title: Functional evidence of reversible ischemic injury immediately after the sympathetic storm associated with experimental brain death.
abstract: BACKGROUND
  Acute brain death from increased intracranial pressure results in a transient increase in myocardial adenosine and lactate, which indicates that oxygen demand exceeds oxygen delivery during the sympathetic "storm". The aim of this study was to determine the functional significance of this period of ischemia.
  
  
  METHODS
  Brain death was inflicted on 40 Westran pigs (36.5-68.0 kg) by inflating a 21-ml subdural balloon over 3 minutes. In 38 animals, micromanometry and sonomicrometry were used to obtain left ventricular pressure-volume loops to determine the preload recruitable stroke work (PRSW) relationship. Data files were recorded before and at 15-minute intervals after beginning balloon inflation. Plasma troponin I was measured before and 60 minutes after beginning balloon inflation in the 38 instrumented and 2 non-instrumented animals.
  
  
  RESULTS
  All animals experienced the classical sympathetic storm. The slope of the PRSW relationship decreased, and the volume-axis intercept shifted to the right 15 minutes after beginning balloon inflation (p < 0.0001). Progressive incremental recovery (leftward shift) occurred between subsequent time points (p < or = 0.0018). In the instrumented animals, the mean plasma troponin I level increased from 1.4 +/- 1.6 microg/liter to 2.8 +/- 2.3 microg/liter (p < 0.001). However, troponin I was not detected before or after induction of brain death in the plasma of either non-instrumented animal (p = 0.001).
  
  
  CONCLUSIONS
  The sympathetic storm produced transient contractile dysfunction, consistent with ischemic injury. However, troponin I release reflected surgical instrumentation and not brain death.
authors.affiliation: Heart and Lung Transplant Unit, St. Vincent's Hospital and the Victor Chang Cardiac Research Institute, Sydney, NSW, Australia. j.ryan@garvan.unsw.edu.au
authors.forename: Jonathon B
authors.initials: JB
authors.lastname: Ryan
authors.forename: Mark
authors.initials: M
authors.lastname: Hicks
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Cropper
authors.forename: Sarah R
authors.initials: SR
authors.lastname: Garlick
authors.forename: Scott H
authors.initials: SH
authors.lastname: Kesteven
authors.forename: Michael K
authors.initials: MK
authors.lastname: Wilson
authors.forename: Michael P
authors.initials: MP
authors.lastname: Feneley
authors.forename: Peter S
authors.initials: PS
authors.lastname: Macdonald
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D001926:Brain Death / Q000503:physiopathology*; D002102:Cadaver; D003326:Coronary Circulation / Q000502:physiology; D004195:Disease Models, Animal; D006339:Heart Rate / Q000502:physiology*; D016027:Heart Transplantation; D019586:Intracranial Hypertension / Q000150:complications / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000209:etiology / Q000503:physiopathology*; D013552:Swine; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D019210:Troponin I / Q000097:blood
chemical_list: D019210:Troponin I