title: Effect and Mechanism of Portal Blood Stasis Removal on Intestinal Endotoxemia and Hepatic Ischemia Reperfusion Injury.
abstract: OBJECTIVE
  We used a rabbit model of hepatic ischemia reperfusion in situ to observe the change of portal venous endotoxin level before reperfusion, and the effect of portal blood stasis removal on intestinal endotoxemia and hepatic ischemia reperfusion injury. The purpose was to find an ideal method for portal blood stasis removal and provide the experimental proof for clinical application of hepatectomy.
  
  
  METHODS
  To investigate the effect of portal blood stasis removal on intestinal endotoxemia and hepatic ischemia reperfusion injury, a rabbit hepatic ischemia reperfusion injury model was established and treated with removal of portal blood stasis before the portal blood circulation was resumed. Serum endotoxin content, alanine aminotransferase (ALT), hyaluronic acid (HA), and content of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD) and activation of nuclear factor-κB (NF-κB) in liver tissue were examined respectively.
  
  
  RESULTS
  In portal blood stasis the level of serum endotoxin significantly decreased with each 2.5 mL blood removal (P < .01), subsequently reaching a minima at the 7.5 mL blood removal (P > .05). Removing portal blood stasis ameliorated endotoxemia and hepatic ischemia reperfusion injury as shown by ALT, HA, MDA, SOD, TNF-α, IL-6, and activation of NF-κB compared to no removal. The first 5 mL portal blood stasis contains high volume of endotoxin which may be responsible for hepatic reperfusion injury.
  
  
  CONCLUSIONS
  Removal of portal blood stasis before the resume of splanchnic circulation may ameliorate intestinal endotoxemia and hepatic ischemia reperfusion injury.
authors.affiliation: Department of General Surgery, Haici Hospital of Qingdao University, Qingdao, Shandong Province, China. Electronic address: ytlzs@qq.com.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of General Surgery, Haici Hospital of Qingdao University, Qingdao, Shandong Province, China.
authors.forename: Z-S
authors.initials: ZS
authors.lastname: Liu
authors.affiliation: Department of General Surgery, Haici Hospital of Qingdao University, Qingdao, Shandong Province, China.
authors.forename: S-L
authors.initials: SL
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, Haici Hospital of Qingdao University, Qingdao, Shandong Province, China.
authors.forename: Q-X
authors.initials: QX
authors.lastname: Diao
authors.affiliation: Department of Clinical Medicine, Qingdao Municipal Hospital, Qingdao, Shandong Province, China.
authors.forename: Y-J
authors.initials: YJ
authors.lastname: Ge
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D019446:Endotoxemia / Q000097:blood*; D006488:Hemostasis, Surgical / Q000379:methods*; D015850:Interleukin-6 / Q000097:blood; D007422:Intestines; D007511:Ischemia / Q000097:blood / Q000628:therapy*; D008099:Liver / Q000098:blood supply / Q000293:injuries; D008107:Liver Diseases / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D016328:NF-kappa B / Q000378:metabolism; D011169:Portal Vein; D011817:Rabbits; D011897:Random Allocation; D015427:Reperfusion Injury / Q000097:blood* / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D000410:Alanine Transaminase