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目的:观察增加缝隙连接耦联对兔长QT综合征(LQTS)模型室性心律失常的影响。方法:应用心肌细胞快速延迟整流钾通道(IKr)阻滞剂E-4031(0.5μmol/L)在兔左室楔型心肌块建立LQT2模型,随机分为正常组、LQT2组、100 nmol/L缝隙连接激动剂(AAP-10)干预组(AAP-100组)、500 nmol/L AAP-10干预组(AAP-500组),每组10只。采用浮置玻璃微电极法同步记录心内膜、心外膜心肌细胞跨膜动作电位及跨室壁心电图。结果:LQT2组QT间期,跨室壁复极离散度(TDR)、早期后除极(EAD)、R-on-T期前收缩和尖端扭转性室性心动过速(TdP)发生率均显著高于正常组(P<0.05)。在LQT2模拟状态下,500 nmol/L AAP显著缩短了QT间期和TDR(P<0.05),降低了EAD、R-on-T期前收缩和TdP的发生率(P<0.05)。结论:增加缝隙连接耦联能减少兔LQT2模型TDR和室性心律失常发生率。
Objective: To observe the effect of increased gap junctional coupling on ventricular arrhythmia in rabbit model with long QT syndrome (LQTS). Methods: LQT2 model was established in rabbit left ventricular wedge cardiac muscle by rapid cardiomyocyte delayed rectifier potassium channel (IKr) blocker E-4031 (0.5μmol / L) and randomly divided into normal group, LQT2 group, 100 nmol / L AAP-10 intervention group (AAP-100 group), 500 nmol / L AAP-10 intervention group (AAP-500 group), 10 rats in each group. Floating glass microelectrode method was used to record the transmembrane action potential and transmural electrocardiogram of endocardial and epicardial cardiomyocytes synchronously. Results: The incidences of QT interval, TDR, EAD, R-on-T premature ventricular contractions and torsades de pointes (TdP) in LQT2 group Significantly higher than the normal group (P <0.05). At LQT2 simulation, 500 nmol / L AAP significantly shortened the QT interval and TDR (P <0.05), and reduced the EAD, pre-R-on-T contraction and TdP incidence (P <0.05). Conclusion: Increasing gap junctional coupling can reduce the incidence of TDR and ventricular arrhythmia in rabbit LQT2 model.