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BioMed Research International
Volume 2015 (2015), Article ID 169841, 11 pages
Research Article

Adventitial Alterations Are the Main Features in Pulmonary Artery Remodeling due to Long-Term Chronic Intermittent Hypobaric Hypoxia in Rats

1Institute of Health Studies, Universidad Arturo Prat, Avenue Arturo Prat 2120, 11100939 Iquique, Chile
2Department of Physiology, Faculty of Medicine, Universidad Autónoma de Madrid, c/Arzobispo Morcillo 2, 28029 Madrid, Spain
3Department of Biological and Physiological Sciences, Faculty of Sciences and Philosophy/IIA, Universidad Peruana Cayetano Heredia, Avenue Honorario Delgado 430, Urb. Ingenieria, Distrito, Lima 31, Peru
4Department of Preventive Medicine and Public Health, Faculty of Medicine, Universidad Autónoma de Madrid, c/Arzobispo Morcillo 2, 28029 Madrid, Spain

Received 3 August 2014; Revised 21 October 2014; Accepted 5 November 2014

Academic Editor: Shiro Mizuno

Copyright © 2015 Julio Brito et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Long-term chronic intermittent exposure to altitude hypoxia is a labor phenomenon requiring further research. Using a rat model, we examined whether this type of exposure differed from chronic exposure in terms of pulmonary artery remodeling and other features. Rats were subjected to chronic hypoxia (CH, ) and long-term intermittent hypoxia (CIH2x2; 2 days of hypoxia/2 days of normoxia, ) in a chamber (428 Torr, 4,600 m of altitude) for 46 days and compared to rats under normoxia (NX, ). Body weight, hematocrit, and right ventricle ratio were measured. Pulmonary artery remodeling was assessed using confocal microscopy of tissues stained with a nuclear dye (DAPI) and CD11b antibody. Both hypoxic conditions exhibited increased hematocrit and hypertrophy of the right ventricle, tunica adventitia, and tunica media, with no changes in lumen size. The medial hypertrophy area (larger in CH) depicted a significant increase in smooth muscle cell number. Additionally, CIH2x2 increased the adventitial hypertrophy area, with an increased cellularity and a larger prevalence of clustered inflammatory cells. In conclusion, CIH2x2 elicits milder effects on pulmonary artery medial layer muscularization and subsequent right ventricular hypertrophy than CH. However, CIH2x2 induces greater and characteristic alterations of the adventitial layer.