Cellular electrophysiologic characteristics of surviving subendocardial fibers in chronically infarcted right ventricular myocardium susceptible to inducible sustained ventricular tachycardia.

Cellular electrophysiologic characteristics of surviving subendocardial fibers in chronically infarcted right ventricular myocardium susceptible to inducible sustained ventricular tachycardia.
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慢性梗塞右心室心肌中幸存心内膜下纤维的细胞电生理特征易诱发持续性室性心动过速。

DOI:
10.1016/0002-8703(87)90753-8
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发表时间:
1987
影响因子:
4.8
通讯作者:
Peter,T
Peter,T
中科院分区:
医学2区
文献类型:
--
作者:
Sugi,K;Karagueuzian,HS;Fishbein,MC;Mandel,WJ;Peter,T

文献摘要

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右冠状动脉(RCA)的永久性闭塞与清醒犬RCA闭塞后第3 - 10天内可诱导的持续性室性快速性心律失常(VT)相关;在此闭塞后时间段之后,无法再诱导VT。本研究的目的是确定是否在梗死的右心室(RVI)的内膜下(SE)纤维在VT的诱导和非诱导阶段仍然可行,如果是这样的话,其跨膜电位特性与微电极和评估其形态学特征。在13只闭胸麻醉犬中,冠状动脉内球囊扩张闭塞RCA。在一组(N = 7)中,在VT诱导期分离梗死组织,在另一组(N = 6)中,在VT非诱导期分离这些组织。静息膜电位,动作电位振幅,最大上行速度,和动作电位时程的存活SE浦肯野纤维(PF)和心室肌(VM)在IZ(第一层)在两组中没有显着差异。两组从基底部到心尖部的基本和过早刺激的传导速度相似。在两组中,周期长度为300至200毫秒的快速刺激未能诱导触发自动活动。与24小时梗死相比,IZ中SEPF的电子显微镜显示胞质脂滴积聚急剧减少。我们的结论是:(1)在RVI的慢性期,梗死区的SEPF和VM网络保持电活性;(2)该纤维网络的跨膜电位特性保持恒定,且与VT诱导性的时间变化无关;(3)该纤维网络的超微结构改善表明向正常进化。
Permanent occlusion of the right coronary artery (RCA) is associated with inducible sustained ventricular tachyarrhythmias (VT) during days 3 to 10 post RCA occlusion period in the conscious dog; VT could no longer be induced beyond this post occlusion period. The aims of the present study were to determine if subendocardial (SE) fibers in the infarcted right ventricle (RVI) during both inducible and noninducible phases of VT remain viable, and if so, to characterize their transmembrane potential properties with the microelectrode and to assess their morphologic features. The RCA was occluded in 13 closed-chest anesthetized dogs with intracoronary balloon inflation. In one group (N = 7), the infarcted tissues were isolated during the VT inducible phase and in another group (N = 6) these tissues were isolated during the VT noninducible phase. Resting membrane potential, action potential amplitude, maximum upstroke velocity, and action potential duration of the surviving SE Purkinje fibers (PF) and ventricular muscle (VM) in the IZ (first layer) were not significantly different in the two groups. Conduction velocity for both basic and premature stimuli from the base to the apex were similar in the two groups. Rapid stimulation at cycle lengths of 300 to 200 msec failed to induce triggering of automatic activity in the two groups. Electron microscopy of SEPF in the IZ showed a drastic reduction in cytosolic lipid droplet accumulation when compared to 24-hour-old infarct. We conclude that: (1) SEPF and VM network in the infarct zone remain electrically viable during the chronic phase of RVI; (2) transmembrane potential properties of this fiber network remain constant and independent of temporal changes of VT inductibility; and (3) ultrastructural improvement of this fiber network suggests an evolution toward normaicy.