title: Chronic hypoxia does not cause wall thickening of intra-acinar pulmonary supernumerary arteries.
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.
authors.affiliation: Department of Pharmacology, University of South Alabama, Mobile, Alabama Center for Lung Biology, University of South Alabama, Mobile, Alabama.
authors.forename: Kaori
authors.initials: K
authors.lastname: Oshima
authors.affiliation: Center for Lung Biology, University of South Alabama, Mobile, Alabama Department of Biochemistry and Molecular Biology, University of South Alabama, Mobile, Alabama.
authors.forename: Jared M
authors.initials: JM
authors.lastname: McLendon
authors.affiliation: Department of Pharmacology, University of South Alabama, Mobile, Alabama Center for Lung Biology, University of South Alabama, Mobile, Alabama.
authors.forename: Wiltz W
authors.initials: WW
authors.lastname: Wagner
authors.affiliation: Department of Pharmacology, University of South Alabama, Mobile, Alabama Center for Lung Biology, University of South Alabama, Mobile, Alabama Department of Internal Medicine, University of South Alabama, Mobile, Alabama.
authors.forename: Ivan F
authors.initials: IF
authors.lastname: McMurtry
authors.affiliation: Department of Pharmacology, University of South Alabama, Mobile, Alabama Center for Lung Biology, University of South Alabama, Mobile, Alabama Department of Internal Medicine, University of South Alabama, Mobile, Alabama moka@southalabama.edu.
authors.forename: Masahiko
authors.initials: M
authors.lastname: Oka
mesh_terms: D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D006439:Hemodynamics / Q000502:physiology*; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000473:pathology; D000860:Hypoxia / Q000150:complications*; D008168:Lung / Q000098:blood supply / Q000473:pathology*; D008297:Male; D011651:Pulmonary Artery / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D066253:Vascular Remodeling / Q000502:physiology*
keywords: Chronic hypoxia; pulmonary supernumerary artery; vascular remodeling
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