title: Argon reduces neurohistopathological damage and preserves functional recovery after cardiac arrest in rats.
abstract: BACKGROUND
  Xenon has profound neuroprotective effects after neurological injury and is currently undergoing phase 2 clinical trials in cardiac arrest patients. However, xenon is very costly, which might preclude its widespread use. We hypothesized argon, which is more available, might also protect central nervous tissues and allow better functional recovery in a rodent model of global cerebral ischaemia.
  
  
  METHODS
  Fourteen male Sprague-Dawley rats were subjected to 7 min of cardiac arrest and 3 min of cardiopulmonary resuscitation (CPR). One hour after successful CPR, animals were randomized to either ventilation with 70% argon in oxygen (n = 7) for 1 h or 70% nitrogen (controls, n=7). A neurological deficit score (NDS) was calculated daily for the following 7 days, then the animals were killed and the brains harvested for histopathological analyses.
  
  
  RESULTS
  All animals survived. Control rats had severe neurological dysfunction, while argon-treated animals showed significant improvements in the NDS at all time points. This was paralleled by a significant reduction in the neuronal damage index in the neocortex and the hippocampal CA 3/4 region.
  
  
  CONCLUSIONS
  Our study demonstrates that a single 1 h application of 70% argon significantly reduced histopathological damage of the neocortex and hippocampus, associated with a marked improvement in functional neurological recovery.
authors: Department of Surgical Intensive Care, University Hospital RWTH Aachen, Aachen, Germany. uecken@ukaachen.de
authors: A
authors: A
authors: Brücken
authors: A
authors: A
authors: Cizen
authors: C
authors: C
authors: Fera
authors: A
authors: A
authors: Meinhardt
authors: J
authors: J
authors: Weis
authors: K
authors: K
authors: Nolte
authors: R
authors: R
authors: Rossaint
authors: T
authors: T
authors: Pufe
authors: G
authors: G
authors: Marx
authors: M
authors: M
authors: Fries
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001128:Argon / Q000627:therapeutic use*; D016887:Cardiopulmonary Resuscitation; D004353:Drug Evaluation, Preclinical / Q000379:methods; D006323:Heart Arrest / Q000150:complications* / Q000628:therapy; D006624:Hippocampus / Q000473:pathology; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D018782:Maze Learning; D019579:Neocortex / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects
chemical_list: D018696:Neuroprotective Agents; D001128:Argon
keywords: argon; cardiopulmonary resuscitation; hypoxia–ischaemia, brain