Rate-related electrophysiologic effects of long-term administration of amiodarone on canine ventricular myocardium in vivo.

Rate-related electrophysiologic effects of long-term administration of amiodarone on canine ventricular myocardium in vivo.
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长期施用胺碘酮对体内犬心室心肌的速率相关电生理效应。

DOI:
10.1161/01.cir.79.4.948
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发表时间:
1989
期刊:
影响因子:
37.8
通讯作者:
Urie,PM
Urie,PM
中科院分区:
医学1区
文献类型:
--
作者:
Anderson,KP;Walker,R;Dustman,T;Lux,RL;Ershler,PR;Kates,RE;Urie,PM

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在13只犬中检查了胺碘酮的电生理效应,这些犬在3周内口服30 g胺碘酮,并与13只未接受胺碘酮的对照犬进行了比较。纵向和横向心外膜传导速度估计与一个正方形阵列的64个紧密间隔的电极和计算机辅助采集和分析系统。胺碘酮引起传导速度的速率依赖性降低,对纵向传播的影响略大。在突然缩短起搏周期长度后,与频率相关的传导速度下降迅速发展; 67%的变化发生在快速序列的前两次搏动之间,在第10次搏动后几乎没有变化。传导速度的使用依赖性抑制恢复呈指数关系,纵向平均时间常数为447 +/- 172 msec,横向为452 +/- 265 msec。复极间期(定义为单极电描记图中激动时间和复极时间之间的间期)与在不存在和存在胺碘酮的情况下在每个测试周期长度下的不应期测定高度相关。胺碘酮治疗引起的复极间期和不应期延长不随周期长度变化。胺碘酮治疗还导致收缩压显著降低。接受胺碘酮治疗组的收缩压在1,000和200 msec的稳态起搏周期长度之间平均降低50 +/- 23%,而对照组的相应降低为21 +/- 32%(p <0.05)。血浆和心肌胺碘酮和去乙基胺碘酮水平与临床观察到的水平相当。我们得出结论,长期胺碘酮给药导致传导速度和血压的频率依赖性降低,并导致复极间期的频率非依赖性增加。
The electrophysiologic effects of amiodarone were examined in 13 dogs that received 30 g amiodarone orally during 3 weeks and compared with 13 control dogs that did not receive amiodarone. Longitudinal and transverse epicardial conduction velocities were estimated with a square array of 64 closely spaced electrodes and a computer-assisted acquisition and analysis system. Amiodarone caused a rate-dependent decrease in conduction velocity with a slightly greater effect in the longitudinal direction of propagation. Rate-related depression of conduction velocity developed rapidly after abrupt shortening of the pacing cycle length; 67% of the change occurred between the first two beats of the rapid train, and little change occurred after the 10th beat. Recovery from use-dependent depression of conduction velocity was exponential with a mean time constant of 447 +/- 172 msec in the longitudinal direction and 452 +/- 265 msec in the transverse direction. Repolarization intervals, defined as the interval between the activation time and the repolarization time in the unipolar electrograms, correlated highly with refractory period determinations in the absence and presence of amiodarone at each cycle length tested. The increase in repolarization intervals and refractory periods resulting from amiodarone treatment did not vary with cycle length. Amiodarone treatment also resulted in a significant rate-related reduction in systolic blood pressure. The systolic blood pressure in the group that received amiodarone decreased by a mean of 50 +/- 23% between steady-state pacing cycle lengths of 1,000 and 200 msec, whereas the corresponding decrease in the control group was 21 +/- 32% (p less than 0.05). Plasma and myocardial amiodarone and desethylamiodarone levels were comparable to those observed clinically. We conclude that long-term amiodarone administration causes rate-dependent reductions in conduction velocity and blood pressure and causes rate-independent increases in repolarization intervals.
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