Health & Environmental Research Online (HERO)


Print Feedback Export to File
2617474 
Journal Article 
Abstract 
Lung inflammation and vascular reactivity in rats exposed to concentrated ambient fine particles (PM2.5) of urban Sao Paulo air pollution 
Davel, AC; Lemos, M; Pastro, LD; Pedro, SSC; Rossoni, LV; Saldiva, PHN 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A1147 
English 
WOS:000208771000148 
is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Rationale: This study was designed to evaluate structural alterations and reactivity of pulmonary artery and trachea of rats exposed to urban air pollution.

Methods: Rats were daily exposed to 600ug/m^3 concentrated ambient fine particles (PM2.5) from urban São Paulo, during 2 weeks, 5 hours per day. After exposure rats were sacrificed by exsanguination of abdominal aorta and, then, trachea, lungs and heart were removed and immersed in Krebs-Henseleit solution at 4°C. Trachea and extralobar pulmonary artery were isolated and transversely cut. Rings of distal trachea and pulmonary artery were immersed in a container with Krebs-Henseleit solution, at 37°C, continuously gasefied with carbogenic mixture, at 7.4 pH. Two metals probes were positioned through the lumen of the rings. One end was fixed to the bath wall and the other end was connected vertically to a isometric tension transducer connected to a data acquisition system (Biopac Austrália). Viability of rings was tested with KCl. Concentration-response curves were obtained by trachea rings subjected to baths with Carbacol (10pM-100uM) and isoproterenol (100pM-1uM) and pulmonary artery rings subjected to bath solutions of acetylcholine (1nM-30uM), phenylephrine (100pM-30uM, evaluating endothelium dependent vessel relaxation), and sodium nitroprusside (1pM-3mM, evaluating endothelium independent relaxation). Morphometric analysis of pulmonary arterioles was also performed, specifically targeting the bronchiole alveoli transition region.

Results: Trachea rings from the exposed group showed significant reduction of smooth muscle relaxation in response to isoproterenol administration, but contractile responses to KCl and carbacol were similar. Pulmonary arteries rings of exposed animals showed significant reduction of induced relaxation by acetylcholine, indicating endothelium disfunction. There was not differences for induced relaxation by sodium nitroprusside. Contractile responses to KCl and phenylephrine were similar for both groups. Morphometry showed that the relationship between vessel lumen and wall increased with increasing vessel size. PM2.5 exposure promoted pulmonary arteriole narrowing, specially on the smaller arterioles, which is compatible with the functional results above.

Conclusion: This results indicate that low levels of exposure to PM2.5 can cause adverse impact to the pulmonary vascular territory and structure.

This abstract is Funded by: Fapesp grants 2002/09804-0. 
American Thoracic Society 2010 International Conference 
New Orleans, LA 
May 14-19, 2010