Modelling of effects of gap junction voltage gating on propagation of excitation in cardiac tissue under pathological conditions
| Author | Affiliation | |
|---|---|---|
Kauno technologijos universitetas | ||
Kauno technologijos universitetas | ||
Verselis, Vytautas Kazimieras | Albert Einstein College of Medicine, Department of Neuroscience, New York, USA |
| Date |
|---|
2020-11-19 |
Basic Science
The Conference is organized by the Student’s Scientific Society of Lithuanian University of Health Sciences The content of the abstract book is redacted. The Student’s Scientific Society of Lithuanian University of Health Sciences did not have control over the abstracts. The authors remain responsible for the content of their respective abstracts. All abstracts presented in the conference were reviewed.
Bibliogr.: p. 18-19
Introduction Gap junctions (GJ) are composed of connexin proteins and ensures metabolic and electrical communication between cells. One of most the important function of GJ is transfer of electrical excitation in heart. Disrupted gap junction coupling has been linked to and increased risk of arrhythmias [1]. Previous studies of propagation of excitation in cardiac tissue assumed that conductance of GJ (gj) is constant, but it is well established that it depends on intracellular voltage [2]. In addition, gj depends on chemical factors, such as changes of intracellular pH or Ca2+ concentration, which are observed under cardiac ischemia. Aim The aim of this study was to evaluate effects of GJ voltage gating on propagation of excitation in heart under pathological conditions. Methods We developed 2-D model of cardiomyocytes network. The model combines Fenton-Karma equations, which describes excitation of cardiomyocyte, and published 36-state model of voltage gating of GJ [3]. We used C++ language and parallel programming to accelerate computations. Results Simulations revealed that high amplitude transjunctional voltage transients could develop during propagation of excitation. Such change of transjuctional voltage could weakly reduce gj, however they accumulate over time into larger decay if pulses of transjunctional voltage are of high frequency and sensitivity of GJ is increased. Further, slow conduction, that is associated with pathological conditions (e.g. cardiac ischemia), can result to higher amplitude and longer transjunctional voltage pulses. [...].