Fig. 1. The pulmonary vasorelaxation to 0.4, 4, and 40 ppm inhaled nitric oxide (NO) in mice, 16 h after intraperitoneal challenge with saline (open circles) or lipopolysaccharide (LPS; closed circles). Endotoxin attenuated the pulmonary vasorelaxation to inhaled NO (*P < 0.001). Responsiveness to inhaled NO was partially preserved in mice treated with lipopolysaccharide and given 150 mg/kg intraperitoneal N -acetylcysteine (NAC; open squares) immediately thereafter. Responsiveness to inhaled NO was fully preserved after lipopolysaccharide and two doses of 150 mg/kg N -acetylcysteine given 3.5 h apart (closed triangles;P = nonsignificant vs. saline). ΔPAP = decrease in pulmonary artery pressure as percentage of the U46619-induced increase.