Skip Navigation

European Heart Journal 2003 24(20):1854-1856; doi:10.1016/S0195-668X(03)00439-1
Copyright © 2003 by the 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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Opie, L. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Opie, L. H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Current opinion

Preconditioning and metabolic anti-ischaemic agents

Lionel H. Opie*

Hatter Institute for Cardiology Research, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa

* Corresponding author. Lionel H. Opie, MD, Ph.D., Director, Hatter Institute for Cardiology Research, Univ. of Cape Town Medical School, Observatory, 7925, South Africa. Tel.: +27-21-406-6358; fax: +27-21-447-8789
E-mail address: opie{at}capeheart.uct.ac.za

Received 25 July 2003; accepted 28 July 2003

Abstract

Preconditioning a powerful protective mechanism, is the response to transient ischemia and reperfusion. However, the best way to achieve total protection is to avoid ischemia altogether. Therefore prevention of ischemia and protection by preconditioning are differently mediated so that anti-ischemic agents may not precondition, whereas paradoxically pro-ischemic agents may precondition. Metabolically active agents such as glucose-insulin-potassium, trimetazidine and ranolazine that protect from ischemia, increase glucose metabolism relative to that of fatty acids. By promoting glycolysis they tend to close the ATP-dependent potassium channels that help to mediate preconditioning. By lessening the oxygen-wasting effects of fatty acids, they are mitochondrial protective and oxygen-sparing. These qualities should help in the therapy of myocardial ischemia and also heart failure.

Key Words: Preconditioning • Anti-ischaemic agents • Metabolic protection


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
J. Pharmacol. Exp. Ther.Home page
S. Wisel, M. Khan, M. L. Kuppusamy, I. K. Mohan, S. M. Chacko, B. K. Rivera, B. C. Sun, K. Hideg, and P. Kuppusamy
Pharmacological Preconditioning of Mesenchymal Stem Cells with Trimetazidine (1-[2,3,4-Trimethoxybenzyl]piperazine) Protects Hypoxic Cells against Oxidative Stress and Enhances Recovery of Myocardial Function in Infarcted Heart through Bcl-2 Expression
J. Pharmacol. Exp. Ther., May 1, 2009; 329(2): 543 - 550.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
N. Sambandam, D. Morabito, C. Wagg, B. N. Finck, D. P. Kelly, and G. D. Lopaschuk
Chronic activation of PPAR{alpha} is detrimental to cardiac recovery after ischemia
Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H87 - H95.
[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.