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 p47(phox)-/- 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.

Urinary waste products (UWP) in the amniotic fluid have been held responsible for the intestinal damage (ID) in gastroschisis, based on the fact that the fetus urinates physiologically into the amniotic cavity. However, experimental and clinical evidence suggests that intrauterine defecation is a physiological event; thus gastrointestinal waste products (GWP) may also be responsible for ID in gastroschisis. An experimental study was performed to investigate the effects of intraperitoneal human neonatal urine and diluted meconium on rat intestines. Adult Wistar albino rats were used. Sterile urine and meconium were obtained from newborn humans and 5% meconium suspension was prepared. Histopathological features of the intestines of the rats injected with urine did not differ from the intestines of the untreated rats. The bowel in rats injected with a meconium suspension showed serosal thickening, inflammation, focal fibrin and collagen deposits. Histopathological changes in intestines induced by intraperitoneal diluted meconium were consistent with those described for human gastroschisis specimens. We conclude that GWP, rather than UWP, seems to be responsible for the ID in gastroschisis.

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An experimental study was conducted to determine the end-results of two different defects on the anterior abdominal wall: an abdominal wall defect (AWD) versus an umbilical cord defect (UCD) using chick embryos. The AWD was created by leaving an intact skin bridge between the defect and the umbilical cord in group 1; the UCD was created on the umbilical cord near the junction of the skin in group 2. At the end of incubation, the intestines appeared hemorrhagic in the AWD group, but not in the UCD group. During microscopic examination, hemorrhagic areas were observed in the bowel wall and mucosal villi in the AWD group but not in the UCD group. The end-result of the defect causing the physiological umbilical hernia resulted in bowel damage resembling the classic picture of gastroschisis (GS). We conclude that the site of the defect in GS is not the abdominal wall itself, but the physiological umbilical hernia.

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