Document Detail


Cardiac effects of postconditioning depend critically on the duration of index ischemia.
MedLine Citation:
PMID:  17122197     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Postconditioning (POC) is known as the phenomenon whereby brief intermittent ischemia applied at the onset of reperfusion following index ischemia limits myocardial infarct size. Whereas there is evidence that the algorithm of the POC stimulus is an important determinant of the protective efficacy, the importance of the duration of index ischemia on the outcome of the effects of POC has received little attention. Pentobarbital sodium-anesthetized Wistar rats were therefore subjected to index ischemia produced by coronary artery occlusions (CAO) of varying duration (15-120 min) followed by reperfusion, without or with postconditioning produced by three cycles of 30-s reperfusion and reocclusion (3POC30). 3POC30 limited infarct size produced by 45-min CAO (CAO45) from 45 +/- 3% to 31 +/- 5%, and CAO60 from 60 +/- 3% to 47 +/- 6% (both P < or = 0.05). In contrast, 3POC30 increased infarct size produced by CAO15 from 3 +/- 1% to 19 +/- 6% and CAO30 from 36 +/- 6 to 48 +/- 4% (both P < or = 0.05). This deleterious effect of 3POC30 was not stimulus sensitive because postconditioning with 3POC5 and 3POC15 after CAO30 also increased infarct size. The cardioprotection by 3POC30 after CAO60 was accompanied by an increased stimulation of Akt phosphorylation at 7 min of reperfusion and a 36% lower superoxide production, measured by dihydroethidium fluorescence, after 2 h of reperfusion. Consistent with these results, cardioprotection by 3POC30 was abolished by phosphatidylinositol-3-OH-kinase inhibition, as well as nitric oxide (NO) synthase inhibition. The deleterious effect of 3POC30 after CAO15 was accompanied by an increased superoxide production with no change in Akt phosphorylation and was not affected by NO synthase inhibition. In conclusion, the effect of cardiac POC depends critically on the duration of the index ischemia and can be either beneficial or detrimental. These paradoxical effects of POC may be related to the divergent effects on Akt phosphorylation and superoxide production.
Authors:
Olivier C Manintveld; Maaike Te Lintel Hekkert; Ewout Jan van den Bos; Grietje M Suurenbroek; Dick H Dekkers; Pieter D Verdouw; Jos M Lamers; Dirk J Duncker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-11-22
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  292     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-06     Completed Date:  2007-04-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1551-60     Citation Subset:  IM    
Affiliation:
Division Experimental Cardiology, Erasmus MC, 3000DR Rotterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Atrial Fibrillation / physiopathology
Disease Models, Animal
Male
Myocardial Ischemia / physiopathology*,  therapy*
Myocardial Reperfusion*
Rats
Rats, Wistar
Time Factors
Ventricular Fibrillation / physiopathology

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


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