Stability of genetically engineered cardiac pacemaker - role of intracellular CA/sup 2+/ handling

Author

Zhang, H. ; Tong, W.-C. ; Garratt, CJ ; Holden, AV

Author_Institution

Biol. Phys. Group, Manchester Univ.

fYear

2005

fDate

25-28 Sept. 2005

Firstpage

969

Lastpage

972

Abstract

Down-regulation of Kir2.1 channel reduces the inward-rectifier potassium current (i_K1), and transforms excitable ventricular myocytes to pacemaker cells. This provides a possible bio-technique to induce a biological pacemaker, as an alternative to an implantable electronic pacemaker. However there are two fundamental issues: (i) the stability of the pacemaker activity; (ii) the critical size of the biological pacemaker necessary for robust pacing and driving the surrounding ventricular muscle. In this study, we address the two issues by computer modelling

Keywords

bioelectric phenomena; biomembrane transport; calcium; cardiovascular system; genetic engineering; medical computing; muscle; neurophysiology; patient treatment; physiological models; potassium; Kir2.1 channel; biological pacemaker; computer modelling; genetically engineered cardiac pacemaker stability; intracellular Ca²⁺ channel; inward-rectifier potassium current; ventricular myocytes; Astronomy; Biological system modeling; Biological tissues; Biology computing; Biomembranes; Genetic engineering; Medical treatment; Pacemakers; Physics; Robust stability;

fLanguage

English

Publisher

ieee

Conference_Titel

Computers in Cardiology, 2005

Conference_Location

Lyon

Print_ISBN

0-7803-9337-6

Type

conf

DOI

10.1109/CIC.2005.1588270

Filename

1588270