Pulmonary neutrophil recruitment and bronchial reactivity in formaldehyde-exposed rats are modulated by mast cells and differentially by neuropeptides and nitric oxide

摘要: We have used a pharmacological approach to study the mechanisms underlying rat lung injury and airway reactivity changes induced by inhalation of formaldehyde (FA) (1% formalin solution, 90 min once day, 4 days). The isolated tracheae intrapulmonary bronchi were assessed in dose-response curves methacholine (MCh). Local systemic inflammatory phenomena evaluated terms leukocyte countings bronchoalveolar lavage (BAL) fluid, blood, bone marrow spleen. Whereas tracheal MCh did not change, significant bronchial hyporesponsiveness (BHR) was found after FA as compared with naive rats. Also, exposure significantly increased total cell numbers BAL, peripheral blood spleen, but modify counts marrow. Capsaicin hindered increase number recovered BAL fluid exposure. Both compound 48/80 indomethacin able prevent neutrophil influx FA, had no effect on that mononuclear cells. Following inhalation, treatment sodium cromoglycate (SCG), nitric oxide (NO) synthase inhibitor L-NAME, reduced BAL. Compound 48/80, L-NAME SCG prevented BHR whereas capsaicin inactive this regard. On other hand, exacerbated BHR. These data suggest resulting may involve oxide, sensory fibers mast cell-derived mediators. NO seemed be largely restricted tonus, neuropeptides appeared linked response, therefore indicating responsible for responsiveness caused separate from those its effects.