Endothelial dysfunction in the pulmonary artery induced by concentrated fine particulate matter exposure is associated with local but not systemic inflammation.

摘要: 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≤2.5 μm, PM2.5) induces endothelial dysfunction isolated arteries. We aimed investigate effects vivo urban concentrated PM2.5 on rat artery reactivity and mechanisms involved. For this, adult Wistar rats were exposed 2 weeks Sao Paulo city at accumulated daily dose approximately 600 μg/m3. Pulmonary arteries from PM2.5-exposed animals exhibited impaired endothelium-dependent relaxation acetylcholine without significant changes nitric oxide donor response compared control rats. caused vascular oxidative stress enhanced protein expression Cu/Zn- Mn-superoxide dismutase artery. Protein synthase (eNOS) reduced, while tumor necrosis factor (TNF)-α by inhalation There a positive correlation between eNOS maximal (Emax) acetylcholine. A negative found TNF-α Emax Plasma cytokine levels, blood cells count coagulation parameters similar The present findings showed could decrease associated with local high level but not systemic pro-inflammatory factors. Taken together, results elucidate underlying trigger cardiopulmonary diseases induced ambient levels PM2.5.