title: Does brain death induce a pro-inflammatory response at the organ level in a porcine model?
abstract: BACKGROUND
  Organs from brain-dead donors have a poorer prognosis after transplantation than organs from living donors. A possible explanation for this is that brain death might initiate a systemic inflammatory response, elicited by a metabolic stress response or brain ischemia. The aim of this study was to investigate the effect of brain death on the cytokine content in the heart, liver, and kidney. In addition, the metabolic and hemodynamic response caused by brain death was carefully registered.
  
  
  METHODS
  Fourteen pigs (35-40 kg) were randomized into two groups (1) eight brain-dead pigs and (2) six pigs only sham operated. Brain death was induced by inflation of an epidurally placed balloon. Blood samples for insulin, glucose, catecholamine, free fatty acids (FAA), and glucagon were obtained during the experimental period of 360 min. At the conclusion of the experiment, biopsies were taken from the heart, liver, and kidney and were analyzed for cytokine mRNA and proteins [tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, and IL-10).
  
  
  RESULTS
  We found a dramatic response to brain death on plasma levels of epinephrine (P=0.004), norepinephrine (P=0.02), FAA (P=0.0001), and glucagon (P=0.0003) compared with the sham group. There was no difference in cytokine content in any organ between the groups.
  
  
  CONCLUSIONS
  In this porcine model, brain death induced a severe metabolic response in peripheral blood. At the organ level, however, there was no difference in the cytokine response between the groups.
authors.affiliation: Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark. Barklin@ki.au.dk
authors.forename: A
authors.initials: A
authors.lastname: Barklin
authors.forename: A
authors.initials: A
authors.lastname: Larsson
authors.forename: C
authors.initials: C
authors.lastname: Vestergaard
authors.forename: J
authors.initials: J
authors.lastname: Koefoed-Nielsen
authors.forename: A
authors.initials: A
authors.lastname: Bach
authors.forename: R
authors.initials: R
authors.lastname: Nyboe
authors.forename: L
authors.initials: L
authors.lastname: Wogensen
authors.forename: E
authors.initials: E
authors.lastname: Tønnesen
mesh_terms: D000818:Animals; D001706:Biopsy; D001786:Blood Glucose / Q000032:analysis; D001926:Brain Death / Q000378:metabolism* / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood / Q000378:metabolism; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D016753:Interleukin-10 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007668:Kidney / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D011897:Random Allocation; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D001786:Blood Glucose; D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D005934:Glucagon; D009638:Norepinephrine; D004837:Epinephrine