Surfactant dysfunction after inhalation of nitric oxide.
Hallman, Mikko, Feizal Waffarn, Kristina Bry, Robert Turbow, Michael
T. Kleinman, William J. Mautz, Ronald E. Rasmussen, Deepak K. Bhalla,
and Robert F. Phalen.
Division of Neonatal Medicine, Department of Pediatrics, and
Department of Community and Environmental Medicine, University of
California, Irvine, California 92717
APStracts 3:0081A, 1996.
To study whether nitric oxide (NO) affects surfactant function, 36
young rats inhaled one of the following humidified environments for
24 h: 1. air; 2. 95% O2; 3. air and NO 100 ppm; 4. 95% O2 and NO 100
ppm. The treatments did not change the recovery of phospholipid from
bronchoalveolar lavage (BAL). Exposure to NO of animals that breathed
either air or 95% O2 increased the minimum surface tension of
surfactant from BAL at low (1.5 [mu]mol/ml), but not at high (4
[mu]mol/ml) phosphatidylcholine (PC) concentration. After inhaled NO,
the non-sedimentable protein of BAL decreased the surface activity of
surfactant (1 [mu]mol PC/ml) more than the protein from the controls.
NO treatment of animals that breathed either air or 95% O2 affected
neither the quantity nor the molecular weight distribution of non
-sedimentable protein. Hyperoxia increased the amount of the non
-sedimentable protein, whereas NO increased the iron saturation of
transferrin. The surfactant fraction and the non-sedimentable protein
from BAL were separately exposed to NO 80 ppm in vitro. NO exposure
had no effect on the surface activity of surfactant fraction. NO
exposure of non-sedimentable protein from the control animals (no NO)
increased the inhibition of the surface activity and changed the
adsorption spectrum of the protein, suggesting conversion of Hb to
methemoglobin. Non-sedimentable protein from NO-exposed animals
contained methemoglobin. We propose that surfactant dysfunction
caused by inhaled NO is in part due to alteration of protein(s) in
epithelial lining fluid that in turn inactivate surfactant.
Received 11 April 1995; accepted in final form 17 January 1996.
APS Manuscript Number A397-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96