Kunysz A M, Shrier A, Glass L
Department of Physiology, McGill University, Montreal, Quebec, Canada.
Am J Physiol. 1997 Jul;273(1 Pt 1):C331-46. doi: 10.1152/ajpcell.1997.273.1.C331.
Spontaneously beating embryonic chick atrial heart cell aggregates were stimulated with depolarizing current pulses delivered at a fixed delay after each action potential. This preparation is an experimental model of a reentrant tachycardia. During fixed-delay stimulation, bursting behavior was typically observed for a wide range of delays. Episodes of bursting at a rate faster (slower) than control were followed by overdrive suppression (underdrive acceleration). We use a simple nonlinear model, based on the interaction between excitability and overdrive suppression, to describe these dynamics. A modified version of the Shrier-Clay ionic model of electrical activity of the embryonic chick heart cell aggregates that includes a simplified Na+ pump term is also presented. We show that the complex patterns during fixed-delay stimulation arise as a result of delicate interactions between overdrive suppression and phase resetting, which can be described in terms of the underlying ionic mechanisms. This study may provide a basis for understanding incessant tachycardias in the intact heart, as well as an alternative mechanism for the emergence of bursting activity in other biologic tissue.
在每次动作电位后以固定延迟施加去极化电流脉冲，刺激自发搏动的鸡胚心房心脏细胞聚集体。该制备物是折返性心动过速的实验模型。在固定延迟刺激期间，在很宽的延迟范围内通常观察到爆发行为。比对照更快（更慢）速率的爆发发作之后是超速抑制（欠驱动加速）。我们使用一个基于兴奋性和超速抑制之间相互作用的简单非线性模型来描述这些动力学。还提出了胚胎鸡心脏细胞聚集体电活动的Shrier-Clay离子模型的修改版本，其中包括简化的Na +泵项。我们表明，固定延迟刺激期间的复杂模式是由于超速抑制和相位重置之间的微妙相互作用而产生的，这可以根据潜在的离子机制来描述。这项研究可能为理解完整心脏中的持续性心动过速提供基础，以及为其他生物组织中爆发活动的出现提供另一种机制。
