Billette J, Janse M J, van Capelle F J, Anderson R H, Touboul P, Durrer D
Am J Physiol. 1976 Oct;231(4):1129-39. doi: 10.1152/ajplegacy.1976.231.4.1129.
Cycle-length-dependent changes in AV nodal cell activation were studied in isolated preparations from rabbit hearts. Transmembrane action potentials were recorded from the node while it was propagating impulses initiated in the atrium with an accelerating train of stimuli. This train consisting of five successive stimuli separated by progressively shorter intervals was uniformly repeated at every 10th basic beat, each time reproducing a sequence of five different increasing AV nodal delays. The AN and NH cells were found to contribute only slightly to the cycle-length-dependent AV nodal delay which developed mainly in the small N zone, located centrally in the AV node. With the increasing delay, the action potentials from this N zone typically dissociated into two components synchronous with late AN and early NH activity, respectively. The amplitude of the first component decreased, wheareas that of the second increased progressively in N cells activated progressively later. No cells were activated at an intermediate time between the two components. This dissociation was not accompanied by changes in the activation pattern of the AV node. The different nodal cells classified according to their response to the accelerating train delineated functional zones corresponding to different anatomic structures. The possible mechanisms which would explain the cycle-length-dependent AV nodal delay are discussed.
在兔心脏的离体标本中研究了房室结细胞激活的周期长度依赖性变化。在房室结传导由心房加速刺激序列引发的冲动时,记录其跨膜动作电位。该刺激序列由五个连续刺激组成,刺激间隔逐渐缩短,每十个基本搏动均匀重复一次,每次再现五个不同的、逐渐增加的房室结延迟序列。发现心房肌(AN)细胞和结希区(NH)细胞对周期长度依赖性房室结延迟的贡献很小,这种延迟主要发生在房室结中央的小N区。随着延迟增加,来自该N区的动作电位通常分解为两个成分,分别与晚期AN活动和早期NH活动同步。在逐渐延迟激活的N细胞中,第一个成分的幅度减小,而第二个成分的幅度逐渐增加。在两个成分之间的中间时间没有细胞被激活。这种分离并不伴随着房室结激活模式的变化。根据对加速刺激序列的反应分类的不同结细胞描绘了与不同解剖结构相对应的功能区。讨论了解释周期长度依赖性房室结延迟的可能机制。