Journal of Applied Physiology
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J Appl Physiol 79: 886-891, 1995;
8750-7587/95 $5.00
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Journal of Applied Physiology, Vol 79, Issue 3 886-891, Copyright © 1995 by American Physiological Society

ARTICLES

Inhaled nitric oxide prevents the increase in pulmonary vascular permeability caused by hydrogen peroxide

W. B. Poss, O. D. Timmons, I. S. Farrukh, J. R. Hoidal and J. R. Michael
Department of Medicine, Veterans Affairs Medical Center, Salt Lake City, Utah, USA.

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 peroxide with glucose and glucose oxidase (GOX). Experiments were performed at a constant pulmonary arterial pressure. GOX substantially augmented vascular permeability, as demonstrated by an increase in the lung-to-perfusate 125I-labeled albumin ratio, lavage-to-perfusate 125I-albumin ratio, 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 125I-albumin ratios that were not significantly different from control values and intermediate between the control and GOX groups. Inhaled NO. also prevented the increase in wet-to-dry lung weight ratio and pulmonary vascular filtration coefficient caused by GOX.. Thus inhaled NO. substantially reduced in the isolated lung the increase in pulmonary vascular permeability produced by the intravascular generation of hydrogen peroxide.


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