急性心肌梗死L-型钙离子通道变化的仿真模拟  

Simulation of L-type Calcium Channel Alteration in Acute Myocardial Infarction

作　　者：斯小琴 陈大伟 张季谦[2] SI Xiao-qin;CHEN Da-wei;ZHANG Ji-qian(Urban Construction College,Anhui Jianzhu University,Hetei Anhui 238076,China;College of Physics and Electronic Information,Anhui Normal University,Wuhu Anhui 241000,China)

机构地区：[1]安徽建筑大学城市建设学院,安徽合肥238079 [2]安徽师范大学物理与电子信息学院,安徽芜湖241000

出　　处：《长春师范大学学报》2018年第6期135-138,141,共5页Journal of Changchun Normal University

基　　金：安徽高校自然科学重点项目"外界扰动对窦房结体系起搏动力学过程调控作用的理论研究"(KJ2017A810);安徽省自然科学基金"心肌组织螺旋波与时空混沌的调控作用研究"(1508085MA15);高校学科(专业)拔尖人才学术资助重点项目(gxbj ZD2016014);安徽省学术和技术带头人后备人选科研资助项目(2017H117)

摘　　要：本文利用Zhang等构建的完整兔子的心脏窦房结—心房细胞体系二维解剖模型为研究对象,通过计算机仿真模拟,研究了细胞外钙离子浓度和迷走神经调节对心肌细胞L-型钙离子通道电流的影响。结果发现:一方面,细胞外钙离子浓度在一定范围内升高时,心律会适当加快;在钙离子浓度较高的情况下,心脏会停止跳动。另一方面,迷走神经释放的递质——乙酰胆碱浓度升高,心肌细胞运动电位周期变短,心律加快。上述结果表明,细胞外钙离子浓度和乙酰胆碱浓度对心肌细胞L-型钙离子通道电流具有明显的抑制作用,可导致心肌细胞产生负性肌力作用,诱发心律失常。A two-dimensional anatomical model of the intact sinoatrial node（ SAN） and surrounding atrial muscle of rabbit proposed by Zhang et al. was used as a research subject,and by computer simulation,the effect of extracellular calcium ion concentration（ [Ca^（2＋）]i） and the regulation of the vagal nerve on L-type calcium channel current of cardiomyocytes were studied. The results showed that,on the one hand that,when the [Ca^（2＋）]iincreases within a certain range,the heart rhythm will be accelerated properly. At higher concentrations of calcium ions,the heart will stop beating. On the other hand,as the concentration of acetylcholine（ ACh） increases,a transmitter of the vagus nerve,the activity of myocardial cells becomes shorter and the rhythm beats faster. Above results suggest that the[Ca^（2＋）]iand ACh concentration have a significant inhibitory effect on L-type calcium channel current. It will help us to reveal the pathology of various arrhythmias resulting from the acute myocardial infarction（ AMI）,and it will provide a theoretical reference for clinical diagnosis and prevention.

关 键 词：心肌梗死 L-型钙离子通道 乙酰胆碱 仿真模拟 

分 类 号：R331.38[医药卫生—人体生理学]