NITRIC-OXIDE ATTENUATES LUNG ENDOTHELIAL INJURY CAUSED BY SUBLETHAL HYPEROXIA IN RATS

Inhaled nitric oxide (NO) has been shown to prevent oxidant-induced lu ng injury in isolated-perfused lung models, whereas NO-derived oxidant s may contribute to acute lung injury secondary to hyperoxia. Whether inhaled NO improves or contributes to oxidant-mediated lung injury may depend on the timing of NO administration or how lung injury is asses sed. The objective of these studies was to determine whether inhaled N O (20 ppm) was protective or harmful to the different lung barriers wh en it was administered with 95% O-2 for 60 h in Sprague-Dawley rats by measuring fluid transport and permeability to protein across the lung endothelium and the alveolar epithelium. Inhaled NO significantly att enuated the O-2-mediated lung endothelial injury and abolished the inc rease in the bronchoalveolar lavage fluid content of rTI40, a specific and sensitive marker of alveolar epithelial type I cell injury, that occurs secondary to hyperoxia. In conclusion, inhaled NO administered with high concentrations of O-2 may protect the lung endothelium and t he alveolar epithelium against O-2-mediated injury.