Salama G, Kanai A, Efimov I R
Department of Physiology, University of Pittsburgh School of Medicine, Pa.
Circ Res. 1994 Apr;74(4):604-19. doi: 10.1161/01.res.74.4.604.
The effects of subthreshold stimulation (STS) delivered during right atrial pacing and ventricular tachycardia (VT) were investigated in Langendorff-perfused guinea pig hearts. The hearts were stained with a voltage-sensitive dye (RH 421) to map the propagation of optical action potentials. Sustained VT was reliably induced by 5-second trains (cycle length [CL], 25 to 50 milliseconds; duration, 0.5 to 10 milliseconds; and voltage, 2x threshold voltage) of impulses (n = 12 hearts) or a single premature beat (n = 6). The location of extrastimuli was not critical to the induction of VT, but the diameter of the heart had to be > or = 14.5 mm. During VT, heart rate increased from 200 to 600 beats per minute; action potential durations decreased from 112 to 175 milliseconds to 60 to 105 milliseconds, with no diastolic interval. Activation on the epicardium spread anisotropically, but VT decreased the "apparent" maximum conduction velocity (theta max) by 68% and altered the orientation of the major axis from beat to beat. Activation patterns and theta max measured during VT were similar to patterns recorded during direct pacing of the ventricle and indicated that Purkinje fibers no longer propelled ventricular excitation. STS (CL, 25 to 50 milliseconds; duration, 0.5 to 25 milliseconds; and voltage, 0.5x to 0.8x threshold; trains of 2.0 to 2.5 seconds) interrupted VT when applied to Purkinje fibers lining the endocardium (n = 6) but failed to interrupt VT when applied to the epicardium (n = 8). In atrial pacing, STS delivered to the endocardium increased theta max from 2.44 +/- 0.32 (mean +/- SEM) to 3.63 +/- 0.21 m/s in a local region surrounding the first activation sites (n = 4). Alternatively, VT could be terminated by reducing theta max (approximately 55%) with procainamide (10 mumol/L) (n = 6). STS terminates VT by synchronizing ventricular excitation most likely by increasing local conduction and/or improving the coupling between Purkinje and ventricular cells.
在Langendorff灌注的豚鼠心脏中，研究了右心房起搏和室性心动过速（VT）期间阈下刺激（STS）的作用。用电压敏感染料（RH 421）对心脏进行染色，以绘制光学动作电位的传播情况。通过5秒的冲动序列（周期长度[CL]，25至50毫秒；持续时间，0.5至10毫秒；电压，2倍阈电压）（n = 12只心脏）或单个早搏（n = 6）可靠地诱发持续性VT。额外刺激的位置对VT的诱发并不关键，但心脏直径必须≥14.5毫米。在VT期间，心率从每分钟200次增加到600次；动作电位持续时间从112至175毫秒减少到60至105毫秒，且无舒张间期。心外膜的激活呈各向异性传播，但VT使“表观”最大传导速度（θmax）降低了68%，并使主轴线方向逐搏改变。VT期间测量的激活模式和θmax与心室直接起搏期间记录的模式相似，表明浦肯野纤维不再推动心室兴奋。当应用于心内膜内衬的浦肯野纤维时（n = 6），STS（CL，25至50毫秒；持续时间，0.5至25毫秒；电压，0.5倍至0.8倍阈电压；2.0至2.5秒的序列）可中断VT，但应用于心外膜时（n = 8）未能中断VT。在心房起搏时，应用于心内膜的STS在第一个激活部位周围的局部区域将θmax从2.44±0.32（平均值±标准误）增加到3.63±0.21米/秒（n = 4）。或者，可通过用普鲁卡因胺（10μmol/L）将θmax降低约55%来终止VT（n = 6）。STS最有可能通过增加局部传导和/或改善浦肯野细胞与心室细胞之间的耦联来同步心室兴奋，从而终止VT。
