| Contribution of ventricular remodeling to pathogenesis of heart failure in rats. | |
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MedLine Citation:
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PMID: 11158966 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We previously reported an approximately 50% incidence of rats with symptoms of congestive heart failure (CHF) at 8 wk postinfrarenal aorto-caval fistula. However, it was not clear whether compensatory ventricular remodeling could continue beyond 8 wk or whether the remaining animals would have developed CHF or died. Therefore, the intent of this study was to complete the characterization of this model of sustained volume overload by determining the morbidity and mortality and the temporal response of left ventricular (LV) remodeling and function beyond 8 wk. The findings demonstrate an upper limit to LV hypertrophy and substantial increases in LV volume and compliance, matrix metalloproteinase activity, and collagen volume fraction associated with the development of CHF. There was an 80% incidence of morbidity and mortality following 21 wk of chronic volume overload. These findings indicate that the development of CHF is triggered by marked ventricular dilatation and increased compliance occurring once the myocardial hypertrophic response is exhausted. |
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Authors:
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G L Brower; J S Janicki |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 280 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2001 Feb |
Date Detail:
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Created Date: 2001-02-22 Completed Date: 2001-03-22 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H674-83 Citation Subset: IM |
Affiliation:
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Department of Anatomy, Physiology, and Pharmacology, Auburn University, Auburn, Alabama 36849-5517, USA. browegl@auburn.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arteriovenous Fistula / mortality, physiopathology Cardiac Volume / physiology Disease Models, Animal Heart Failure / etiology*, mortality, physiopathology* Hypertrophy, Left Ventricular / etiology, mortality, physiopathology Hypertrophy, Right Ventricular / etiology, mortality, physiopathology Male Matrix Metalloproteinases / metabolism Myocardium / enzymology Rats Rats, Sprague-Dawley Systole / physiology Ventricular Dysfunction, Left / etiology, mortality, physiopathology Ventricular Remodeling / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL-59981/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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EC 3.4.24.-/Matrix Metalloproteinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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