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It was recently demonstrated that nitric oxide (NO) inhalation improves arterial oxygenation in patients with the adult respiratory distress syndrome (ARDS). However, the potential adverse reaction of NO on inflammatory cells and mediators in the lung has not yet been investigated. In this study, we evaluated the impact of NO inhalation on lung polymorphonuclear neutrophil (PMN) activation and proinflammatory cytokine release, both of which are involved in the pathophysiology of ARDS. Two groups of patients with ARDS of similar etiologies were compared; one received NO (n=9) and the other did not (n=5). After 4 d of NO inhalation (18 ppm), PMN form bronchoalveolar lavage (BAL) showed a reduction in both spontaneous H2O2 production (p<0.05) and beta 2 integrin CD11b/CD18 expression (p<0.05). Moreover, the high levels of IL8 and IL-6 decreased in BAL fluid supernatants after NO inhalation (p<0.05). In the NO-untreated group of patients with ARDS, neither PMN activation nor levels of IL-8 and IL-6 in BAL fluid changed significantly on Day 4. These results suggest that NO inhalation might reduce lung inflammation in ARDS, as reflected by PMN activation status and IL-8/IL-6 release.

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