| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Cardiac Rhythm Management Laboratory and Department of Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama 35294; and 2 Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112
Many studies suggest that early
afterdepolarizations (EADs) arising from Purkinje fibers initiate
triggered arrhythmias under pathological conditions. However,
electrotonic interactions between Purkinje and ventricular myocytes may
either facilitate or suppress EAD formation at the Purkinje-ventricular
interface. To determine conditions that facilitated or suppressed EADs
during Purkinje-ventricular interactions, we coupled single Purkinje
myocytes and aggregates isolated from rabbit hearts to a passive model
cell via an electronic circuit with junctional resistance
(Rj). The model cell had input resistance
(Rm,v) of 50 M
, capacitance of 39 pF, and a
variable rest potential (Vrest,v). EADs were
induced in Purkinje myocytes during superfusion with 1 µM
isoproterenol. Coupling at high Rj to normally
polarized Vrest,v established a repolarizing
coupling current during all phases of the Purkinje action potential.
This coupling current preferentially suppressed EADs in single cells with mean membrane resistance (Rm,p) of 297 M, whereas EAD suppression in larger aggregates with mean
Rm,p of 80 M required larger coupling currents. In contrast, coupling to elevated
Vrest,v established a depolarizing coupling
current during late phase 2, phase 3, and phase 4 that facilitated
EAD formation and induced spontaneous activity in single Purkinje
myocytes and aggregates. These results have important implications for
arrhythmogenesis in the infarcted heart when reduction of the
ventricular mass due to scarring alters the
Rm,p-to-Rm,v ratio and in
the ischemic heart when injury currents are established during coupling
between polarized Purkinje myocytes and depolarized ventricular myocytes.
Purkinje-ventricular junction; injury current; membrane resistance
This article has been cited by other articles:
|
|
 |
|
  V. E. Bondarenko and R. L. Rasmusson Simulations of propagated mouse ventricular action potentials: effects of molecular heterogeneity Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1816 - H1832. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Wilders Dynamic clamp: a powerful tool in cardiac electrophysiology J. Physiol., October 15, 2006; 576(2): 349 - 359. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Xing, A. L. Kjolbye, J. S. Petersen, and J. B. Martins Pharmacological stimulation of cardiac gap junction coupling does not affect ischemia-induced focal ventricular tachycardia or triggered activity in dogs Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H511 - H516. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Huelsing, K. W. Spitzer, and A. E. Pollard Spontaneous activity induced in rabbit Purkinje myocytes during coupling to a depolarized model cell Cardiovasc Res, September 1, 2003; 59(3): 620 - 627. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E Pollard, W. E Cascio, V. G Fast, and S. B Knisley Modulation of triggered activity by uncoupling in the ischemic border: A model study with phase 1b-like conditions Cardiovasc Res, December 1, 2002; 56(3): 381 - 392. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
