Stabilization of lung surfactant particles against conversion by a
cycling interface.
Halla, S. B., R. W. Hydeb, and M. C. Kahna.
Department of Medicinea, Oregon Health Sciences University,
Portland, Oregon and Departments of Medicine and Environmental
Medicine, University of Rochester, Rochester, New York
APStracts 3:0213E, 1996.
The large active particles of pulmonary surfactant are depleted in
patients with the Acute Respiratory Distress Syndrome and in animal
models of this disorder. We studied in vitro conversion of large to
small particles, separated by differential sedimentation, to
determine how factors lavaged from rabbits injured by intravenous
oleic acid would affect conversion. In half-filled test tubes rotated
end-over-end, samples from injured animals increased the recovery of
large particles from 40 6% of uncycled samples for controls to 62
21%. We hypothesized that proteins in the injured samples, and
perhaps also the proteinase inhibitors used previously by Gross and
Schultz to block conversion (9), stabilized surfactant particles by
limiting access to the cycling interface. Hemoglobin, neutrophil
elastase, and a1-antiproteinase (a1-PI) oxidized to eliminate its
antiproteinase activity all stabilized large particles against
conversion. Hemoglobin was most effective, increasing recovery from
18 5% for controls to 86 5% with 0.4 mg/ml hemoglobin. Native a1-PI
had no effect on conversion. Our results suggest that acceleration of
normal conversion is unlikely to explain the depletion of large
particles in injured lungs. They also suggest that conversion of
surfactant particles separated by differential sedimentation requires
no proteinase susceptible to inhibition by a1-PI. They provide an
alternate hypothesis related to interfacial effects rather than
proteinase inhibition for the previously reported effect of a1-PI on
conversion of particles separated according to density.
Received 26 July 1996; accepted in final form 2 October 1996.
APS Manuscript Number E362-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996