No abstract

The role of endogenous NO in the regulation of acute lung injury is not well defined. We investigated the effects of inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) on the acute inflammatoryThere is abundant evidence that lung inflammatory injury, occurring after a variety of insults, is due to activation of lung phagocytic cells, which produce numerous chemokines (reviewed).1 CXC chemokines are thought to attract neutrophils into the lung, while CC chemokines attract lymphocytes and monocytes and also have the ability to activate macrophages.2 It is well known that a variety of lung cells other than phagocytic cells have the ability to generate cytokines and chemokines.3 For inflammatory reactions that lead to injury, the role of NO is controversial, with evidence for pro-inflammatory as well as antiinflammatory effects. 4 In various lung injury models, neutrophil recruitment, cytokine production, and oxygen radical production were reduced in the presence of either inhaled NO or exogenous NO donors, suggesting a beneficial role for NO in acute lung injury. [5][6][7] In contrast, a decrease in lung permeability and neutrophil recruitment was shown in various models of lung injury using NO synthase (NOS) inhibitors, suggesting a harmful effect of NO on lung injury. 8 -10