Document Detail


Endothelial dysfunction in the pulmonary artery induced by concentrated fine particulate matter exposure is associated with local but not systemic inflammation.
MedLine Citation:
PMID:  22361244     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Clinical evidence has identified the pulmonary circulation as an important target of air pollution. It was previously demonstrated that in vitro exposure to fine particulate matter (aerodynamic diameter ≤2.5μm, PM(2.5)) induces endothelial dysfunction in isolated pulmonary arteries. We aimed to investigate the effects of in vivo exposure to urban concentrated PM(2.5) on rat pulmonary artery reactivity and the mechanisms involved. For this, adult Wistar rats were exposed to 2 weeks of concentrated São Paulo city air PM(2.5) at an accumulated daily dose of approximately 600μg/m(3). Pulmonary arteries isolated from PM(2.5)-exposed animals exhibited impaired endothelium-dependent relaxation to acetylcholine without significant changes in nitric oxide donor response compared to control rats. PM(2.5) caused vascular oxidative stress and enhanced protein expression of Cu/Zn- and Mn-superoxide dismutase in the pulmonary artery. Protein expression of endothelial nitric oxide synthase (eNOS) was reduced, while tumor necrosis factor (TNF)-α was enhanced by PM(2.5) inhalation in pulmonary artery. There was a significant positive correlation between eNOS expression and maximal relaxation response (E(max)) to acetylcholine. A negative correlation was found between vascular TNF-α expression and E(max) to acetylcholine. Plasma cytokine levels, blood cells count and coagulation parameters were similar between control and PM(2.5)-exposed rats. The present findings showed that in vivo daily exposure to concentrated urban PM(2.5) could decrease endothelium-dependent relaxation and eNOS expression on pulmonary arteries associated with local high TNF-α level but not systemic pro-inflammatory factors. Taken together, the present results elucidate the mechanisms underlying the trigger of cardiopulmonary diseases induced by urban ambient levels of PM(2.5).
Authors:
Ana Paula Davel; Miriam Lemos; Luciana Manfré Pastro; Sibelli Cosme Pedro; Paulo Afonso de André; Cristina Hebeda; Sandra Helena Farsky; Paulo Hilário Saldiva; Luciana Venturini Rossoni
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-2-16
Journal Detail:
Title:  Toxicology     Volume:  -     ISSN:  1879-3185     ISO Abbreviation:  -     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-2-24     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0361055     Medline TA:  Toxicology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Ireland Ltd.
Affiliation:
Department of Anatomy, Cellular Biology, Physiology and Biophysics, Institute of Biology, State University of Campinas-UNICAMP, Campinas, Brazil; Department of Physiology and Biophysics of Biomedical Science Institute, University of São Paulo, São Paulo, Brazil.
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