在体心脏早期后除极起源的电生理学研究

探讨在体心脏早期后除极 (EAD)的起源及其与室性心律失常的关系。采用单相动作电位 (MAP)记录技术 ,同步记录 12只开胸兔左室心外膜下心肌 (Epi)、中层心肌 (Mid)、心内膜下心肌 (Endo)的MAP ,并静脉注射 (简称静注 )索他洛尔诱发EAD后 ,观察三层心肌EAD的发生。结果 :①索他洛尔呈剂量依赖性地增加EAD和尖端扭转型室性心动过速 (TdP)的发生率。静注索他洛尔 0 .5mg kg和 1.0mg kg后无EAD和Tdp ;剂量增至 2 .0mg kg后 ,7只兔的MAP上出现了EAD ,其中 4只兔诱发了TdP。②静注索他洛尔后 ,在Mid比Epi和Endo更容易记录EAD并具有剂量依赖性。三层心肌中以Mid的EAD振幅最高 ,当索他洛尔的剂量为 2 .0mg kg时 ,Epi、Mid和Endo的EAD振幅分别为 2 .5± 1.35 ,6 .0 8± 1.96和 3 .8± 1.46mV。此外 ,Mid的EAD出现的时相早于Epi和Endo,其中Epi和Endo的EAD的耦联间期分别与Mid的EAD的耦联间期具有相关性。③Endo的EAD的出现率多于Epi。静注索他洛尔2 .0mg kg后 ,有 3只兔的Endo的MAP上记录到了EAD ,而Epi的MAP上出现EAD的兔只有 2只。结论 :在体心脏EAD起源于中层心室肌和蒲肯野氏纤维。Ⅲ类抗心律失常药物索他洛尔致心律失常的发生机制与其诱导三层心肌EAD的程度不同有关

Electrophysiological Studies of Origin for Early Afterdepolarization Induced by Sotalol in Vivo

The purpose of this research is to investigate the origin of early afterdepolarization (EAD) and its relationship with ventricular arrhyhmia in the rabbit in vivo.With the monophasic action potential (MAP) recording technique,MAPs of epicardium (Epi),midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plungeneedle electrodes across the left ventricular myocardium in 12 chestopening rabbits.After intravenous administration of Sotalol with different doses,EADs of all three myocardial layers were observed.Results: (1) sotalol increased dosedependently the incidence of EAD and torsade de pointes (TdP).After intravenous administration of 0.5 mg/kg and 1.0 mg/kg sotalol,no EAD and TdP occurred.When 1.5 mg/kg sotalol injected,EAD appeared in 3 of 12 rabbits,in which TdP was induced in 1 rabbit.When dose of sotalol was increased to 2.0 mg/kg,EAD appeared in 7 of 12 rabbits,in which TdP was induced in 4 rabbits.(2)EAD was much more readily induced in Mid than in Epi and Endo with dosedependence.Amplitude was 2.5±1.3 mV,6.08±1.96 mV,and 3.8±1.46 mV in Epi,Mid,and Endo respectively.In addition,the appearance of EAD in Mid was earlier than that of Epi and Endo.The coupling interval of EAD in Epi and Endo both were relative to that of EAD in Mid.(3)the incidence of EAD was higher in Endo than in Epi.Conclusion:EAD induced by sotalol originate from Mid and Purkinje fibers,proarrhythmic effect of sotalol is relate to the discrepancy of EAD in all three myocardial layers.Chinese Journal of Cardiac Pacing and Electrophysiology,2000,14(2):117～120] Monophaic action potential Early afterdepolarization Sotalol Rabbit