INHALED NITRIC-OXIDE PREVENTS THE INCREASE IN PULMONARY VASCULAR-PERMEABILITY CAUSED BY HYDROGEN-PEROXIDE

Given the interest in using inhaled nitric oxide (NO .) to treat acute lung injury and the importance of oxygen radicals in its pathogenesis , we studied the effects, in buffer-perfused isolated rabbit lungs, of inhaled NO . (24 ppm) on the injury caused by generating hydrogen per oxide with glucose and glucose oxidase (GOX). Experiments were perform ed at a constant pulmonary arterial pressure. GOX substantially augmen ted vascular permeability, as demonstrated by an increase in the lung- to-perfusate I-125-labeled albumin ratio, lavage-to-perfusate I-125-al bumin wet-to-dry lung weight ratio, and pulmonary vascular filtration coefficient. Lungs treated with inhaled NO . before perfusion with GOX had lung-to-perfusate and lavage-to-perfusate I-125-albumin ratios th at were not significantly different from control values and intermedia te between the control and GOX groups. Inhaled NO. also prevented the increase in wet-to-dry lung weight ratio and pulmonary vascular filtra tion coefficient caused by GOX .. Thus inhaled NO . substantially redu ced in the isolated lung the increase in pulmonary vascular permeabili ty produced by the intravascular generation of hydrogen peroxide.