Nilius B, Boldt W
Acta Biol Med Ger. 1980;39(2-3):255-64.
The paper reports on changes of the configuration of the action potential recorded from atrial trabecular preparations of the rabbit. Trabeculae, which were isolated from the right atrial cavum (initial length between 2.6 and 5.4 mm) were stretched up to 160% of the initial length. After stretching the steady state action potentials were analysed. While increasing the trabecular length, the duration of 90% repolarization was prolonged and the duration of 25% repolarization was shortened drastically. The conductance for a time-independent potassium outward current gK, measured from the trajectories of the repolarization phase of the action potential, was reduced by increasing the trabecular length. The reconstruction of the measured action potential suggests an increased anomalous rectification for the time-independent potassium current, a decreased amount of the inward transported calcium during the action potential, and a more rapid inactivation of the Ca++-inward current by stretching the atrial myocardium. The results concerning the gK and the anomalous rectification for the potassium current may explain the alleviated generation of the extrasystoles and arrhythmias in the stretched atrial myocardium. The reduction of the Ca++-transport during the action potential may be a control mechanism protecting the heart tissue from the destabilizing effect of an increased anomalous rectification for a time-independent potassium current.
该论文报道了从兔心房小梁制备物记录的动作电位构型的变化。从小右心房腔分离出的小梁(初始长度在2.6至5.4毫米之间)被拉伸至初始长度的160%。拉伸后,对稳态动作电位进行了分析。在增加小梁长度时,90%复极化的持续时间延长,而25%复极化的持续时间急剧缩短。从动作电位复极化阶段的轨迹测量的与时间无关的钾外向电流gK的电导,随着小梁长度的增加而降低。对测量的动作电位的重建表明,与时间无关的钾电流的反常整流增加,动作电位期间内向转运的钙量减少,并且通过拉伸心房心肌,Ca++内向电流的失活更快。关于gK和钾电流反常整流的结果可能解释了拉伸心房心肌时早搏和心律失常的产生减轻。动作电位期间Ca++转运的减少可能是一种控制机制,保护心脏组织免受与时间无关的钾电流反常整流增加的破坏作用。