This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oulton, M. R. Articles by Scott, J. E. Search for Related Content PubMed PubMed Citation Articles by Oulton, M. R. Articles by Scott, J. E.

American Journal of Pathology, Vol 145, 941-950, Copyright © 1994 by American Society for Investigative Pathology

REGULAR ARTICLES

Effects of smoke inhalation on alveolar surfactant subtypes in mice

MR Oulton, DT Janigan, JM MacDonald, GT Faulkner and JE Scott
Department of Obstetrics/Gynecology, Dalhousie University, Halifax, Nova Scotia, Canada.

The effects of smoke inhalation on alveolar surfactant subtypes were examined in mice exposed for 30 minutes to smoke generated from the burning of a flexible polyurethane foam. At 4 or 12 hours after the exposure, three surfactant pellets, P10, P60, and P100, and a supernatant, S100, were prepared by sequential centrifugation of lavage fluids at 10,000 g for 30 minutes (P10), 60,000 g for 60 minutes (P60), and 100,000 g for 15 hours (P100 and S100). Phospholipid analysis and electron microscopy were performed on each fraction. Smoke exposure dramatically altered the normal distributions of these fractions: it significantly increased the phospholipid content of the heavier subtype, P10, which is thought to represent newly secreted surfactant; had no effect on the intermediate form, P60; and dramatically increased the phospholipid content (approximately fivefold) of the lighter subtypes, P100 and S100, which are believed to represent catabolic end- products of alveolar surfactant. Only P100 was structurally altered by the smoke. These results represent alterations of the normal metabolic processing of alveolar surfactant. Whereas the mechanism is yet to be defined, it seems to involve a small but significant increase in the newly secreted surfactant, as well as an excessively high accumulation of the structurally altered catabolic forms of the secreted surfactant.

This article has been cited by other articles:

				L. G. Vazquez de Lara, T. M. Umstead, S. E. Davis, and D. S. Phelps Surfactant protein A increases matrix metalloproteinase-9 production by THP-1 cells Am J Physiol Lung Cell Mol Physiol, October 1, 2003; 285(4): L899 - L906. [Abstract] [Full Text] [PDF]

				D. M. Kuhn and M. A. Ghannoum Indoor Mold, Toxigenic Fungi, and Stachybotrys chartarum: Infectious Disease Perspective Clin. Microbiol. Rev., January 1, 2003; 16(1): 144 - 172. [Abstract] [Full Text] [PDF]

				Shengjun Wang, R. C. Lantz, R. F. Robledo, V. Breceda, A. M. Hays, and M. L. Witten Early Alterations of Lung Injury Following Acute Smoke Exposure and 21-Aminosteroid Treatment Toxicol Pathol, May 1, 1999; 27(3): 334 - 341. [Abstract] [PDF]