SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
Journal of Cardiovascular Pharmacology and Therapeutics
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Dow, J.
Right arrow Articles by Kloner, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dow, J.
Right arrow Articles by Kloner, R. A.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

The Mechanism by Which Ischemic Postconditioning Reduces Reperfusion Arrhythmias in Rats Remains Elusive

Joan Dow, BS

Heart Institute, Good Samaritan Hospital

Anil Bhandari, MD

Heart Institute, Good Samaritan Hospital

Robert A. Kloner, MD, PhD

Heart Institute, Good Samaritan Hospital, rkloner{at}goodsam.org, Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California Los Angeles, California

We have observed that ischemic postconditioning markedly reduces reperfusion-induced ventricular arrhythmias, but whether the mechanism is related to previously described pathways of preconditioning or postconditioning for infarct size reduction is unknown. The purpose of this study was to determine whether known pathways were involved in postconditioning's protective effect on arrhythmias.

Anesthetized female rats were subjected to 5 minutes of proximal coronary artery occlusion and 5 minutes of reperfusion. They were either not postconditioned or subjected to 4 cycles of 20 seconds reperfusion, 20 seconds reocclusion before final reperfusion (postconditioned). Electrocardiogram and blood pressure were monitored throughout. Alleged agonists and antagonists to postconditioning representing a number of mechanisms were evaluated.

Nonpostconditioned rats treated with the suppressor of the mitochondrial permeability transition pore, cyclosporine A, did not show a reduction in

reperfusion-induced ventricular arrhythmias compared to control nonpostconditioned rats. Neither Wortmannin (p13-kinase inhibitor), 5 hydroxydecanoate (selective inhibitor of mitochondrial KATP channel), nor 8-sulfophenyl theophylline (blocker of adenosine receptors) blocked the reduction in ventricular tachycardia of postconditioning.

The mechanism by which postconditioning reduces reperfusion-induced ventricular arrhythmias may be independent of known pathways that have been implicated in the infarct sparing effects of preconditioning and postconditioning—including adenosine, mitochondrial KATP channel, mitochondrial permeability transition pore, and p13-kinase-pAKt pathways. Alternative protective pathways may exist to explain the antiarrhythmic effect of postconditioning.

Key Words: ischemia • reperfusion • postconditioning • arrhythmias

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 14, No. 2, 99-103 (2009)
DOI: 10.1177/1074248408329606
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




Advertisement