Nitric oxide attenuates lung endothelial injury caused by sublethal
hyperoxia in rats.
McElroy, M. C., J. P. Wiener-Kronish, H. Miyazaki, T. Sawa, K.
Modelska, L. G. Dobbs, and J. F. Pittet.
Cardiovascular Research Institute, and Departments of Anesthesia
and Medicine, Univ. of California, San Francisco, CA, 94143
APStracts 3:0222L, 1996.
Inhaled nitric oxide (NO) has been shown to prevent oxidant-induced
lung injury in isolated perfused lung models whereas NO-derived
oxidants 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 assessed. The objective of these studies was to determine
whether inhaled NO (20 ppm) was protective or harmful to the
different lung barriers when it was administered with 95% O2 for 60h
in Sprague-Dawley rats by measuring fluid transport and permeability
to protein across the lung endothelium and the alveolar epithelium.
Inhaled NO significantly attenuated the oxygen-mediated lung
endothelial injury and abolished the increase in the bronchoalveolar
lavage fluid content of TIrat40, 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 oxygen may protect the lung endothelium and the
alveolar epithelium against oxygen-mediated injury.
Received 23 February 1996; accepted in final form 8 November
1996.
APS Manuscript Number L64-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996