Received: 15 February 2000 Accepted: 7 May 2002 Published online: 12 July 2002 © Springer-Verlag 2002 This study was supported in part a grant from the Ohmeda Corporation Abstract Objective: We tested the hypothesis that NO contamination of hospital compressed air also im- proves PaO 2 in patients with acute lung injury (ALI) and following lung transplant (LTx). Design: Prospec- tive clinical study. Setting: Cardio- thoracic intensive care unit. Patients: Subjects following cardiac surgery (CABG, n=7); with ALI (n=7), and following LTx (n=5). Interventions: Four sequential 15-min steps at a constant FiO 2 were used: hospital compressed air-O 2 (H1), N 2 -O 2 (A1), repeat compressed air-O 2 (H2), and repeat N 2 -O 2 (A2). Measurements and results: NO lev- els were measured from the endotra- cheal tube. Cardiorespiratory values included PaO 2 were measured at the end of each step. FiO 2 was 0.46±0.05, 0.53±0.15, and 0.47±0.06 (mean±SD) for three groups, respectively. In- haled NO levels during H1 varied among subjects (30–550 ppb, 27–300 ppb, and 5–220 ppb, respec- tively). Exhaled NO levels were not detected in 4/7 of CABG (0–300 ppb), 3/6 of ALI (0–140 ppb), and 3/5 of LTx (0–59 ppb) patients during H1, whereas during A1 all but one pa- tient in ALI and three CABG pa- tients had measurable exhaled NO levels (P<0.05). Small but signifi- cant decreases in PaO 2 occurred for all groups from H1 to A1 and H2 to A2 (132–99 Torr and 128–120 Torr, P <0.01, respectively). There was no correlation between inhaled NO dur- ing H1 and exhaled NO during A1 or the change in PaO 2 from H1 to A1. Conclusions: Low-level NO contam- ination improves PaO 2 in patients with ALI and following LTx. Keywords Acute respiratory distress syndrome (ARDS) · Compressed air · Intrapulmonary shunt · Lung transplantation · Mechanical ventilation · Oxygenation Intensive Care Med (2002) 28:1064–1072 DOI 10.1007/s00134-002-1366-7 ORIGINAL P. Seow Koon Tan F. Genc E. Delgado J.A. Kellum M.R. Pinsky Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury Introduction Nitric oxide (NO) is a potent smooth muscle vasodilating agent that, when inhaled at levels of 2 ppm to 40 ppm, can reverse the increased pulmonary vasomotor tone in- duced by hypoxia and transiently increase oxygenation in some, but not all, subjects with acute lung injury (ALI) [1, 2, 3]. Unfortunately, in the published large and small multi-center clinical trials of inhaled NO in pa- tients with ALI no consistent improvement in arterial oxygenation after the first 24 h could be seen, nor was there any reduced mortality or reduction in need for me- chanical ventilation in the subset of patients in whom an initial improvement in oxygenation did occur [4, 5, 6, 7]. Based on these negative studies, the routine use of in- haled NO in the ventilatory management of adult pa- tients has been questioned [8] despite the clear evidence of a physiologic response to inhaled NO in specific sub- jects [9]. Inhaled NO may have other effects other than selective pulmonary vasodilation. Low levels of ambient NO are anti-inflammatory, reducing white cell accumu- lation in the lung thus promoting repair [10]. Thus, as a P.S.K. Tan Department of Anaesthesiology, University of Malaya Medical Centre, Kuala Lumpur, Malaysia F. Genc · E. Delgado · J.A. Kellum M.R. Pinsky ( ✉ ) Department of Anesthesiology & Critical Care Medicine, University of Pittsburgh Medical Center, 604 Scaife Hall, Pittsburgh, Pa., USA e-mail: pinskymr@anes.upmc.edu Tel.: +1-412-6475387 Fax: +1-412-6478060