Cobbe S M, Manley B S
Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, U.K.
Eur Heart J. 1987 Nov;8(11):1241-8. doi: 10.1093/oxfordjournals.eurheartj.a062199.
The effects of 30 min zero-flow ischaemia and reperfusion on the electrophysiological properties of amiodarone were studied in 11 rabbits treated with oral amiodarone (mean 117 mg kg-1, day-1) for 2-3 months, and 11 controls. Experiments were performed in vitro in the isolated perfused interventricular septum, and preischaemic values were compared with those obtained in right ventricular papillary muscles from the same hearts. Prior to ischaemia, mean values of action potential duration (APD90) and effective refractory period (ERP) were prolonged by 13% in the amiodarone-treated septa. Action potential upstroke velocity (Vmax) was reduced by 14% in the septa, but by 42% in papillary muscles. Ischaemia resulted in shortening of APD90 in both control and amiodarone-treated septa, with a loss of the ability of amiodarone to prolong APD90. In contrast, ischaemia resulted in a greater fall in Vmax, gross lengthening in conduction time and increase in stimulation threshold in the amiodarone-treated septa compared with controls. Reperfusion resulted in a restoration of the action of amiodarone on repolarization, and resolution of the marked effects on excitability and conduction. The electrophysiological properties of amiodarone are considerably altered in ischaemic myocardium, with a reversible loss of its ability to prolong repolarization, but evidence suggestive of a marked enhancement of its effect on the inward sodium current.
在11只口服胺碘酮（平均剂量117mg·kg-1，每日1次）2 - 3个月的家兔及11只对照家兔中，研究了30分钟零流量缺血及再灌注对胺碘酮电生理特性的影响。实验在离体灌注的室间隔上进行，缺血前的值与取自同一心脏的右心室乳头肌所获得的值进行比较。缺血前，胺碘酮处理的室间隔动作电位时程（APD90）和有效不应期（ERP）的平均值延长了13%。室间隔动作电位上升速度（Vmax）降低了14%，但乳头肌中降低了42%。缺血导致对照和胺碘酮处理的室间隔中APD90均缩短，胺碘酮延长APD90的能力丧失。相比之下，与对照组相比，缺血导致胺碘酮处理的室间隔中Vmax下降幅度更大，传导时间显著延长，刺激阈值增加。再灌注导致胺碘酮对复极化的作用恢复，对兴奋性和传导的显著影响消退。在缺血心肌中，胺碘酮的电生理特性发生了显著改变，其延长复极化的能力可逆性丧失，但有证据表明其对内向钠电流的作用显著增强。
