Abstract
Despite no reported survival benefit by inhaled nitric oxide (NO) among patients with acute respiratory distress syndrome (ARDS) until now, NO inhalation is still deemed acceptable as a rescue therapy for ARDS patients with refractory hypoxemia to various therapeutic measures. However, it is unclear whether inhaled NO exerts either detrimental or beneficial effects on the pathogenesis of ARDS. Laboratory studies suggest that inhaled NO might reduce some types of acute lung injury (ALI). By contrast, NO and nitrite could interact with neutrophil myeloperoxidase or high oxygen in the alveoli to stimulate oxidative reactions during inflammation. Recent experimental data suggest that inhaled NO might attenuate endotoxin-induced ALI. Considering the diverse role of NO as an important endogenous regulatory molecule on both proinflammatory and antiinflammatory processes, the effects of early and continued therapy with low dose of inhaled NO on ALT should be determined.
