索他洛尔诱导尖端扭转型室性心动过速发生机制的实验研究  

Experiment Study of Mechanism on Acquired Torsade de Points in Vivo

作　　者：李运田[1] 张存泰[1] 陆再英 吴杰[1] 王晨[1] 

机构地区：[1]同济医科大学同济医院心内科,湖北省武汉市430030

出　　处：《中国循环杂志》2000年第4期237-238,共2页Chinese Circulation Journal

摘　　要：目的 :探讨索他洛尔诱导在体心脏尖端扭转型室性心动过速 (Td P)的发生机制。　　方法 :同步记录 12只开胸兔左心室心外膜心肌、中层心肌、心内膜心肌的单相动作电位 ,静脉注射索他洛尔后 ,探讨Td P的发生机制。　　结果 :12只兔共诱发了 19次 Td P,Td P的第 1个室性激动均起自单相动作电位上早期后除极 (EAD)的峰值 ,其中10次 Td P其后的室性激动均由前一个室性激动的 EAD引起 ,最后一个室性激动复极电位降至阈下后 Td P终止 ;其余 9次 Td P第 1个室性激动之后的室性激动在与之相应的各层心肌的单相动作电位上均无 EAD。　　结论 :EAD是 Td P发生的始动因素 ,EAD产生的触发活动和三层心肌间复极离散度的明显增加在 Td P的维持中起重要作用。Objective:To investigate the mechanism on acquired torsade de points (TdP) induced by sotalol in rabbit in vivo. Methods:Monophasic action potential of epimyocardium、midmyocardium and endomyocardium were simultaneously recorded by specially designed plunge needle electrodes at the left ventricular myocardium in 12 open chest rabbits.After TdP were developed by injecting sotalol intravenously,the mechanism of TdP was studied. Results:Nineteen TdP occurred in 12 rabbits.They were triggered by early afterdepolarization (EAD),subsequent ventricular ectopic beats in 10 TdP were induced by successive EAD,and it terminated when the repolarization of the last beat fell below the threshold potentials.There was no EAD on subsequent ventricular ectopic beats in 9 TdP. Conclusion:EAD is the initiating factor of TdP,and triggered activity induced by EAD and increased transmural dispersion of repolarization among the three myocardial layers play important role in the maintenance of TdP.

关 键 词：尖端扭转型室性心动过速 索他洛尔 实验研究 

分 类 号：R541.71[医药卫生—心血管疾病]