Journal article
Chronic hypoxia does not cause wall thickening of intra-acinar pulmonary supernumerary arteries
Physiological reports, Vol.4(2), pp.e12674-n/a
01/2016
DOI: 10.14814/phy2.12674
PMCID: PMC4760391
PMID: 26811053
Abstract
Chronic exposure to hypoxia causes pulmonary hypertension and pulmonary arterial remodeling. Although the exact mechanisms of this remodeling are unclear, there is evidence that it is dependent on hemodynamic stress, rather than on hypoxia alone. Pulmonary supernumerary arteries experience low hemodynamic stress as a consequence of reduced perfusion due to 90° branching angles, small diameters, and "valve-like" structures at their orifices. We investigated whether or not intra-acinar supernumerary arteries undergo structural remodeling during the moderate pulmonary hypertension induced by chronic hypoxia. Rats were exposed to either normoxia or hypoxia for 6 weeks. The chronically hypoxic rats developed pulmonary hypertension. For both groups, pulmonary arteries were selectively filled with barium-gelatin mixture, and the wall thickness of intra-acinar pulmonary arteries was measured in histological samples. Only thin-walled arteries were observed in normoxic lungs. In hypertensive lungs, we found both thin- and thick-walled pulmonary arteries with similar diameters. Disproportionate degrees of arterial wall thickening between parent and daughter branches were observed with supernumerary branching patterns. While parent arteries developed significant wall thickening, their supernumerary branches did not. Thus, chronic hypoxia-induced pulmonary hypertension did not cause wall thickening of intra-acinar pulmonary supernumerary arteries. These findings are consistent with the idea that hemodynamic stress, rather than hypoxia alone, is the cause of structural remodeling during chronic exposure to hypoxia.
Details
- Title: Subtitle
- Chronic hypoxia does not cause wall thickening of intra-acinar pulmonary supernumerary arteries
- Creators
- Kaori Oshima - University of South AlabamaJared M McLendon - University of South AlabamaWiltz W Wagner Jr - University of South AlabamaIvan F McMurtry - University of South AlabamaMasahiko Oka - University of South Alabama
- Resource Type
- Journal article
- Publication Details
- Physiological reports, Vol.4(2), pp.e12674-n/a
- DOI
- 10.14814/phy2.12674
- PMID
- 26811053
- PMCID
- PMC4760391
- ISSN
- 2051-817X
- eISSN
- 2051-817X
- Language
- English
- Date published
- 01/2016
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Internal Medicine
- Record Identifier
- 9984618506902771
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