title: [Potential molecular mechanism of multiple organ dysfunction syndrome induced by hemorrhage and endotoxin].
abstract: OBJECTIVE
  To investigate the possible molecular mechanism of multiple organ dysfunction syndrome (MODS) associated with hemorrhagic shock followed by resuscitation and endotoxin.
  
  
  METHODS
  A rabbit model of MODS after hemorrhagic shock followed by resuscitation and endotoxin was used in this study. The expression of I-kappaB kinase-beta (IKK-beta), the activity of nuclear factor-kappaB (NF-kappaB) in macrophage (PAM) and Kupffer cell (KC), the concentration of tumor necrosis factor-alpha (TNF-alpha) in the culture supernatant were measured by in situ hybridization (ISH), electrophoretic mobility shift assay (EMSA) and enzyme linked immunoadsorbent assay (ELISA), respectively. Then the blood gas, biochemistrical and pathological changes in lungs, liver and intestines were examined in each groups.
  
  
  RESULTS
  In the MODS group, the expression of IKK-beta mRNA (0.15+/-0.03, 0.17+/-0.04), the activity of NF-kappaB (1.49+/-0.30, 1.72+/-0.36) and the levels of TNF-alpha[(279.74+/-25.91)ng/L, (300.05+/-30.86)ng/L] in PAM and KCs were significantly higher than those of normal controls[IKK-beta mRNA 0.03+/-0.01 and 0.02+/-0.01; NF-kappaB 0.25+/-0.06 and 0.31+/-0.10, TNF-alpha (137.33+/-6.09)ng/L and (134.85+/-12.09)ng/L, respectively, all P<0.01]. Also, the contents of blood urea nitrogen (BUN), alanine aminotransferase (ALT) in plasma significantly increased, the arterial oxygen partial pressure decreased, and the severity of organ damages in lungs, liver as well as intestines increased following MODS.
  
  
  CONCLUSIONS
  The IKK-beta expression, NF-kappaB activation and cytokine release may play important roles in the pathogenesis of acute lung injury and MODS.
authors.affiliation: Department of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, Shanxi, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Yin
authors.forename: Xiao-min
authors.initials: XM
authors.lastname: Hu
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
authors.forename: Jian-hong
authors.initials: JH
authors.lastname: Yang
authors.forename: Jin-shan
authors.initials: JS
authors.lastname: Zhang
authors.forename: Jian-ming
authors.initials: JM
authors.lastname: Pei
authors.forename: Yan-jun
authors.initials: YJ
authors.lastname: Luo
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay / Q000379:methods; D004731:Endotoxins / Q000633:toxicity*; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D006470:Hemorrhage / Q000150:complications*; D051550:I-kappa B Kinase; D017403:In Situ Hybridization / Q000379:methods; D007728:Kupffer Cells / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D009102:Multiple Organ Failure / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D011817:Rabbits; D012128:Respiratory Distress Syndrome / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004731:Endotoxins; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D017346:Protein Serine-Threonine Kinases; D051550:I-kappa B Kinase