Skip Navigation

Cardiovascular Research 2001 49(4):779-789; doi:10.1016/S0008-6363(00)00300-X
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Huelsing, D. J.
Right arrow Articles by Spitzer, K. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Huelsing, D. J.
Right arrow Articles by Spitzer, K. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Transient outward current modulates discontinuous conduction in rabbit ventricular cell pairs

Delilah J. Huelsinga,*, Andrew E. Pollarda and Kenneth W. Spitzerb

aCardiac Rhythm Management Lab and 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

* Corresponding author. Tel.: +1-205-975-4718; fax: +1-205-975-4720 djh{at}crml.uab.edu

Objective: While several studies have demonstrated that the L-type calcium current maintains discontinuous conduction, the contribution of the transient outward current (Ito) to conduction remains unclear. This study evaluated the effects of Ito inhibition on conduction between ventricular myocytes. Methods: An electronic circuit with a variable resistance (Rj) was used to electrically couple single epicardial myocytes isolated from rabbit right ventricle. We inhibited Ito with 4-aminopyridine superfusion, rate–acceleration, or premature stimulation to evaluate the subsequent effects on conduction delay and the critical Rj, which was quantified as the highest Rj that could be imposed before conduction failed. Results: Ito inhibition significantly enhanced conduction in all cell pairs (n = 23). Pharmacologic inhibition of Ito resulted in a 32±5% decrease in conduction delay and a 36±7% increase in critical Rj. Similarly, reduction of the basic cycle length from 2 to 0.5 s resulted in a 31±3% decrease in conduction delay and a 31±3% increase in critical Rj. Finally, premature action potentials conducted with a 41±4% shorter conduction delay and a 73±24% higher critical Rj than basic action potentials. Conclusions: Ito inhibition significantly enhanced conduction across high Rj. These results suggest Ito may contribute to rate-dependent conduction abnormalities.

KEYWORDS Arrhythmia (mechanisms); Cell communication; Conduction (block); Ion channels; K-channels; Membrane potential; Ventricular arrhythmias


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.