The intestinal lymph pathway plays an important role in the pathogenesis of organ
injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized
that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO
shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the
superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly,
MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by
reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped
and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic
structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO),
intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14),
lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced
activities of NO synthase and myeloperoxidase, and 4) decreased activities of
superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these
deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO
shock, which itself is associated with oxidative stress, excessive release of NO,
recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced
inflammatory responses.