| Chronic pulmonary artery pressure elevation is insufficient to explain right heart failure. | |
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MedLine Citation:
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PMID: 19884466 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The most important determinant of longevity in pulmonary arterial hypertension is right ventricular (RV) function, but in contrast to experimental work elucidating the pathobiology of left ventricular failure, there is a paucity of data on the cellular and molecular mechanisms of RV failure. METHODS AND RESULTS: A mechanical animal model of chronic progressive RV pressure overload (pulmonary artery banding, not associated with structural alterations of the lung circulation) was compared with an established model of angioproliferative pulmonary hypertension associated with fatal RV failure. Isolated RV pressure overload induced RV hypertrophy without failure, whereas in the context of angioproliferative pulmonary hypertension, RV failure developed that was associated with myocardial apoptosis, fibrosis, a decreased RV capillary density, and a decreased vascular endothelial growth factor mRNA and protein expression despite increased nuclear stabilization of hypoxia-induced factor-1alpha. Induction of myocardial nuclear factor E2-related factor 2 and heme-oxygenase 1 with a dietary supplement (Protandim) prevented fibrosis and capillary loss and preserved RV function despite continuing pressure overload. CONCLUSIONS: These data brought into question the commonly held concept that RV failure associated with pulmonary hypertension is due strictly to the increased RV afterload. |
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Authors:
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Harm J Bogaard; Ramesh Natarajan; Scott C Henderson; Carlin S Long; Donatas Kraskauskas; Lisa Smithson; Ramzi Ockaili; Joe M McCord; Norbert F Voelkel |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-11-02 |
Journal Detail:
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Title: Circulation Volume: 120 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2009 Nov |
Date Detail:
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Created Date: 2009-11-17 Completed Date: 2009-12-08 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: 1951-60 Citation Subset: AIM; IM |
Affiliation:
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Divisions of Pulmonary and Critical Care, Virginia Commonwealth University, Richmond, VA 23298-0281, USA. nvoelkel@mcvh-vcu.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Blood Pressure* Disease Models, Animal Fibrosis Gene Expression Regulation Heart Failure / metabolism*, pathology, physiopathology Heme Oxygenase (Decyclizing) / biosynthesis Hypertension, Pulmonary / metabolism*, pathology, physiopathology Hypertrophy, Right Ventricular / metabolism*, pathology, physiopathology Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis Male Pulmonary Artery / metabolism*, pathology, physiopathology RNA, Messenger / biosynthesis Rats Rats, Sprague-Dawley Vascular Endothelial Growth Factor A / biosynthesis Ventricular Function, Right |
| Grant Support | |
ID/Acronym/Agency:
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5P30NS047463/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hif1a protein, rat; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; 0/vascular endothelial growth factor A, rat; EC 1.14.99.3/Heme Oxygenase (Decyclizing); EC 1.14.99.3/Hmox1 protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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