心脏收缩调节刺激对心肌细胞钙动力学的影响  

Effects of non-excitatory electrical signal on intracellular calcium handling:a computational study

作　　者：张凡 方祖祥[2] 韩晓东[3] 

机构地区：[1]上海邦德职业学院,上海200241 [2]复旦大学电子工程系 [3]通用电气全球研究中心

出　　处：《中国心脏起搏与心电生理杂志》2011年第2期154-160,共7页Chinese Journal of Cardiac Pacing and Electrophysiology

摘　　要：目的通过计算机理论模拟心肌细胞电生理模型,在心肌动作电位(AP)绝对不应期内施加非兴奋性电刺激,观察胞内自由钙离子浓度变化及心脏收缩调节。方法在人心室细胞电生理模型的基础上,根据近年相关实验成果,通过改造以模拟衰竭心肌细胞的电生理特性。结果改造后模型的AP和胞内钙浓度变化,和临床发现非常相似。心脏收缩调节刺激大大增强了钠-钙交换器活性,在AP间期更多的钙离子经过此交换器进入胞内,逐拍提高了肌浆网内的钙浓度峰值,因而下一搏中有更多的钙离子释放到胞浆中,从而逐渐提高了细胞内的自由钙浓度,最后收敛于一个稳定值,AP的延长和胞内钙活动密切相关。结论适宜的AP绝对不应期刺激能提高肌浆网内钙的集聚,增强心肌收缩。Objective Non-excitatory electrical stimulus during the absolute refractory period is called the cardiac contractility modulation （CCM）. The changes of calcium handling by CCM signal were computationally studied. Methods The current electrophysiological model of human ventricular cell was altered to simulate the failing cell. Results The falling heart cell had very consistent action potential and intracellular calcium concentration in agreement with clinic findings. The activation of sodium-calcium exchanger was greatly strengthened by CCM signal and more calcium enters cell through it. CCM gradually increased the peak calcium concentration in the sarcoplasmic reticulum, which would release more calcium in sequent cardiac cycles, until a balance state was reached and kept. The prolonging of action potential duration by CCM signal was very accordant with the enhancing of calcium handling by the CCM signal. Conclusion CCM could change the calcium handling, increase the free calcium concentration in cells, so to enhance the contractility.

关 键 词：电生理学 心脏收缩调节 钙活动 心力衰竭 人心室细胞模型 

分 类 号：R541.61[医药卫生—心血管疾病] R331.38[医药卫生—内科学]