title: The Early Endocrine Stress Response in Experimental Subarachnoid Hemorrhage.
abstract: BACKGROUND
  In patients with severe illness, such as aneurysmal subarachnoid hemorrhage (SAH), a physiologic stress response is triggered. This includes activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. The aim of this study was to investigate the very early responses of these systems.
  
  
  METHODS
  A porcine animal model of aneurysmal SAH was used. In this model, blood is injected slowly to the basal cisterns above the anterior skull base until the cerebral perfusion pressure is 0 mm Hg. Sampling was done from blood and urine at -10, +15, +75 and +135 minutes from time of induction of SAH. Analyses of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, catecholamines and chromogranin-A were performed.
  
  
  RESULTS
  Plasma ACTH, serum cortisol and plasma aldosterone increased in the samples following induction of SAH, and started to decline after 75 minutes. Urine cortisol also increased after SAH. Urine catecholamines and their metabolites were found to increase after SAH. Many samples were however below detection level, not allowing for statistical analysis. Plasma chromogranin-A peaked at 15 minutes after SAH, and thereafter decreased.
  
  
  CONCLUSIONS
  The endocrine stress response after aneurysmal SAH was found to start within 15 minutes in the HPA axis with early peak values of ACTH, cortisol and aldosterone. The fact that the concentrations of the HPA axis hormones decreased 135 minutes after SAH may suggest that a similar pattern exists in SAH patients, thus making it difficult to catch these early peak values. There were also indications of early activation of the sympathetic nervous system, but the small number of valid samples made interpretation difficult.
authors.affiliation: Department of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
authors.forename: Christoffer
authors.initials: C
authors.lastname: Nyberg
authors.affiliation: Department of Surgical Sciences, Section of Anesthesiology and Intensive care, Uppsala University, Uppsala, Sweden.
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Karlsson
authors.affiliation: Department of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
authors.forename: Lars
authors.initials: L
authors.lastname: Hillered
authors.affiliation: Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: Mats
authors.initials: M
authors.lastname: Stridsberg
authors.affiliation: Department of Neuroscience, Section of Neurosurgery, Uppsala University, Uppsala, Sweden.
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Ronne Engström
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000450:Aldosterone / Q000097:blood; D000818:Animals; D002395:Catecholamines / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System; D008297:Male; D010913:Pituitary-Adrenal System; D013312:Stress, Physiological; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D013552:Swine
chemical_list: D002395:Catecholamines; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone