HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science 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 ISI Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Bailey, T.C. Articles by Veldhuizen, R.A.W. Search for Related Content PubMed PubMed Citation Articles by Bailey, T.C. Articles by Veldhuizen, R.A.W.

Sepsis and hyperoxia effects on the pulmonary surfactant system in wild-type and iNOS knockout mice

Depts of ¹ Physiology, ² Medicine, and ³ Pharmacology & Toxicology, Lawson Health Research Institute, University of Western Ontario

CORRESPONDENCE: T.C. Bailey, Lawson Health Research Institute, H417, 268 Grosvenor Street, London, ON, Canada, N6A 4V2. Fax: 519 6466110. E-mail: tbailey2@uwo.ca

Keywords: acute lung injury, nitric oxide, pulmonary surfactant

Received: August 28, 2001
Accepted January 18, 2002

The present study was supported by the Dept of Medicine, University of Western Ontario and the Canadian Institute of Health Research.

Alterations of pulmonary surfactant and increases in inducible nitric oxide synthase (iNOS) have been implicated in the pathophysiology of acute lung injury. It was hypothesised that these two observations are related and that alterations of the endogenous surfactant, due to either sepsis or hyperoxia, would be reduced in mice lacking the iNOS gene compared to wild-type mice.

Wild-type and iNOS (–/–) mice were randomised into sham or sepsis, and in a separate experiment animals were randomised to normoxia or hyperoxia exposure for 48 h. Lungs were lavaged and analysed for total surfactant levels and surfactant subfractions (large (LA) and small (SA) aggregates).

Both sepsis groups had decreased SA compared to sham groups with no significant difference between the two genotypes. Mice exposed to hyperoxia had a decreased amount of total surfactant when compared to normoxia controls and there was no significant difference between the two genotypes.

It is concluded that inducible nitric oxide synthase does not influence the amount of pulmonary surfactant or surfactant subfractions recovered in lavage after 18 h of sepsis or 48 h of hyperoxia.

This article has been cited by other articles:

				W. Huang, L. A. McCaig, R. A. W. Veldhuizen, L-J. Yao, and J. F. Lewis Mechanisms responsible for surfactant changes in sepsis-induced lung injury Eur. Respir. J., December 1, 2005; 26(6): 1074 - 1079. [Abstract] [Full Text] [PDF]

				J. W. Lee, B. Ovadia, A. Azakie, S. Salas, J. Goerke, J. R. Fineman, and J. A. Gutierrez Increased pulmonary blood flow does not alter surfactant protein gene expression in lambs within the first week of life Am J Physiol Lung Cell Mol Physiol, June 1, 2004; 286(6): L1237 - L1243. [Abstract] [Full Text] [PDF]

				T. C. Bailey, K. A. Da Silva, J. F. Lewis, K. Rodriguez-Capote, F. Possmayer, and R. A. W. Veldhuizen Physiological and inflammatory response to instillation of an oxidized surfactant in a rat model of surfactant deficiency J Appl Physiol, May 1, 2004; 96(5): 1674 - 1680. [Abstract] [Full Text] [PDF]

				E. L. Martin, B. Z. Moyer, M. C. Pape, B. Starcher, K. J. Leco, and R. A. W. Veldhuizen Negative impact of tissue inhibitor of metalloproteinase-3 null mutation on lung structure and function in response to sepsis Am J Physiol Lung Cell Mol Physiol, December 1, 2003; 285(6): L1222 - L1232. [Abstract] [Full Text] [PDF]

				T. C. Bailey, E. L. Martin, L. Zhao, and R. A. W. Veldhuizen High oxygen concentrations predispose mouse lungsto the deleterious effects of high stretch ventilation J Appl Physiol, March 1, 2003; 94(3): 975 - 982. [Abstract] [Full Text] [PDF]