Kodama I, Sakuma I, Shibata N, Knisley S B, Niwa R, Honjo H
Department of Circulation, Nagoya University, Japan.
Pacing Clin Electrophysiol. 2000 May;23(5):807-17. doi: 10.1111/j.1540-8159.2000.tb00848.x.
Regional differences of the aftereffects of high intensity DC stimulation were investigated in isolated rabbit hearts stained with a voltage-sensitive dye (di-4-ANEPPS). Optical action potential signals were recorded from the epicardial surface of the right and left ventricular free wall (RVep, LVep) and from the right endocardial surface of the interventricular septum (IVS). Ten-millisecond monophasic DC stimulation (S2, 20-120 V) was applied to the signal recording spots during the early plateau phase of the action potential induced by basic stimuli (S1, 2.5 Hz). There was a linear relationship between S2 voltage and the S2 field intensity (FI). S2 caused postshock additional depolarization, giving rise to a prolongation of the shocked action potential. With S2 > or = 40 V (FI > or = approximately 20 V/cm), terminal repolarization of action potential was inhibited, and subsequent postshock S1 action potentials for 1-5 minutes were characterized by a decrease in the maximum diastolic potential and a decrease in the amplitude and a slowing of their upstroke phase. The higher the S2 voltage, the larger the aftereffects. The changes in postshock action potential configuration in RVep were significantly greater than those observed in LVep and IVS when compared at the same levels of S2 intensity. In RVep, 12 of 20 shocks of 120 V resulted in a prolonged refractoriness to S1 (> 1 s), and the arrest was often followed by oscillation of membrane potential. Ventricular tachycardia or fibrillation ensued from the oscillation in five cases. No such long arrest or serious arrhythmias were elicited in LVep and IVS. These results suggest that RVep is more susceptible than LVep and IVS for arrhythmogenic aftereffects of high intensity DC stimulation.
利用电压敏感染料（di-4-ANEPPS）对离体兔心脏进行染色，研究了高强度直流电刺激后效应的区域差异。从右心室和左心室游离壁的心外膜表面（RVep、LVep）以及室间隔右心内膜表面（IVS）记录光学动作电位信号。在基础刺激（S1，2.5Hz）诱发的动作电位早期平台期，对信号记录点施加10毫秒的单相直流电刺激（S2，20 - 120V）。S2电压与S2场强（FI）之间存在线性关系。S2引起电击后额外去极化，导致电击动作电位延长。当S2≥40V（FI≥约20V/cm）时，动作电位的终末复极化受到抑制，随后1 - 5分钟的电击后S1动作电位表现为最大舒张电位降低、幅度减小以及上升相减慢。S2电压越高，后效应越大。在相同S2强度水平下比较时，RVep中电击后动作电位形态的变化显著大于LVep和IVS中观察到的变化。在RVep中，120V的20次电击中有12次导致对S1的不应期延长（>1秒），并且这种阻滞之后常伴有膜电位振荡。5例中振荡引发了室性心动过速或颤动。LVep和IVS中未引发这种长时间的阻滞或严重心律失常。这些结果表明，对于高强度直流电刺激的致心律失常后效应，RVep比LVep和IVS更敏感。
