title: Xenon attenuates cerebral damage after ischemia in pigs.
abstract: BACKGROUND
  Cerebral blood flow may be compromised in a variety of anesthetic procedures, and ischemic cerebral complications represent the leading cause of morbidity after cardiac operations. With the growing importance of neuroprotective strategies, the current study was designed to determine whether xenon would attenuate cardiac arrest-induced brain injury in pigs.
  
  
  METHODS
  Twenty-four pigs (aged 12-16 weeks) were investigated in a randomized design. General hemodynamics, intracranial pressure, brain tissue oxygenation, and cerebral microdialysis parameters were investigated. The animals were assigned to two groups to receive anesthesia with either xenon (75%) in oxygen (25%) or total intravenous anesthesia combined with air in oxygen (25%) ventilation 15 min before cardiac arrest. After induction (t0) of cardiac arrest of 4 min, cardiopulmonary resuscitation was performed for 1 min, and the induced ventricular fibrillation was terminated by electrical defibrillation. The investigation time was 240 min.
  
  
  RESULTS
  Approximately 60 s after cardiac arrest, brain tissue oxygenation decreased to a critical level of less than 5 mmHg, paralleled by a decrease in electroencephalographic activity. Glycerol as a damage marker increased significantly (> 200 m; P < 0.05), with a peak 90 min after cardiac arrest in both groups. Glycerol concentrations during reperfusion were significantly lower and normalized faster in the xenon group as compared with the total intravenous anesthesia group.
  
  
  CONCLUSIONS
  Although the primary ischemic lesion in this model was similar in both groups, the cerebral microdialysis data show that xenon induces a differential neurochemical benefit in cerebral cell damage and metabolism as compared with total intravenous anesthesia in vivo during cerebral reperfusion after cardiac arrest in a pig model.
authors.affiliation: Department of Cardiac Anesthesia, University of Ulm, Germany. michael.schmidt@medizin.uni-ulm.de
authors.forename: Michael
authors.initials: M
authors.lastname: Schmidt
authors.forename: Thomas
authors.initials: T
authors.lastname: Marx
authors.forename: Egon
authors.initials: E
authors.lastname: Glöggl
authors.forename: Helmut
authors.initials: H
authors.lastname: Reinelt
authors.forename: Uwe
authors.initials: U
authors.lastname: Schirmer
mesh_terms: D000771:Anesthesia, Intravenous; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D001784:Blood Gas Analysis; D001831:Body Temperature; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D004569:Electroencephalography / Q000187:drug effects; D018698:Glutamic Acid / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D006323:Heart Arrest / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D007427:Intracranial Pressure / Q000187:drug effects; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D019344:Lactic Acid / Q000097:blood; D017551:Microdialysis; D018696:Neuroprotective Agents; D010101:Oxygen Consumption / Q000187:drug effects; D019289:Pyruvic Acid / Q000378:metabolism; D013552:Swine; D014978:Xenon / Q000494:pharmacology*
chemical_list: D018685:Anesthetics, Inhalation; D018696:Neuroprotective Agents; D019344:Lactic Acid; D014978:Xenon; D018698:Glutamic Acid; D019289:Pyruvic Acid; D005990:Glycerol