ObjectiveTo investigate whether inhaled nitric oxide (NO) enhances pulmonary lipid peroxidation as indicated by arterial blood levels of malondialdehyde, hexanal, and pentanal in patients with acute respiratory distress syndrome (ARDS).DesignProspective, nonrandomized, controlled trial.SettingSurgical intensive care unit in a university hospital.PatientsTwenty-five patients with ARDS, as defined by the American-European Consensus Conference, and a Pao2/Fio2≤170 mm Hg were enrolled in the study. Four healthy subjects were studied as controls.InterventionsOn enrollment of the patients in the study, a dose-response test with increasing concentrations of inhaled NO (0, 2, 10, 40, 0 ppm) was performed. Patients who showed an increase of >20% in Pao2were designated as responders and all others as nonresponders. In responders, this dose-response test was followed by 24 hrs of continuous treatment with inhaled NO at the best NO concentration determined during the dose-response test, whereas nonresponders received standard care. For healthy volunteers, the dose-response test took the form of spontaneous breathing of the same NO concentrations.Measurements and Main ResultsEighteen patients (72%) showed an increase of >20% in Pao2during the dose-response test. This significant improvement in arterial oxygenation in responders led to a significant reduction in Fio2(responders, 0.73 ± 0.05 vs. nonresponders, 0.89 ± 0.05) after 24 hrs of therapy. On enrollment, arterial blood concentrations of malondialdehyde, hexanal, and pentanal were significantly higher than those of healthy volunteers. In addition, arterial concentrations of hexanal and pentanal exceeded mixed venous levels two- to ten-fold. Inhalation of NO did not significantly alter these blood concentrations either during the dose response test or during 24 hrs of therapy.ConclusionsIn patients with ARDS, malondialdehyde, hexanal, and pentanal were significantly elevated, indicating lipid peroxidation. Lipid peroxidation was not further affected by inhalation of NO.