© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Spontaneous activity induced in rabbit Purkinje myocytes during coupling to a depolarized model cell
aCardiac Rhythm Management Lab, Department of Biomedical Engineering, University of Alabama-Birmingham, Volker Hall B140, 1670 University Blvd., Birmingham, AL 35294, USA
bNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
pollard{at}crml.uab.edu
* Corresponding author. Tel.: +1-205-975-4710; fax: +1-205-975-4720.
Objective: The development of an "injury current" secondary to heterogeneous ion accumulation and cellular uncoupling across the ischemic border zone has been implicated as a trigger for arrhythmias arising during acute ischemia. The purpose of the present study was to determine the effects of injury current across the Purkinje–ventricular interface in the development of abnormal automaticity. Methods: Patch clamp and electronic cell coupling techniques were used to record action potentials from and to apply injury current to isolated rabbit Purkinje myocytes. Injury current was dependent upon: (1) a coupling resistance, which was varied to simulate different degrees of cellular uncoupling, and (2) the difference in Purkinje membrane potential and depolarized ischemic myocardium, which was represented by a passive resistor–capacitor circuit with initial voltages of –70, –60, or –50 mV. Results: During coupling to the moderately depolarized cell (–60 or –50 mV), Purkinje myocytes developed repetitive, spontaneous activity within a window of coupling resistances. This abnormal automaticity was dependent upon L-type calcium current, as cadmium or nifedipine completely suppressed coupling-induced spontaneous activity. Conclusions: Our results demonstrate that injury current alone can induce spontaneous activity in normal Purkinje myocytes. The level of myocardial depolarization and the degree of cellular uncoupling required to induce this activity suggest spontaneous Purkinje activity induced by injury current as a potent trigger for acute ischemic arrhythmias.
KEYWORDS Arrhythmia (mechanisms); Calcium current; Cell communication; Gap junctions; Ischemia
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  E. M. Aliot, W. G. Stevenson, J. M. Almendral-Garrote, F. Bogun, C. H. Calkins, E. Delacretaz, P. D. Bella, G. Hindricks, P. Jais, M. E. Josephson, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: Developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA) Europace, June 1, 2009; 11(6): 771 - 817. [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]
|
|
|
|
|
|
S. P. Patel and D. L. Campbell Transient outward potassium current, 'Ito', phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms J. Physiol., November 15, 2005; 569(1): 7 - 39. [Abstract] [Full Text] [PDF]
|
|