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Published on: September 27, 2024
Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock
1Institute of Microcirculation, Hebei North University, Zhangjiakou, Hebei, China.
Abstract:
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.
Insights
Mesenteric lymph reperfusion worsens spleen injury after superior mesenteric artery occlusion shock. This exacerbation involves oxidative stress, nitric oxide release, and inflammation.
Area of Science:
- Physiology
- Pathology
- Surgical Research
Background:
- The intestinal lymph pathway is crucial in organ injury pathogenesis after superior mesenteric artery occlusion (SMAO) shock.
- Superior mesenteric artery occlusion (SMAO) shock can lead to significant organ damage, particularly affecting the spleen.
Purpose of the Study:
- To investigate the role of mesenteric lymph reperfusion (MLR) in exacerbating spleen injury following SMAO shock.
- To elucidate the underlying mechanisms contributing to spleen injury during SMAO shock and MLR.
Main Methods:
- Induction of SMAO shock in Wistar rats by clamping the superior mesenteric artery for 1 hour, followed by 2 hours of reperfusion.
- Performance of MLR by clamping the mesenteric lymph duct (MLD) for 1 hour, followed by 2 hours of reperfusion.
- Assessment of spleen injury in rats subjected to SMAO shock alone, MLR alone, and combined MLR and SMAO shock.
Main Results:
- SMAO shock alone caused splenic structural injury and increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, CD14, lipopolysaccharide-binding protein, and tumor necrosis factor-α.
- SMAO shock led to enhanced NO synthase and myeloperoxidase activities, and decreased superoxide dismutase and ATPase activities.
- MLR following SMAO shock significantly aggravated these pathological changes, indicating a synergistic detrimental effect.
Conclusions:
- Mesenteric lymph reperfusion exacerbates spleen injury induced by superior mesenteric artery occlusion shock.
- The exacerbation of spleen injury is linked to oxidative stress, excessive NO release, neutrophil recruitment, endotoxin translocation, and heightened inflammatory responses.
