Skip Navigation

Cardiovascular Research 2003 57(4):934-941; doi:10.1016/S0008-6363(02)00836-2
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Allen, D. G
Right arrow Articles by Xiao, X.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Allen, D. G
Right arrow Articles by Xiao, X.-H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Role of the cardiac Na+/H+ exchanger during ischemia and reperfusion

David G Allen* and Xiao-Hui Xiao

Department of Physiology and Institute for Biomedical Research, University of Sydney F13, Sydney, NSW 2006, Australia

* Corresponding author. Tel.: +61-2-9351-4602; fax: +61-2-9351-2058. davida{at}physiol.usyd.edu.au

The coupled exchanger theory describes one of the central mechanisms of damage in the ischemic heart. The theory proposes that anaerobic glycolysis produces lactate and protons and that the protons can leave the cardiac cell on the cardiac Na+/H+ exchanger (NHE1). The subsequent rise in [Na+]i stimulates the cardiac Na+/Ca2+ exchanger (NCX) and results in an increase in [Ca2+]i which promotes myocardial cell damage. Although the general features of this theory are widely accepted, there is dispute about some aspects, specifically whether the NHE1 remains active during ischemia or not. We review the evidence on this issue and conclude that NHE1 is substantially inhibited during ischemia. This issue is central to the design of a clinical trial of NHE1 inhibitors in the treatment of human cardiac ischemia and the existing clinical trials are considered in this light.

KEYWORDS Ischemia; Na/Ca-exchanger; Na/H-exchanger; Reperfusion


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


This article has been cited by other articles:


Home page
 Circ. Res.Home page
E. Murphy and D. A. Eisner
Regulation of Intracellular and Mitochondrial Sodium in Health and Disease
Circ. Res., February 13, 2009; 104(3): 292 - 303.
[Abstract] [Full Text] [PDF]

Home page
 Phil Trans R Soc AHome page
E. J Crampin, N. P Smith, A. E. Langham, R. H Clayton, and C. H Orchard
Acidosis in models of cardiac ventricular myocytes
Phil Trans R Soc A, May 15, 2006; 364(1842): 1171 - 1186.
[Abstract] [Full Text] [PDF]


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.