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1 Department of Pediatric Surgery, School of Medicine, Dokuz Eylül University, Izmir, Turkey 35340; Departments of 2 Surgery and 3 Molecular and Cellular Physiology, School of Medicine, Louisiana State University, Shreveport, Louisiana 71130; 4 Department of Pediatrics, University of California, San Francisco, California 94143; and 5 Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506
Superoxide has been implicated in the regulation of endothelial
cell adhesion molecule expression and the subsequent initiation of
leukocyte-endothelial cell adhesion in different experimental models of
inflammation. The objective of this study was to assess the
contribution of oxygen radicals to P-selectin expression in a murine
model of whole body ischemia-reperfusion, i.e.,
hemorrhage-resuscitation (H/R), with the use of different strategies
that interfere with either the production (allopurinol,
CD11/CD18-deficient or p47phox
/ mice) or accumulation
[intravenous superoxide dismutase (SOD), mutant mice that overexpress
SOD] of oxygen radicals. P-selectin expression was quantified in
different regional vascular beds by use of the dual-radiolabeled
monoclonal antibody technique. H/R elicited a significant increase in
P-selectin expression in all vascular beds. This response was blunted
in SOD transgenic mice and in wild-type mice receiving either
intravenous SOD or the xanthine oxidase inhibitor allopurinol. Mice
genetically deficient in either a subunit of NADPH oxidase or the
leukocyte adhesion molecule CD11/CD18 also exhibited a reduced
P-selectin expression. These results implicate superoxide, derived from
both xanthine oxidase and NADPH oxidase, as mediators of the increased
P-selectin expression observed in different regional vascular beds
exposed to hemorrhage and retransfusion.
ischemia-reperfusion; leukocyte-endothelial cell adhesion; xanthine
oxidase; 
2-integrins
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