Document Detail

Severity of myocardial injury following ischemia-reperfusion is increased in a mouse model of allergic asthma.
MedLine Citation:
PMID:  16905595     Owner:  NLM     Status:  MEDLINE    
Cardiovascular disease is common in asthmatic patients but often is attributed to respiratory drug therapy. With mounting evidence for an inflammatory role in the development of cardiovascular disease, we hypothesized that the inflammation associated with asthma adversely affects the cardiovascular system independent of therapeutic interventions. The hypothesis was tested in a murine model of myocardial ischemia-reperfusion injury. BALB/C mice were sensitized by intraperitoneal injection of ragweed (RW) or normal saline (NS) and challenged by intratracheal instillation of RW or NS. Effective allergic sensitization and challenge were confirmed by hyperresponsiveness to aerosolized methacholine and bronchoalveolar lavage. In vivo myocardial ischemia-reperfusion injury was induced by ligation of the left anterior descending artery for 20 min, followed by reperfusion for 2 h. The infarct size (% risk area) and neutrophil density in the myocardial area at risk were significantly higher in the RW/RW group than in the control groups. The tissue neutrophil count correlated with the infarct size but did not correlate with blood neutrophil counts. Furthermore, in the RW/RW group, circulating granulocytes showed an enhanced expression of CD11b and P-selectin glycoprotein ligand-1, enhanced stimulated release of myeloperoxidase, and enhanced expression of P-selectin in the coronary vasculature. These results indicate that allergic responses in the airways enhance expression of attachment molecules in coronary vasculature and activate circulating neutrophils, resulting in recruitment of highly activated neutrophils to the infarct zone during an acute ischemia-reperfusion event, thereby enhancing tissue destruction.
Surovi Hazarika; Michael R Van Scott; Robert M Lust
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Publication Detail:
Type:  Journal Article     Date:  2006-08-11
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 Jan 
Date Detail:
Created Date:  2007-01-10     Completed Date:  2007-02-20     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:  H572-9     Citation Subset:  IM    
Dept. of Physiology, East Carolina Univ. School of Medicine, 600 Moye Blvd., 6N-98, Greenville, NC 27834, USA.
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MeSH Terms
Asthma / chemically induced,  complications,  immunology*,  pathology*
Disease Models, Animal*
Mice, Inbred BALB C
Myocardial Reperfusion Injury / complications,  immunology*,  pathology*
Myocardial Stunning / complications,  immunology*,  pathology*
Severity of Illness Index
Reg. No./Substance:

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

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