Document Detail


Myocardium tolerant to an adenosine-dependent ischemic preconditioning stimulus can still be protected by stimuli that employ alternative signaling pathways.
MedLine Citation:
PMID:  15486028     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Clinical studies on cardioprotection by preinfarct angina are ambiguous, which may involve development of tolerance to repeated episodes of ischemia. Not all preconditioning stimuli use identical signaling pathways, and because patients likely experience varying numbers of episodes of preinfarct angina of different degrees and durations, it is important to know whether myocardium tolerant to a particular preconditioning stimulus can still be protected by stimuli employing alternative signaling pathways. We tested the hypothesis that development of tolerance to a particular stimulus does not affect cardioprotection by stimuli that employ different signaling pathways. Anesthetized rats underwent classical, remote or pharmacological preconditioning. Infarct size (IS), produced by a 60-min coronary artery occlusion (CAO), was determined after 120 min of reperfusion. Preconditioning by two 15-min periods of CAO (2CAO15, an adenosine-dependent stimulus) limited IS from 69 +/- 2% to 37 +/- 6%, but when 2CAO15 was preceded by 4CAO15, protection by 2CAO15 was absent (IS = 68 +/- 1%). This development of tolerance coincided with a loss of cardiac interstitial adenosine release, whereas two 15-min infusions of adenosine (200 microg/min i.v.) still elicited cardioprotection (IS = 40 +/- 4%). Furthermore, cardioprotection was produced when 4CAO15 was followed by the adenosine-independent stimulus 3CAO3 (IS = 50 +/- 8%) or the remote preconditioning stimulus of two 15-min periods of mesenteric artery occlusion (IS = 49 +/- 6%). In conclusion, development of tolerance to cardioprotection by an adenosine-dependent preconditioning stimulus still allows protection by pharmacological or ischemic stimuli intervention employing different signaling pathways.
Authors:
David A Liem; Maaike te Lintel Hekkert; Olivier C Manintveld; Frans Boomsma; Pieter D Verdouw; Dirk J Duncker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-10-14
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  288     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-11     Completed Date:  2005-03-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1165-72     Citation Subset:  IM    
Affiliation:
Experimental Cardiology, Thoraxcenter, Erasmus MC, University Medical Center Rotterdam, PO Box 1738, 3000 DR Rotterdam, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / drug effects,  physiology
Adenosine / pharmacology*
Animals
Blood Pressure
Disease Models, Animal
Heart Rate
Ischemic Preconditioning, Myocardial / methods*
Male
Myocardial Infarction / metabolism,  mortality,  physiopathology*
Myocardium / metabolism*
Rats
Rats, Wistar
Signal Transduction / drug effects,  physiology*
Vasodilator Agents / pharmacology*
Chemical
Reg. No./Substance:
0/Vasodilator Agents; 58-61-7/Adenosine

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


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