标题:
心肌组织死亡细胞分布对窦房结搏动信号传导功能的影响Effect of Distribution of Dead Cells on Pacemaking and Driving Function of Sinoatrail Node in the Myocardium
作者:
斯小琴, 张季谦, 陈春磊, 王业遒, 张恒贵
关键字:
传导阻滞, 心脏瘁死, 仿真模拟, 死亡细胞分布Conduction Block; Cardiac Sudden Death; Computer Simulation; Dead Cell Distribution
期刊名称:
《Applied Physics》, Vol.1 No.2, 2011-07-29
摘要:
本文利用Zhang等人构建的兔子心脏窦房结–心房细胞完整的二维解剖模型，通过计算机仿真模拟研究了死亡细胞分布对心脏起搏和传导的影响。模拟结果发现，一方面，利用该模型可以重现有生理缺陷的心脏体系异常搏动现象，例如老龄化的心脏因部分心肌细胞死亡数达到一定比例时所引起的窦房结传导受阻，甚至会产生心脏瘁死现象。另一方面，我们可以通过分析心肌组织中死亡细胞的分布情况，了解其对心脏搏动功能的影响：在神经系统分泌一定浓度的乙酰胆碱调节作用下，心肌组织中细胞死亡达到一定比例时，引起起搏活动的传导阻滞与死亡细胞的空间分布密切相关。其不仅与组织中某区域内细胞死亡数及占正常细胞比例大小成正比，而且还与离死亡细胞所在位置的距离成反比。最后我们讨论了不同乙酰胆碱浓度对这种分布效果的影响。上述结果将有助于揭示复杂的心脏体系异常搏动的内在形成机理，并为病态窦房结综合症的临床诊断和预防提供一定的理论指导。
In this paper, by using a 2D anatomical model of the intact sinoatrial node (SA) node and surrounding atrial muscle of the rabbit heart proposed by Zhang et al., the effect of the distribution of death cells on the pacemaking and conductibility of SA node is investigated by computer simulation. The results show, on the one hand, using this model, we can obtain the phenomenon of abnormal rhythm in heart with physiological defect, such as, once the number of the myocardial death cell to reach a certain level in the aging heart due to SA-atrium conduction block, etc., and these will induce the cardiac sudden death. On the other hand, more importantly, the effect of the cardiac pacemaker can be understood by analyzing the spacial distribution of dead cells in the myocardium: Under the regulation of acetylcholine with certain concentration excreted by nervous system, and as well as the number of dead cells reaches in a certain proportion, such conduction block of pacemaker activity is closely relate to the spatial distribution of dead cells. It is not only proportional to the number of death cells, and the ratio of dead cells to normal cells in the organization, but also inverse proportion to the distance of dead cells location. Finally, we discussed the effect of thus distribution for dif-ferent concentrations of acetylcholine. Our simulation results may contribute to the understanding about the internal mechanism of the abnormal rhythm in complex cardiac system, and provide a theoretical guidance on the clinical diagnosis of sick sinus syndrome and prevention.