Wang Juan, Zhang Hong, Yang Lin, Wu Ruijuan, Zhang Zhenxi
School of Electrical Engineering, Xi'an Jiaotong University, Xi'an 710049, China.
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2012 Aug;29(4):764-8.
Electrical instability easily induces a unidirectional conduction block, resulting in ventricular tachycardia (VT) or even fibrillation (VF). Cardiac memory affects dynamic electrical characteristics through previous pacing so that it makes the memory important in arrhythmia study. This paper investigates the impact of the rapid pacing duration on cellular excitability and its mechanism. Based on the canine endocardial single cell, a one-dimensional tissue model was developed. Simulations were realized with OpenMP parallel programming method. The results showed that with repetitive pacing, the cellular excitability became low while the conduction velocity decreased. Accumulation of intracellular [Ca2+]i and [Na+]i and depletion of [K+]i led to the shift of membrane current-voltage curves, changing the membrane resistance. Excitability determined by the resistance at the large width of stimulus pulse, therefore, it suggested that [Ca2+]i and [K+]i-induced memory formed the ionic substrates for the alteration of excitability.
电不稳定容易诱发单向传导阻滞，导致室性心动过速（VT）甚至颤动（VF）。心脏记忆通过先前的起搏影响动态电特性，因此其在心律失常研究中具有重要意义。本文研究快速起搏持续时间对细胞兴奋性的影响及其机制。基于犬心内膜单细胞，建立了一维组织模型。采用OpenMP并行编程方法进行模拟。结果表明，重复起搏时，细胞兴奋性降低，传导速度减慢。细胞内[Ca2+]i和[Na+]i的积累以及[K+]i的耗竭导致膜电流-电压曲线的移位，改变了膜电阻。兴奋性由宽刺激脉冲时的电阻决定，因此，提示[Ca2+]i和[K+]i诱导的记忆形成了兴奋性改变的离子基础。
