LQT2模型室性心律失常电生理机制研究

The Study of Electrophysiological Mechanisms of Ventricular Arrhythmia in LQT2 Models of the Long QT Syndrome

为探讨心室肌跨壁复极离散度 (TDR)和心脏兴奋的恢复性质在长QT综合征 (LQTS)室性心律失常发生过程中的作用 ,应用冠状小动脉灌流的兔左室肌楔形组织块标本 ,分模型组和对照组 ,采用浮置玻璃微电极法同步记录心室肌内、外膜心肌细胞动作电位和跨壁心电图。模型组以 30 μmol/L的d sotalol台氏液灌流 ,制备LQT2模型。对照组以标准台氏液灌流。结果 :模型组和对照组比较TDR有显著性差异 (83.6± 14 .0msvs 4 8.6± 5 .3ms,P <0 .0 1,n =10 )。模型组内、外膜动作电位时程 (APD)恢复曲线最大斜率均大于 1,而对照组均小于 1,两组间APD恢复曲线最大斜率比较有显著性差异 (P <0 .0 1,n =2 0 )。模型组在S1S2 程序刺激下尖端扭转型室性心动过速的发生率为70 %。对照组无 1例发生室性心律失常。结论 :心脏兴奋的恢复性质和心室肌TDR均参与了LQT2室性心律失常的发生。

Arterially perfused rabbit left ventricular preparations were used in the present study to simulate LQT2 by perfusing with d-sotalol. Transmembrane action potentials from epicardium and endocardium were recorded simultaneously, together with a trasmural ECG, in arterially perfused rabbit left ventricular preparations by use of 2 separate intracellular floating mocroelectrodes. The ventricular preparations were perfused by blockade of I kr d-sotalol (30μmol/L) and stimulated with S 1S 2 program stimulations.Action potential duration( APD) was measured at 90% repolarization (APD 90).Transmural dispersion of repolarization( TDR) was defined as the difference between the longest and shortest repolarization time across the left ventricular wall. The APD restitution curves were drawn and the slopes were measured. Results: Preferential prolongation of endocardium APD was associated with a marked increase in TDR from 48.6±5.3ms to 83.6±14.0ms (P<0.01, n=10). The slopes of APD restitution curve had marked difference ( P<0.01, n=20) with or without d-sotalol.Tdp was induced with programmed stimulation in 7 of 10(70%) preparations in LQT2 model group and Tdp never induced in the absence of d-sotalol. Conclusion:Both transmural dispersion of repolarization and restitution properties are involved in the occurrence of ventricular arrhythmia in LQT2.