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氙气可阻止与减压相关的神经元损伤。

Xenon Blocks Neuronal Injury Associated with Decompression.

作者信息

Blatteau Jean-Eric, David Hélène N, Vallée Nicolas, Meckler Cedric, Demaistre Sebastien, Lambrechts Kate, Risso Jean-Jacques, Abraini Jacques H

机构信息

Institut de Recherche Biomédicale des Armées, Équipe Résidente de Recherche Subaquatique Opérationnelle, BP 600 Toulon Cedex 9, France.

Centre de recherche Hôtel-Dieu de Lévis, CSSS Alphonse-Desjardins, Lévis, QC, Canada.

出版信息

Sci Rep. 2015 Oct 15;5:15093. doi: 10.1038/srep15093.

DOI:10.1038/srep15093
PMID:26469983
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4606806/
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.

摘要

尽管采用了最先进的高压氧(HBO)治疗,但约30%的神经性减压病(DCS)患者恢复不完全。由于神经性DCS的机制涉及导致兴奋性毒性的缺血过程,HBO联合抗兴奋性毒性治疗可能会改善DCS患者的治疗效果。因此,在本研究中,我们在神经性DCS的体外模型中研究了稀有气体氙的作用。氙已被证明在多种急性缺血性损伤模型中具有神经保护作用。与缓慢减压相比,快速减压导致乳酸脱氢酶(LDH)增加,LDH是亚致死性细胞损伤的一个众所周知的标志物。减压后给予氙可阻止快速减压诱导的LDH释放增加。这些数据表明,氙可能是HBO治疗神经性DCS的一种有效的辅助治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39b2/4606806/4e815b875b67/srep15093-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39b2/4606806/4e815b875b67/srep15093-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/39b2/4606806/4e815b875b67/srep15093-f1.jpg

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本文引用的文献

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J Neurosci Methods. 2014 Oct 30;236:40-3. doi: 10.1016/j.jneumeth.2014.07.010. Epub 2014 Jul 23.
2
Oxygen for the ischemic organ: Much more than an oxygen provider.用于缺血器官的氧气:远不止是一个氧气供应者。
Undersea Hyperb Med. 2013 Mar-Apr;40(2):211-2.
3
Hyperintense white matter lesions in 50 high-altitude pilots with neurologic decompression sickness.
常压与高压氧对急性脑片氧糖剥夺诱导的细胞损伤的影响。
Med Gas Res. 2016 Oct 14;6(3):169-173. doi: 10.4103/2045-9912.191364. eCollection 2016 Jul-Sep.
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Prothrombolytic action of normobaric oxygen given alone or in combination with recombinant tissue-plasminogen activator in a rat model of thromboembolic stroke.常压氧单独或联合重组组织型纤溶酶原激活物对血栓栓塞性卒中大鼠模型的促纤溶作用。
J Appl Physiol (1985). 2012 Jun;112(12):2068-76. doi: 10.1152/japplphysiol.00092.2012. Epub 2012 Apr 5.
5
Neuroprotective role of the TREK-1 channel in decompression sickness.TREK-1 通道在减压病中的神经保护作用。
J Appl Physiol (1985). 2012 Apr;112(7):1191-6. doi: 10.1152/japplphysiol.01100.2011. Epub 2012 Feb 9.
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Pressure-response analysis of anesthetic gases xenon and nitrous oxide on urate oxidase: a crystallographic study.Xe 和 N2O 对尿酸氧化酶的压力-反应分析:晶体学研究。
FASEB J. 2011 Jul;25(7):2266-75. doi: 10.1096/fj.11-183046. Epub 2011 Mar 18.
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Anesthesiology. 2010 Mar;112(3):614-22. doi: 10.1097/ALN.0b013e3181cea398.
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