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 Till, G. O. Articles by Ward, P. A. Search for Related Content PubMed PubMed Citation Articles by Till, G. O. Articles by Ward, P. A.

American Journal of Pathology, Vol 119, 376-384, Copyright © 1985 by American Society for Investigative Pathology

REGULAR ARTICLES

Lipid peroxidation and acute lung injury after thermal trauma to skin. Evidence of a role for hydroxyl radical

GO Till, JR Hatherill, WW Tourtellotte, MJ Lutz and PA Ward

The authors have previously shown that thermal injury to the skin of rats results in the development of acute lung injury that is susceptible to systemic treatment of animals with catalase and dependent on the presence of neutrophils. The current studies have been expanded for exploration of the nature of the neutrophil-derived oxygen products responsible for the lung injury and have also focused on evidence of the appearance of products of lipid peroxidation (conjugated dienes). With respect to the former, treatment of rats with iron chelators (deferoxamine mesylate, 2,3-dihydroxybenzoic acid), with scavengers of hydroxyl radical (dimethyl sulfoxide, dimethyl thiourea, sodium benzoate), or with vitamin E affords a significant degree of protection from acute lung injury as assessed by changes in lung vascular permeability and by morphologic parameters. These data suggest that lung vascular injury after thermal trauma of the skin is related to the generation by neutrophils of the hydroxyl radical. Conjugated dienes have been demonstrated to appear sequentially both in the burned skin (at 1/4 hour) and in the lungs (at 2 hours), as well as in the plasma (with peaks at 1/2 and at 3 hours) after thermal injury. The appearance of the conjugated dienes in plasma at the two intervals of time is greatly diminished if animals are pretreated with the iron chelator deferoxamine, with catalase, or with scavengers of hydroxyl radical. Furthermore, the appearance of conjugated dienes in plasma at 30 minutes and 3 hours is significantly diminished if animals are depleted of neutrophils, complement-depleted, or the burned skin is excised immediately after thermal injury. These data indicate a linkage between thermal trauma of skin, secondary injury of lung, and appearance in plasma and tissues of products of lipid peroxidation.

This article has been cited by other articles:

				A. Mizutani, P. Enkhbaatar, A. Esechie, L. D. Traber, R. A. Cox, H. K. Hawkins, D. J. Deyo, K. Murakami, T. Noguchi, and D. L. Traber Pulmonary changes in a mouse model of combined burn and smoke inhalation-induced injury J Appl Physiol, August 1, 2008; 105(2): 678 - 684. [Abstract] [Full Text] [PDF]

				L. Xing and D. G. Remick Mechanisms of Dimethyl Sulfoxide Augmentation of IL-1{beta} Production J. Immunol., May 15, 2005; 174(10): 6195 - 6202. [Abstract] [Full Text] [PDF]

				K. Soejima, F. C. Schmalstieg, H. Sakurai, L. D. Traber, and D. L. Traber Pathophysiological analysis of combined burn and smoke inhalation injuries in sheep Am J Physiol Lung Cell Mol Physiol, June 1, 2001; 280(6): L1233 - L1241. [Abstract] [Full Text] [PDF]