Inhaled NO prevents IL-1-induced neutrophil accumulation and associated acute edema in isolated rat lungs.

摘要: We determined previously that inhaled nitric oxide (NO) prevented oxidant-dependent capillary leak in isolated rat lungs perfused with human neutrophils and fMLP via a mechanism was independent of vasodilatation. In the present investigation we NO (50 ppm) acute (as reflected by weight gain Ficoll retention) given recombinant interleukin-1 alpha (IL-1, 50 ng) intratracheally neutrophils. Inhaled also reduced neutrophil migration from vascular to airway compartment lung lavage fluid numbers levels myeloperoxidase), rats IL-1 However, did not prevent IL-1-mediated increases cytokine-induced chemoattractant (CINC), potent chemokine produced alveolar macrophages other resident cells mediates IL-1-induced infiltration vivo. conclude caused intratracheal administration perfusion lungs. speculate directly inhibits responsivity during inflammation, premise is consistent known effects on function vitro. This study provides further evidence may have important anti-inflammatory as well vasodilator injury.