title: A study of the biologic activity of trauma-hemorrhagic shock mesenteric lymph over time and the relative role of cytokines.
abstract: BACKGROUND
  Gut-derived factors in intestinal lymph have been recently shown to cause lung injury, activate neutrophils, and injure endothelial cells in rats subjected to hemorrhagic shock (T/HS). However, the time course of the appearance and disappearance of these factors in intestinal lymph is unclear. Thus the goal of this study was to characterize the biologic activity of T/HS lymph collected at various times during and after shock.
  
  
  METHODS
  Male rats subjected to trauma (laparotomy) plus hemorrhagic shock (mean arterial pressure, 90 mm Hg x 90 min) (T/HS) or trauma plus sham shock (T/SS) had their mesenteric lymph duct catheterized. Mesenteric lymph collected before shock, during shock, and hourly for 6 hours after shock was assayed for cytokine levels (tumor necrosis factor, granulocyte-macrophage colony-stimulating factor, interleukin-1, and transforming growth factor-beta) as well as biologic activity on endothelial cells (cytotoxicity and permeability) and neutrophils (CD11b adhesion molecule expression and respiratory burst activity).
  
  
  RESULTS
  T/HS, but not T/SS, lymph injured endothelial cells and activated neutrophils, although the cytokine levels did not differ between the T/HS and T/SS lymph samples. The biologic activity of T/HS lymph appeared during the shock (gut ischemic) period. The temporal pattern of activity varied on the basis of the biologic activity being tested, with the neutrophil-activating properties of the T/HS lymph persisting longest.
  
  
  CONCLUSIONS
  These results suggest that gut ischemia itself is sufficient to induce the production of biologically active T/HS lymph and that the temporal pattern of biologic activity varies over time on the basis of the property being tested. Consequently, studies directed at identifying the active factors in T/HS lymph must take these temporal patterns of activity into account.
authors.affiliation: Department of Surgery, University of Medicine and Dentistry of New Jersey, Newark, 07103, USA.
authors.forename: Marson T
authors.initials: MT
authors.lastname: Davidson
authors.forename: Edwin A
authors.initials: EA
authors.lastname: Deitch
authors.forename: Qi
authors.initials: Q
authors.lastname: Lu
authors.forename: Adena
authors.initials: A
authors.lastname: Osband
authors.forename: Eleonora
authors.initials: E
authors.lastname: Feketeova
authors.forename: Zoltán H
authors.initials: ZH
authors.lastname: Németh
authors.forename: Gyorgy
authors.initials: G
authors.lastname: Haskó
authors.forename: Da-Zhong
authors.initials: DZ
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D002463:Cell Membrane Permeability / Q000276:immunology; D016207:Cytokines / Q000032:analysis; D042783:Endothelial Cells / Q000276:immunology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis; D007375:Interleukin-1 / Q000032:analysis; D007422:Intestines / Q000166:cytology / Q000276:immunology / Q000503:physiopathology*; D008196:Lymph / Q000737:chemistry / Q000276:immunology*; D008297:Male; D008643:Mesentery / Q000503:physiopathology*; D023421:Models, Animal; D018375:Neutrophil Activation / Q000276:immunology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014947:Wounds and Injuries / Q000276:immunology*
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor