A Simulation Study on the Pacing and Driving of the Biological Pacemaker

被引:1
|
作者
Zhang, Yue [1 ,2 ]
Zhang, Lei [3 ]
Wang, Yong [1 ]
Wang, Kuanquan [4 ]
机构
[1] Harbin Engn Univ, Coll Comp Sci & Technol, Harbin 150001, Peoples R China
[2] Univ New South Wales, Sch Engn & Comp Sci, Sydney, NSW 2052, Australia
[3] Univ Maryland, Dept Diagnost Radiol & Nucl Med, Baltimore, MD 21201 USA
[4] Harbin Inst Technol, Sch Comp Sci & Technol, Harbin 150001, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
CARDIAC-PACEMAKERS; CARDIOMYOCYTES; DYSFUNCTION; GENERATION; MECHANISM; THERAPY; DEVICES;
D O I
10.1155/2020/4803172
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The research on the biological pacemaker has been very active in recent years. And turning nonautomatic ventricular cells into pacemaking cells is believed to hold the key to making a biological pacemaker. In the study, the inward-rectifier K+ current (IK1) is depressed to induce the automaticity of the ventricular myocyte, and then, the effects of the other membrane ion currents on the automaticity are analyzed. It is discovered that the L-type calcium current (ICaL) plays a major part in the rapid depolarization of the action potential (AP). A small enough ICaL would lead to the failure of the automaticity of the ventricular myocyte. Meanwhile, the background sodium current (IbNa), the background calcium current (IbCa), and the Na+/Ca2+ exchanger current (INaCa) contribute significantly to the slow depolarization, indicating that these currents are the main supplementary power of the pacing induced by depressing IK1, while in the 2D simulation, we find that the weak electrical coupling plays a more important role in the driving of a biological pacemaker.
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页数:9
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