• MourgeonEUnité de Réanimation Chirurgicale, Département d'Anesthésie, Hôpital de la Pitié-Salpétrière, 83 Boulevard de I'Hôpital, 75013 Paris, France. jjRouby.pitie@invivo.edu, PuybassetL, Law-KouneJD, LuQ, AbdennourL, GallartL, MalassineP, RaoGU, CluzelP, BennaniA, CoriatP, and RoubyJJ.
• Unité de Réanimation Chirurgicale, Département d'Anesthésie, Hôpital de la Pitié-Salpétrière, 83 Boulevard de I'Hôpital, 75013 Paris, France. jjRouby.pitie@invivo.edu
• Crit Care. 1997 Jan 1; 1 (1): 25-39.

BackgroundThe aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). ResultsEight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (QVA/QT), and a dose-dependent increase in PaO2/FiO2 (P ConclusionFor similar NOinduced decreases in MPAP and PVRI in both groups, the increase in arterial oxygenation was more marked in patients with septic shock.

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