Document Detail

Myocardial reperfusion injury management: erythropoietin compared with postconditioning.
MedLine Citation:
PMID:  19617412     Owner:  NLM     Status:  MEDLINE    
Ischemic postconditioning (IPost) and erythropoietin (EPO) have been shown to attenuate myocardial reperfusion injury using similar signaling pathways. The aim of this study was to examine whether EPO is as effective as IPost in decreasing postischemic myocardial injury in both Langendorff-isolated-heart and in vivo ischemia-reperfusion rat models. Rat hearts were subjected to 25 min ischemia, followed by 30 min or 2 h of reperfusion in the isolated-heart study. Rats underwent 45 min ischemia, followed by 24 h of reperfusion in the in vivo study. In both studies, the control group (n=12; ischemia-reperfusion only) was compared with IPost (n=16; 3 cycles of 10 s reperfusion/10 s ischemia) and EPO (n=12; 1,000 IU/kg) at the onset of reperfusion. The following resulted. First, in the isolated hearts, IPost or EPO significantly improved postischemic recovery of left ventricular developed pressure. EPO induced better left ventricular developed pressure than IPost at 30 min of reperfusion (73.18+/-10.23 vs. 48.11+/-7.92 mmHg, P<0.05). After 2 h of reperfusion, the infarct size was significantly lower in EPO-treated hearts compared with IPost and control hearts (14.36+/-0.60%, 19.11+/-0.84%, and 36.21+/-4.20% of the left ventricle, respectively; P<0.05). GSK-3beta phosphorylation, at 30 min of reperfusion, was significantly higher with EPO compared with IPost hearts. Phosphatidylinositol 3-kinase and ERK1/2 inhibitors abolished both EPO- and IPost-mediated cardioprotection. Second, in vivo, IPost and EPO induced an infarct size reduction compared with control (40.5+/-3.6% and 28.9+/-3.1%, respectively, vs. 53.7+/-4.3% of the area at risk; P<0.05). Again, EPO decreased significantly more infarct size and transmurality than IPost (P<0.05). In conclusion, with the use of our protocols, EPO showed better protective effects than IPost against reperfusion injury through higher phosphorylation of GSK-3beta.
Sophie Tamareille; Nehmat Ghaboura; Frederic Treguer; Dalia Khachman; Anne Croué; Daniel Henrion; Alain Furber; Fabrice Prunier
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-17
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  297     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2010-02-17     Revised Date:  2013-06-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2035-43     Citation Subset:  IM    
Unité Propre de Recherche de l'Enseignement Supérieur Equipe d'Accueil, Protection et Remodelage du Myocarde, Faculté de Médecine d'Angers, Université d'Angers, Service de Cardiologie, Centre Hospitalier Universitaire d'Angers, Angers Cedex 1, France.
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MeSH Terms
Cardiotonic Agents / therapeutic use*
Coronary Circulation / drug effects
Disease Models, Animal
Erythropoietin / analogs & derivatives*,  pharmacology
Glycogen Synthase Kinase 3 / metabolism
Heart Rate / drug effects
Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors,  metabolism
Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors,  metabolism
Myocardial Infarction / enzymology,  pathology,  physiopathology,  prevention & control*
Myocardial Reperfusion Injury / enzymology,  pathology,  physiopathology,  prevention & control*
Myocardium / enzymology,  pathology*
Phosphatidylinositol 3-Kinases / antagonists & inhibitors,  metabolism
Protein Kinase Inhibitors / pharmacology
Proto-Oncogene Proteins c-akt / metabolism
Rats, Wistar
Time Factors
Ventricular Function, Left / drug effects*
Ventricular Pressure / drug effects
Reg. No./Substance:
0/Cardiotonic Agents; 0/Protein Kinase Inhibitors; 11096-26-7/Erythropoietin; 15UQ94PT4P/darbepoetin alfa; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC Proteins c-akt; EC synthase kinase 3 beta; EC Protein Kinase 1; EC Protein Kinase 3; EC Synthase Kinase 3
Erratum In:
Am J Physiol Heart Circ Physiol. 2009 Dec;297:H2035

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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