Document Detail

Postconditioning: from the bench to bedside.
MedLine Citation:
PMID:  20938041     Owner:  NLM     Status:  In-Data-Review    
Infarct size is determined not only by the severity of ischemia but also by pathological processes initiated at reperfusion. Accumulating experimental evidence indicates that lethal reperfusion injury might account for up to half of the final size of the myocardial infarct. Ischemic postconditioning (brief repeated periods of ischemia-reperfusion applied at the onset of coronary reflow) has been recently described as a powerful cardioprotection mechanism that prevents lethal reperfusion injury. This is the first method proven to reduce the final infarct size by about 50% in several in vivo models and to be confirmed in recent preliminary human studies. The molecular pathways are incompletely mapped but they probably converge to a mitochondrial key target: the mitochondrial permeability transition pore (PTP) which opening during early reperfusion is an event that promotes myocardial cell death. In different animal models and experimental settings, pharmacological PTP inhibition at the onset of reperfusion reproduces all the cardioprotective effects of ischemic postconditioning. In a recent proof-of-concept trial, the administration (just before percutaneous coronary intervention) of cyclosporine A, a potent PTP inhibitor, was associated with smaller infarct size. This review will focus on the physiological preclinical data on both ischemic and pharmacological postconditioning that are relevant to their translation to clinical therapeutics.
Martin Cour; Ludovic Gomez; Nathan Mewton; Michel Ovize; Laurent Argaud
Publication Detail:
Type:  Journal Article     Date:  2010-10-11
Journal Detail:
Title:  Journal of cardiovascular pharmacology and therapeutics     Volume:  16     ISSN:  1940-4034     ISO Abbreviation:  J. Cardiovasc. Pharmacol. Ther.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-10     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9602617     Medline TA:  J Cardiovasc Pharmacol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  117-30     Citation Subset:  IM    
INSERM, U886-Cardioprotection, Lyon, France, Hospices Civils de Lyon, Groupement Hospitalier Edouard Herriot, Service de Réanimation Médicale, Lyon, France, Université de Lyon, Université Claude Bernard Lyon 1, Faculté de médecine Lyon-Est, Lyon, France.
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