心脏短期记忆对组织电兴奋的影响及其机制

Effects and the Mechanisms of Cardiac Short-term Memory on Cellular Electrical Excitability

心肌电活动的不稳定易于诱发单向传导阻滞,导致室速/室颤(VT/VF)的发生。心脏记忆使动力学特性受以往所有电刺激的影响而成为心律失常研究中的重要内容。本文主要就快刺激频率下,组织细胞电兴奋与刺激持续时间的关系及机制开展相关研究。在犬心内膜单细胞的基础上,构建了一维传导组织模型,利用OpenMP并行编程实现仿真研究。结果显示,随着刺激的持续,电兴奋降低,传导速度下降。细胞内[Ca2+]i和[Na+]i浓度随刺激持续积累、[K+]i持续减小是导致细胞膜电流电压曲线偏移,进而改变膜电阻的主要原因。对于大脉宽的电刺激,兴奋性取决于膜电阻,因此,由[Ca2+]i、[Na+]i和[K+]i引起的记忆是组织细胞电兴奋改变的离子基础。

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 dura- tion 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. Accumula- tion 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 ,[Na＋ ]i and [K＋ ]i-induced memory formed the ionic substrates for the altera- tion of excitability.