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.
Highlights
And interestingly, animal studies in models of excitotoxic and ischemic insults have provided evidence for the neuroprotective effects of the noble gas xenon[11,12,13,14,15]
We investigated the effect of the noble gas xenon on the release of LDH, known to be a marker of glutamate-mediated sub-lethal cell injury[14,32], using an ex vivo model of neurologic DCS5
We found that administration of xenon after decompression blocked the increase in LDH release induced by fast decompression compared to slow decompression. These data are in excellent agreement with previous studies that have clearly demonstrated the neuroprotective action of xenon in ex vivo and in vivo models of acute hypoxic-ischemic insults[11,12,13,14,15]
Summary
And interestingly, animal studies in models of excitotoxic and ischemic insults have provided evidence for the neuroprotective effects of the noble gas xenon[11,12,13,14,15]. Neuroprotection by xenon is thought to result from its antagonistic action at the NMDA receptor[14,15], whose activation plays a critical role in excitotoxic neuronal death induced by ischemic insults[22,23]. In contrast with prototypical NMDA receptor antagonists, which fail to reach the site of brain injury[24] and possess their own neurotoxicity[25,26,27], xenon crosses the blood-brain barrier and has low blood/gas solubility[28], conditions that are advantageous in terms of rapid inflow and washout, and reduced risk of adverse reactions[29,30,31]. Given the pathophysiological mechanisms of DCS and the neuroprotective properties of xenon described above, we investigated whether xenon may provide neuroprotection in an ex vivo model of neurologic DCS5
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