Splanchnic arteries were clamped for 45 min to induce splanchnic artery occlusion (SAO)
shock in anesthetized rats.
Sham-operated animals were used as controls. Survival time, serum
tumor necrosis factor-alpha (
TNF-alpha), white blood cell (WBC) count, mean arterial blood pressure,
myeloperoxidase (MPO) activity, and serum levels of soluble
E-selectin (sE-
selectin) were investigated. SAO-shocked rats exhibited decreased survival time (95 +/- 11 min, whereas
sham-shocked rats survived for > 5 h), reduced mean arterial blood pressure, increased serum levels of
TNF-alpha (185 +/- 8 U/ml) and MPO activity in the ileum (0.11 +/- 0.03 U x 10(-3)/g tissue) and lung (1.5 +/- 0.4 U x 10(-3)/g tissue),
leukopenia, and enhanced serum levels of sE-
selectin. Furthermore SAO-shocked rats showed histological alterations in the ileum and lung. Administration of
cloricromene (2 mg/kg i.v.), an inhibitor of
TNF-alpha, significantly increased survival time (225 +/- 10 min), decreased serum levels of
TNF-alpha and sE-
selectin, reduced
leukopenia and MPO activity in the ileum (0.035 +/- 0.003 U x 10(-3)/g tissue) and lung (0.3 +/- 0.005 U x 10(-3)/g tissue), improved the cardiovascular changes, and reduced the histological changes in the ileum and lung. Finally, an anti-
E-selectin antibody protected rats against SAO
shock. Our findings are consistent with an involvement of
E-selectin, "in vivo," in the pathogenesis of SAO
shock.