Modulation of propagation from an ectopic focus by electrical load
and by extracellular potassium concentration.
Wagner, Mary B., David Golod, Ronald Wilders, E. Etienne Verheijck,
Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, Antoni C. G. Van
Ginneken and William N. Goolsby.
1 Todd Franklin Cardiac Research Laboratory, The Children's Heart
Center, Department of Pediatrics, Emory University, Atlanta, GA, USA,
2 Department of Medical Physiology and Sports Medicine, Utrecht
University, 3584 CG Utrecht, The Netherlands, 3 Department of
Physiology, University of Amsterdam, 1105 AZ Amsterdam, The
Netherlands, 4Bioengineering Graduate Group, U. California, San
Francisco, and U. California, Berkeley
APStracts 3:0493H, 1996.
We previously developed a technique (12) for study of a mathematical
model cell with spontaneous activity, viz. a "real-time"
simulation of a rabbit sinoatrial node cell (SAN model cell (24))
simultaneously being electrically coupled via our "coupling
clamp" (19) circuit to an real, isolated ventricular myocyte. We
now apply this technique to investigate effects of coupling
conductance (Gc), cell size, and the modulation of membrane potential
by elevated [K+]o on the ability of an ectopic focus, represented by
the SAN model cell, to successfully drive a ventricular cell. Values
of Gc and the relative sizes of the two cells define three possible
outcomes: a) spontaneous pacing of the SAN model cell but not driving
of the ventricular cell, b) cessation of spontaneous pacing, or 3)
pacing of the SAN model cell and driving of the ventricular cell.
Below a critical size of the SAN model cell only the first two of
these outcomes is possible. Above this critical size, there is a
range of Gc which allows successful operation of the system as an
ectopic focus. Elevation of [K+]o from 4 to 8 mM increases both the
lower bound and upper bound of Gc for this range. Elevation of [K+]o,
as commonly observed in myocardial ischemia, may have effects on
either inhibiting or releasing from inhibition an ectopic focus.
Received 26 April 1996; accepted in final form 7 November 1996.
APS Manuscript Number H370-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996