Xenon Blocks Neuronal Injury Associated with Decompression.

Abstract

Despite state-of-the-art hyperbaric oxygen (HBO) treatment, about 30% of patients suffering neurologic decompression sickness (DCS) exhibit incomplete recovery. Since the mechanisms of neurologic DCS involve ischemic processes which result in excitotoxicity, it is likely that HBO in combination with an anti-excitotoxic treatment would improve the outcome in patients being treated for DCS. Therefore, in the present study, we investigated the effect of the noble gas xenon in an ex vivo model of neurologic DCS. Xenon has been shown to provide neuroprotection in multiple models of acute ischemic insults. Fast decompression compared to slow decompression induced an increase in lactate dehydrogenase (LDH), a well-known marker of sub-lethal cell injury. Post-decompression administration of xenon blocked the increase in LDH release induced by fast decompression. These data suggest that xenon could be an efficient additional treatment to HBO for the treatment of neurologic DCS.

• Authors: Jean-Eric Blatteau, Hélène N David, Nicolas Vallée, Cedric Meckler, Sebastien Demaistre, Kate Lambrechts, Jean-Jacques Risso, Jacques H Abraini
• Journal: Scientific reports (Sci Rep) Vol. 5 Pg. 15093 (Oct 15 2015) ISSN: 2045-2322 [Electronic] England
• PMID: 26469983 (Publication Type: Journal Article)

Chemical References

• Neuroprotective Agents
• Xenon
• L-Lactate Dehydrogenase

Topics

• Animals
• Brain (metabolism)
• Decompression Sickness (metabolism, pathology, therapy)
• Disease Models, Animal
• L-Lactate Dehydrogenase (metabolism)
• Male
• Nervous System Diseases (metabolism, pathology, therapy)
• Neuroprotective Agents (administration & dosage)
• Rats
• Time Factors
• Xenon (administration & dosage)