Inhaled no prevents pulmonary endothelial dysfunction in acute lung injury

A major feature of acute lung injury (ALT) is pulmonary vasoconstriction secondary to pulmonary vascular endothelial injury with loss of endothelial-derived nitric oxide (NO). In a rat model of ALI produced by gut ischemia/reperfusion (I/R), our purpose was to examine the effect of exogenous (inhaled) NO on lung neutrophil accumulation (myeloperoxidase, MPO) and 2 modes of endothelial-dependent pulmonary vasorelaxation: (1) receptor-dependent (acetylcholine, ACh) and (2) receptor-independent (A23187). Methods: 5 ventilated rats had gut I/R by superior mesenteric artery occlusion for 1 hr. After 2 hrs of reperfusion, lung MPO was determined. Dose response curves to ACh and A23187 were studied in isolated pulmonary artery rings preconstricted with phenylephrine. NO treated rats (n=5) received inhaled NO (20ppm) for the period of gut I/R. 5 rats had sham laparotomy. Statistics were by ANOVA, *p<0.05. Results: Inhaled NO prevented lung neutrophil accumulation and pulmonary endothelial dysfunction. Conclusion: Inhaled NO prevents pulmonary endothelial dysfunction in ALI.