title: Hormonal profiles in a canine model of the brain-dead organ donor.
abstract: OBJECTIVE
  The aim of the present study was to determine the effect of brain death on the circulating hormone levels.
  
  
  METHODS
  Serum total thyroxine (TT4), total 3,3,5' triiodothyronine (TT3), free thyroxine (FT4), free 3,3,5' triiodothyronine (FT3), reverse 3,3',5' triiodothyronine (RT3) and plasma cortisol (CORT), norepinephrine (NE), epinephrine (EPI), dopamine, insulin (INS), and glucagon (GLUC) concentrations were measured before and for 5 hours after the maintenance of brain death (BD, n = 8), sham-brain death induction (SHAM, n = 3), and the operative procedure alone (time control, n = 3). Brain death in the canine model was induced by increasing and maintaining intracranial pressure above systolic arterial pressure.
  
  
  RESULTS
  Brain death led to a persistent, significant decrease in mean arterial pressure (121 +/- 6 v 40 +/- 4 mm Hg at 5 hours). A significant decrease in the TT4, TT3, FT4, and FT3 concentrations was seen during the experiment for all three groups with the exception of TT4 in the SHAM group; no significant difference was found among the three groups for any of the time points. RT3 was found to increase after the induction of brain death in the BD (n = 5) group. The CORT levels in the BD group were significantly less than the other two groups for all time points 30 minutes after the induction of brain death. The mean 30- to 300-minute plasma NE and EPI levels in the SHAM group were statistically greater than the BD group. The plasma glucose in the BD group was maintained between 60 and 140 mg/dL whereas the trends of the INS/glucose and GLUC/glucose ratios in the BD group were appropriate for the plasma glucose level.
  
  
  CONCLUSIONS
  The operative procedure alone led to the decrease in the plasma thyroid hormone levels. The inability of the BD group to increase plasma CORT, NE, and EPI may contribute to the hemodynamic deterioration and eventual somatic death.
authors.affiliation: Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622.
authors.forename: T S
authors.initials: TS
authors.lastname: Huber
authors.forename: R
authors.initials: R
authors.lastname: Nachreiner
authors.forename: L G
authors.initials: LG
authors.lastname: D'Alecy
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001926:Brain Death / Q000097:blood* / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood*; D004195:Disease Models, Animal; D004285:Dogs; D005069:Evaluation Studies as Topic; D005934:Glucagon / Q000097:blood*; D006439:Hemodynamics; D006706:Homeostasis; D006854:Hydrocortisone / Q000097:blood*; D007328:Insulin / Q000097:blood*; D007427:Intracranial Pressure; D008297:Male; D013963:Thyroid Hormones / Q000097:blood*; D013997:Time Factors; D014019:Tissue Donors
chemical_list: D001786:Blood Glucose; D002395:Catecholamines; D007328:Insulin; D013963:Thyroid Hormones; D005934:Glucagon; D006854:Hydrocortisone