Xenon reduces neurohistopathological damage and improves the early neurological deficit after cardiac arrest in pigs.
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.
Fries
Michael
M
Department of Anesthesiology, University Hospital RWTH Aachen, Aachen, Germany. mfries@ukaachen.de
Nolte
Kay Wilhelm
KW
Coburn
Mark
M
Rex
Steffen
S
Timper
Anne
A
Kottmann
Kai
K
Siepmann
Katharina
K
Häusler
Martin
M
Weis
Joachim
J
Rossaint
Rolf
R
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*
D018696:Neuroprotective Agents; D009418:S100 Proteins; D014978:Xenon