| Persistent vascular collagen accumulation alters hemodynamic recovery from chronic hypoxia. | |
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MedLine Citation:
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PMID: 22183202 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pulmonary arterial hypertension (PAH) is caused by narrowing and stiffening of the pulmonary arteries that increase pulmonary vascular impedance (PVZ). In particular, small arteries narrow and large arteries stiffen. Large pulmonary artery (PA) stiffness is the best current predictor of mortality from PAH. We have previously shown that collagen accumulation leads to extralobar PA stiffening at high strain (Ooi et al. 2010). We hypothesized that collagen accumulation would increase PVZ, including total pulmonary vascular resistance (Z(0)), characteristic impedance (Z(C)), pulse wave velocity (PWV) and index of global wave reflections (P(b)/P(f)), which contribute to increased right ventricular afterload. We tested this hypothesis by exposing mice unable to degrade type I collagen (Col1a1(R/R)) to 21 days of hypoxia (hypoxia), some of which were allowed to recover for 42 days (recovery). Littermate wild-type mice (Col1a1(+/+)) were used as controls. In response to hypoxia, mean PA pressure (mPAP) increased in both mouse genotypes with no changes in cardiac output (CO) or PA inner diameter (ID); as a consequence, Z(0) (mPAP/CO) increased by ~100% in both genotypes (p<0.05). Contrary to our expectations, Z(C), PWV and P(b)/P(f) did not change. However, with recovery, Z(C) and PWV decreased in the Col1a1(+/+) mice and remained unchanged in the Col1a1(R/R) mice. Z(0) decreased with recovery in both genotypes. Microcomputed tomography measurements of large PAs did not show evidence of stiffness changes as a function of hypoxia exposure or genotype. We conclude that hypoxia-induced PA collagen accumulation does not affect the pulsatile components of pulmonary hemodynamics but that excessive collagen accumulation does prevent normal hemodynamic recovery, which may have important consequences for right ventricular function. |
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Authors:
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Diana M Tabima; Alejandro Roldan-Alzate; Zhijie Wang; Timothy A Hacker; Robert C Molthen; Naomi C Chesler |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-12-17 |
Journal Detail:
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Title: Journal of biomechanics Volume: 45 ISSN: 1873-2380 ISO Abbreviation: J Biomech Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-03-05 Completed Date: 2012-09-11 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0157375 Medline TA: J Biomech Country: United States |
Other Details:
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Languages: eng Pagination: 799-804 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Biomedical Engineering, University of Wisconsin-Madison, WI 53706, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia / metabolism*, pathology Blood Flow Velocity / physiology Cardiac Output / physiology Collagen Type I / metabolism* Female Hemodynamics Hypertension, Pulmonary / metabolism*, pathology Lung / blood supply, metabolism, pathology Male Mice Pulmonary Artery / metabolism, pathology Pulmonary Circulation / physiology Vascular Resistance Ventricular Function, Right / physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL086939/HL/NHLBI NIH HHS; R01 HL086939-03/HL/NHLBI NIH HHS; R01 HL086939-04/HL/NHLBI NIH HHS; R01 HL086939-05/HL/NHLBI NIH HHS; R01HL086939/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Collagen Type I |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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