title: Trauma-hemorrhagic shock-induced up-regulation of endothelial cell adhesion molecules is blunted by mesenteric lymph duct ligation.
abstract: OBJECTIVE
  Previous studies have shown that mesenteric lymph duct ligation prevents trauma-hemorrhagic shock-induced lung injury and neutrophil activation. Since endothelial cells rapidly express adhesion molecules, such as P-selectin and intercellular adhesion molecule-1, after shock, and because trauma-hemorrhagic shock-induced lung injury appears to involve neutrophil-endothelial cell interactions, we tested the hypothesis that lymph duct ligation would diminish trauma-hemorrhagic shock-induced P-selectin and intercellular adhesion molecule-1 expression in the lung and other organs.
  
  
  METHODS
  Prospective animal study with concurrent control.
  
  
  METHODS
  Small animal laboratory.
  
  
  METHODS
  Adult male Sprague-Dawley rats.
  
  
  METHODS
  Four groups of male rats were studied: trauma (laparotomy) plus sham shock, trauma-sham shock plus lymph duct ligation, trauma-hemorrhagic shock (90 mins of shock at 30 mm Hg), and trauma-hemorrhagic shock plus lymph duct ligation. At 3 or 24 hrs after trauma-hemorrhagic shock or trauma-sham shock, lung, heart, liver, kidney, intestinal, and other visceral concentrations of P-selectin and intercellular adhesion molecule-1 expression were measured using the dual radiolabeled monoclonal antibody technique.
  
  
  RESULTS
  At 3 and 24 hrs, trauma-hemorrhagic shock increased endothelial cell P-selectin and intercellular adhesion molecule-1 adhesion molecule expression in the lung and liver. At 3 and 24 hrs after trauma-hemorrhagic shock, intercellular adhesion molecule-1 expression was increased in the heart, spleen, pancreas, intestine, and kidney, whereas at 24 hrs, but not 3 hrs, P-selectin expression also was increased in these organs. Lymph duct ligation prevented trauma-hemorrhagic shock-induced increased adhesion molecule expression in all of these organs with the exception of intestinal P-selectin expression.
  
  
  CONCLUSIONS
  Trauma-hemorrhagic shock-induced increases in endothelial cell P-selectin and intercellular adhesion molecule-1 expression in the lung and liver as well as other tissues appear to be related to factors liberated from the ischemic gut and carried in intestinal lymph.
authors.affiliation: Department of Surgery, UMDNJ-New Jersey Medical School, Newark, NJ, USA.
authors.forename: Da-Zhong
authors.initials: DZ
authors.lastname: Xu
authors.forename: Qi
authors.initials: Q
authors.lastname: Lu
authors.forename: Charles A
authors.initials: CA
authors.lastname: Adams
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Issekutz
authors.forename: Edwin A
authors.initials: EA
authors.lastname: Deitch
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D008208:Lymphatic System / Q000502:physiology*; D008297:Male; D008643:Mesentery; D019007:P-Selectin / Q000096:biosynthesis*; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000097:blood; D012771:Shock, Hemorrhagic / Q000097:blood*; D012774:Shock, Traumatic / Q000097:blood*; D015854:Up-Regulation
chemical_list: D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1