Document Detail


Lower risk of postinfarct rupture in mouse heart overexpressing beta 2-adrenergic receptors: importance of collagen content.
MedLine Citation:
PMID:  12352327     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This paper addresses whether the enhanced left ventricular (LV) contractility and heart rate, seen in transgenic mice overexpressing beta -adrenergic receptor in the heart, might raise the incidence of LV rupture after myocardial infarct. Transgenic and wild-type mice underwent left coronary artery occlusion. Postinfarct deaths that occurred 1-7 days after surgery were analyzed. Hemodynamics, morphologic parameters, and collagen content in the LV were determined. A significantly lower incidence of LV rupture was observed in transgenic than in wild-type mice 3-5 days after myocardial infarct (2.5 versus 19.7%, p < 0.05), despite a similar infarct size between the two groups and better hemodynamic function in transgenic mouse hearts. Morphologic analysis showed a more severe infarct expansion in wild-type versus transgenic mice or in mice dying of rupture versus those that died of acute heart failure. Collagen content was higher in the LV of sham-operated transgenic than wild-type mice (p < 0.01) with both type I and type III collagen elevated. Such difference in collagen content between transgenic and wild-type mice was maintained in noninfarcted and infarcted LV. In conclusion, transgenic mice overexpressing beta -adrenergic receptor had a lower risk of cardiac rupture during the acute phase after infarction despite the markedly enhanced LV contractility and heart rate. As a hyperdynamic function due to beta-adrenergic activation would likely increase the risk of cardiac rupture and infarct expansion, the lack of rupture in this transgenic mouse model suggests that the interstitial collagen level is a more important factor than functional status in the pathogenesis of rupture and infarct expansion.
Authors:
Xiao-Ming Gao; Rodney J Dilley; Chrishan S Samuel; Elodie Percy; Meryl J Fullerton; Anthony M Dart; Xiao-Jun Du
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  40     ISSN:  0160-2446     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2002 Oct 
Date Detail:
Created Date:  2002-09-27     Completed Date:  2003-03-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  632-40     Citation Subset:  IM    
Affiliation:
Baker Medical Research Institute, Melbourne, Victoria, Australia. xiaojun.du@baker.edu.au
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MeSH Terms
Descriptor/Qualifier:
Animals
Collagen / genetics,  metabolism*
Female
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Myocardial Infarction / genetics,  metabolism*,  pathology
Myocardium / metabolism,  pathology
Receptors, Adrenergic, beta-2 / biosynthesis*,  genetics
Risk
Ventricular Dysfunction, Left / genetics,  metabolism*,  pathology
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic, beta-2; 9007-34-5/Collagen

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


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