Copyright © 2003 by the European Society of Cardiology.
Current opinion
Preconditioning and metabolic anti-ischaemic agents
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
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