Electrical interactions between a rabbit atrial cell and a nodal cell model

Author:

Joyner Ronald W.1,Kumar Rajiv1,Golod David A.1,Wilders Ronald23,Jongsma Habo J.2,Verheijck E. Etienne23,Bouman Lennart3,Goolsby William N.1,Van Ginneken Antoni C. G.2

Affiliation:

1. Todd Franklin Cardiac Research Laboratory, The Children’s Heart Center, Department of Pediatrics, Emory University, Atlanta, Georgia 30322;

2. Department of Medical Physiology and Sports Medicine, Utrecht University, 3584 CG Utrecht; and

3. Department of Physiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands

Abstract

Atrial activation involves interactions between cells with automaticity and slow-response action potentials with cells that are intrinsically quiescent with fast-response action potentials. Understanding normal and abnormal atrial activity requires an understanding of this process. We studied interactions of a cell with spontaneous activity, represented by a “real-time” simulation of a model of the rabbit sinoatrial (SA) node cell, simultaneously being electrically coupled via our “coupling clamp” circuit to a real, isolated atrial myocyte with variations in coupling conductance ( G c) or stimulus frequency. The atrial cells were able to be driven at a regular rate by a single SA node model (SAN model) cell. Critical G c for entrainment of the SAN model cell to a nonstimulated atrial cell was 0.55 ± 0.05 nS ( n = 7), and the critical G c that allowed entrainment when the atrial cell was directly paced at a basic cycle length of 300 ms was 0.32 ± 0.01 nS ( n = 7). For each atrial cell we found periodic phenomena of synchronization other than 1:1 entrainment when G c was between 0.1 and 0.3 nS, below the value required for frequency entrainment, when the atrial cell was directly driven at a basic cycle length of either 300 or 600 ms. In conclusion, the high input resistance of the atrial cells allows successful entrainment of nodal and atrial cells at low values of G c, but further uncoupling produces arrhythmic interactions.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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