title: Reducing the duration of 100% oxygen ventilation in the early reperfusion period after cardiopulmonary resuscitation decreases striatal brain damage.
abstract: OBJECTIVE
  Previous data indicate that 100% O(2) ventilation during early reperfusion after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) increases neuronal death. However, current guidelines encourage the use of 100% O(2) during resuscitation and for an undefined period thereafter. We retrospectively analyzed data from a porcine CA model and hypothesized that prolonged hyperoxic reperfusion would be associated with increased neurohistopathological damage and impaired neurological recovery.
  
  
  METHODS
  Fifteen male pigs underwent 8 min of CA and 5 min of CPR. After resuscitation animals were ventilated with either 100% oxygen for 60 min (hyperoxia; n=8) or 10 min (normoxia; n=7). Physiological variables were obtained at baseline and 10, 60 and 240 min after resuscitation. Daily functional performance was assessed using an established neurocognitive test in parallel to a neurological deficit score (NDS). On day 5, brains of the re-anaesthetized pigs were harvested for neurohistopathological analyses.
  
  
  RESULTS
  At baseline there were no differences in hemodynamics and neurological status between groups. Post-arrest only PaO(2), as a result of the different inspired oxygen fractions, was significantly higher in the hyperoxia group. There was a numerical trend towards improved clinical recovery in both the NDS and the neurocognitive testing for animals exposed to 10 min of 100% oxygen. However, hyperoxic animals showed a significantly greater degree of necrotic neurons and perivascular inflammation in the striatum in comparison to normoxic animals.
  
  
  CONCLUSIONS
  In this retrospective analysis prolonged hyperoxia after CA aggravated necrotic brain damage and perivascular inflammation in the striatum of pigs.
authors.affiliation: Department of Anesthesiology, University Hospital RWTH Aachen, Pauwelsstraße 30, 52074 Aachen, Germany. abruecken@ukaachen.de
authors.forename: Anne
authors.initials: A
authors.lastname: Brücken
authors.forename: Aaref Bani
authors.initials: AB
authors.lastname: Kaab
authors.forename: Kai
authors.initials: K
authors.lastname: Kottmann
authors.forename: Rolf
authors.initials: R
authors.lastname: Rossaint
authors.forename: Kay Wilhelm
authors.initials: KW
authors.lastname: Nolte
authors.forename: Joachim
authors.initials: J
authors.lastname: Weis
authors.forename: Michael
authors.initials: M
authors.lastname: Fries
mesh_terms: D000818:Animals; D016887:Cardiopulmonary Resuscitation; D003342:Corpus Striatum / Q000473:pathology*; D006323:Heart Arrest / Q000628:therapy; D018496:Hyperoxia / Q000473:pathology*; D008297:Male; D010100:Oxygen / Q000008:administration & dosage* / Q000009:adverse effects; D015427:Reperfusion Injury / Q000473:pathology; D012189:Retrospective Studies; D013552:Swine; D013997:Time Factors
chemical_list: D010100:Oxygen