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Am J Physiol Regul Integr Comp Physiol 260: R413-R420, 1991;
0363-6119/91 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 2 413-R420, Copyright © 1991 by American Physiological Society

ARTICLES

FNLP injures endotoxin-primed rat lung by neutrophil-dependent and -independent mechanisms

B. O. Anderson, D. D. Bensard, J. M. Brown, J. E. Repine, P. F. Shanley, J. A. Leff, L. S. Terada, A. Banerjee and A. H. Harken
Department of Surgery, University of Colorado, Denver 80262.

Bacterial lipopolysaccharide (LPS) and an N-formyl peptide, N-formyl-neoleucyl-leucyl-phenylalanine (FNLP), synergistically promote lung injury in rats as measured by 125I-labeled albumin flux. Concomitantly, neutrophils are sequestered in the lung. We hypothesized that LPS-FNLP-induced lung injury is mediated both by neutrophil-dependent and -independent mechanisms. Rats were depleted of circulating and marginating neutrophils with vinblastine. LPS-FNLP-induced lung protein leak was partially decreased in these neutrophil-depleted animals, although a component of lung injury remained. We hypothesized that LPS-FNLP-induced lung injury was also mediated by xanthine oxidase (XO). Rats were fed a tungsten-enriched diet that inactivates molybdenum-dependent oxidase systems. LPS-FNLP-induced lung leak was partially decreased in these animals as well. When tungsten-fed rats were also neutrophil depleted with vinblastine, no increase in 125I-albumin flux was observed in response to LPS-FNLP. In parallel experiments, lungs from vinblastine-pretreated rats were isolated and perfused. FNLP infusion into the LPS-primed, crystalloid-perfused lungs caused increased 125I-albumin flux, which was prevented by oxidase inhibition. We conclude that LPS-FNLP-induced lung injury is both neutrophil mediated and neutrophil independent. The nonneutrophil component of the LPS-FNLP-induced lung injury appears to be pulmonary XO derived and dependent.


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