Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock

The intestinal lymph pathway plays an important role in the pathogenesis of organinjury following superior mesenteric artery occlusion (SMAO) shock. We hypothesizedthat mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAOshock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping thesuperior 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 byreperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clampedand then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenicstructure 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) enhancedactivities of NO synthase and myeloperoxidase, and 4) decreased activities ofsuperoxide dismutase and ATPase. MLR following SMAO shock further aggravated thesedeleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAOshock, which itself is associated with oxidative stress, excessive release of NO,recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhancedinflammatory responses.