

分 类 号：R331.38[医药卫生—人体生理学]