title: Mesenteric lymph reperfusion after superior mesenteric artery occlusion shock exacerbates endotoxin translocation in brain.
abstract: OBJECTIVE
  To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock.
  
  
  METHODS
  Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats.
  
  
  RESULTS
  SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects.
  
  
  CONCLUSIONS
  Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock.
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, China.
authors.forename: Zi-gang
authors.initials: ZG
authors.lastname: Zhao
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, China.
authors.forename: Li-na
authors.initials: LN
authors.lastname: Yang
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, China.
authors.forename: Yong-quan
authors.initials: YQ
authors.lastname: Zhao
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, China.
authors.forename: Chun-yu
authors.initials: CY
authors.lastname: Niu
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D001930:Brain Injuries / Q000209:etiology* / Q000378:metabolism; D002352:Carrier Proteins / Q000032:analysis; D004195:Disease Models, Animal; D004731:Endotoxins / Q000032:analysis / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008026:Ligation; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D042601:Lymphatic Vessels / Q000502:physiology* / Q000601:surgery; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D017538:Mesenteric Artery, Superior; D008641:Mesenteric Vascular Occlusion / Q000150:complications / Q000503:physiopathology*; D008643:Mesentery; D011897:Random Allocation; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications / Q000503:physiopathology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D004731:Endotoxins; D018799:Intercellular Adhesion Molecule-1; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein