title: [Role of endotoxin translocation on mesenteric lymph reperfusion aggravating multiple organ injury in SMAO shock rats].
abstract: OBJECTIVE
  To investigate the role of mesenteric lymph reperfusion (MLR) aggravates multiple organs injury in superior mesenteric artery occlusion (SMAO) shock and its mechanism.
  
  
  METHODS
  Twenty four Wistar rats were randomly divided into 4 groups (n = 6): Sham group (only anesthetized and operated), MLR group rats performed 1 h occlusion of mesenteric lymph duct (MLD), then followed by 2 h of reperfusion, SMAO group (rats performed 1 h occlusion of superior mesenteric artery (SMA) and then followed by 2 h of reperfusion), SMAO + MLR group (rats performed 1 h occlusion of SMA and MLD and then followed by 2 h of reperfusion). The blood sample was taken out from abdominal aortic for plasma and the liver, kidney, myocardium, lung tissues in fixed position were prepared for making homogenate after reperfusion of 2 h respectively. And the levels of endotoxin (ET) in plasma and homogenates were determined with kinetic turbidimetric technique of tachypleus amebocyte lysate, the contents of lipopolysaccharide-binding protein (LBP), lipopolysaccharide receptor (CD14) and tumor necrosis factor-alpha (TNF-alpha) in homogenates were determined with enzyme-linked immunosorbent assay method.
  
  
  RESULTS
  The indices have no statistics difference between sham group and MLR group. The ET levels of the plasma and hepatic, renal, myocardial, pulmonary homogenates in SMAO and SMAO + MLR groups were significant higher than that of sham and MLR groups, and these indices in SMAO + MLR were increased significantly than those in SMAO group. The CD14, LBP and TNF-alpha contents of the hepatic, renal, myocardial and pulmonary homogenates in SMAO and SMAO + MLR groups were significant higher than those in sham and MLR groups, and these indices in SMAO+ MLR were higher than SMAO group significantly.
  
  
  CONCLUSIONS
  The mechanism of MLR aggravates multiple organs injury in SMAO shock may be associated with enterogenous ET through intestinal lymphatic pathway to translocate, activate the LBP/CD14 as endotoxin sensitizing system and promote inflammatory response.
authors.affiliation: Institution of Microcirculation, Department of Pathophysiololgy of Basic Medical College, Hebei North University, Zhangjiakou 075000, China.
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Yang
authors.forename: Zi-Gang
authors.initials: ZG
authors.lastname: Zhao
authors.forename: Yong-Quan
authors.initials: YQ
authors.lastname: Zhao
authors.forename: Zheng-Jie
authors.initials: ZJ
authors.lastname: Liu
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Niu
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D004731:Endotoxins; D007422:Intestines / Q000098:blood supply; D042601:Lymphatic Vessels / Q000473:pathology*; D008297:Male; D017538:Mesenteric Artery, Superior / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology*; D012772:Shock, Septic / Q000473:pathology*
chemical_list: D004731:Endotoxins