title: Xenon reduces neurohistopathological damage and improves the early neurological deficit after cardiac arrest in pigs.
abstract: OBJECTIVE
  Treatment options to ameliorate brain damage following cardiopulmonary resuscitation from cardiac arrest are limited.
  
  
  METHODS
  In a porcine model, we evaluated the effects of xenon treatment on neuropathologic and functional outcomes after cardiopulmonary resuscitation.
  
  
  METHODS
  Prospective, randomized laboratory animal study.
  
  
  METHODS
  Male pigs.
  
  
  METHODS
  Following successful resuscitation from 8 mins of cardiac arrest and 5 mins of cardiopulmonary resuscitation, 24 pigs were randomized to one of three groups receiving either 70% xenon for 1 or 5 hrs or untreated controls receiving 70% nitrogen.
  
  
  RESULTS
  Gas exchange, hemodynamics, and lactate and glucose levels were measured at baseline and in the postresuscitation period. On four postoperative days, neurocognitive and overall neurologic deficits were assessed before day 5, when the brains were harvested for histologic analysis of predefined regions using a semiquantitative score (0-10% = 1, 10-20% = 2, 20-50% = 3, 50-80% = 4, 80-100% = 5). No differences in gas exchange, hemodynamics, or lactate and glucose levels were observed among the groups. Animals exposed to 1 and 5 hrs of xenon showed significantly reduced scores for necrotic neurons in the putamen (1.25 +/- 0.5 and 1.25 +/- 0.5 vs. 2.5 +/- 1.2; p < 0.05), accompanied by significantly lesser scores for perivascular inflammation in putamen (0.8 +/- 0.5 and 1.1 +/- 0.8 vs. 2.1 +/- 1.1; p < 0.05) and caudate nucleus (1.0 +/- 0.8 and 0.6 +/- 0.7 vs. 2.0 +/- 1.1; p < 0.05). This resulted in improved neurocognitive and neurologic function on day 1 to 3 after cardiopulmonary resuscitation in xenon-treated animals.
  
  
  CONCLUSIONS
  In this experimental study of cardiac arrest-induced neurologic damage, xenon conferred neurohistopathologic protection, translating in transiently improved functional outcome.
authors.affiliation: Department of Anesthesiology, University Hospital RWTH Aachen, Aachen, Germany. mfries@ukaachen.de
authors.forename: Michael
authors.initials: M
authors.lastname: Fries
authors.forename: Kay Wilhelm
authors.initials: KW
authors.lastname: Nolte
authors.forename: Mark
authors.initials: M
authors.lastname: Coburn
authors.forename: Steffen
authors.initials: S
authors.lastname: Rex
authors.forename: Anne
authors.initials: A
authors.lastname: Timper
authors.forename: Kai
authors.initials: K
authors.lastname: Kottmann
authors.forename: Katharina
authors.initials: K
authors.lastname: Siepmann
authors.forename: Martin
authors.initials: M
authors.lastname: Häusler
authors.forename: Joachim
authors.initials: J
authors.lastname: Weis
authors.forename: Rolf
authors.initials: R
authors.lastname: Rossaint
mesh_terms: D000818:Animals; D001927:Brain Diseases / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D016887:Cardiopulmonary Resuscitation / Q000009:adverse effects*; D006323:Heart Arrest / Q000473:pathology / Q000628:therapy*; D008297:Male; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D011597:Psychomotor Performance / Q000187:drug effects*; D009418:S100 Proteins / Q000097:blood; D013552:Swine; D014978:Xenon / Q000627:therapeutic use*
chemical_list: D018696:Neuroprotective Agents; D009418:S100 Proteins; D014978:Xenon