NO PREVENTS NEUTROPHIL-MEDIATED PULMONARY VASOMOTOR DYSFUNCTION IN ACUTE LUNG INJURY

The purpose of this study was to examine the effect of administration of inhaled nitric oxide (NO) on lung neutrophil accumulation and pulmo nary vascular endothelial cell function in endotoxin-induced acute lun g injury. Mechanically ventilated rats were studied 4 hr after endotox in (0.5 mg/kg IP). Inhaled NO (20 ppm) was administered for either the entire 4 hr after endotoxin (continuous group) or for only the first 2 of 4 hr after endotoxin (abbreviated group). Endothelial-dependent ( acetylcholine, ACh) and -independent cGMP-mediated relaxation (nitropr usside, SNP) pulmonary vasorelaxation were studied in isolated pulmona ry arterial rings. Lung neutrophil accumulation was determined by myel operoxidase assay (MPO). Inhaled NO prevented endotoxin-induced lung n eutrophil accumulation as well as pulmonary endothelial cell dysfuncti on. However, this protection required continuous administration of inh aled NO. We conclude that inhaled NO prevents neutrophil-mediated pulm onary vascular endothelial cell dysfunction in acute lung injury. (C) 1996 Academic Press, Inc.