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Multiparametric and longitudinal MRI characterization of mild traumatic brain injury in rats.大鼠轻度创伤性脑损伤的多参数和纵向MRI特征
J Neurotrauma. 2015 Apr 15;32(8):598-607. doi: 10.1089/neu.2014.3563. Epub 2015 Jan 22.
2
Methylene blue is neuroprotective against mild traumatic brain injury.亚甲蓝对轻度创伤性脑损伤具有神经保护作用。
J Neurotrauma. 2014 Jun 1;31(11):1063-71. doi: 10.1089/neu.2013.3193. Epub 2014 Apr 8.
3
Effect of normabaric hyperoxia treatment on neuronal damage following fluid percussion injury in the striatum of mice: a morphological approach.常压高氧处理对小鼠纹状体液压冲击损伤后神经元损伤的影响:形态学方法。
J Biosci. 2013 Mar;38(1):93-103. doi: 10.1007/s12038-012-9290-7.
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Purinergic 2Y1 receptor stimulation decreases cerebral edema and reactive gliosis in a traumatic brain injury model.嘌呤能 2Y1 受体刺激可减少创伤性脑损伤模型中的脑水肿和反应性神经胶质增生。
J Neurotrauma. 2013 Jan 1;30(1):55-66. doi: 10.1089/neu.2012.2488.
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Brain tissue oxygen monitoring and hyperoxic treatment in patients with traumatic brain injury.颅脑创伤患者的脑组织氧监测与高氧治疗。
J Neurotrauma. 2012 Aug 10;29(12):2109-23. doi: 10.1089/neu.2012.2365. Epub 2012 Jul 10.
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Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments.颅脑创伤性脑水肿的发病机制:治疗进展。
Curr Opin Neurol. 2010 Jun;23(3):293-9. doi: 10.1097/WCO.0b013e328337f451.
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Normobaric hyperoxia therapy for traumatic brain injury and stroke: a review.常压高氧疗法治疗创伤性脑损伤和中风:综述
Br J Neurosurg. 2009 Dec;23(6):576-84. doi: 10.3109/02688690903050352.
8
Protection of mitochondrial function and improvement in cognitive recovery in rats treated with hyperbaric oxygen following lateral fluid-percussion injury.高压氧治疗对侧脑液压冲击伤大鼠线粒体功能的保护及认知功能恢复的改善作用
J Neurosurg. 2007 Apr;106(4):687-94. doi: 10.3171/jns.2007.106.4.687.
9
Cerebral perfusion response to hyperoxia.大脑对高氧的灌注反应。
J Cereb Blood Flow Metab. 2007 Jan;27(1):69-75. doi: 10.1038/sj.jcbfm.9600319. Epub 2006 May 3.
10
Mitochondrial damage and dysfunction in traumatic brain injury.创伤性脑损伤中的线粒体损伤与功能障碍
Mitochondrion. 2004 Sep;4(5-6):705-13. doi: 10.1016/j.mito.2004.07.021.

常压氧会使中度创伤性脑损伤后的预后恶化。

Normobaric oxygen worsens outcome after a moderate traumatic brain injury.

作者信息

Talley Watts Lora, Long Justin Alexander, Manga Venkata Hemanth, Huang Shiliang, Shen Qiang, Duong Timothy Q

机构信息

1] Research Imaging Institute, University of Texas Health Science Center, San Antonio, Texas, USA [2] Department of Cellular and Structure Biology, University of Texas Health Science Center, San Antonio, Texas, USA [3] Department of Neurology, University of Texas Health Science Center, San Antonio, Texas, USA.

Research Imaging Institute, University of Texas Health Science Center, San Antonio, Texas, USA.

出版信息

J Cereb Blood Flow Metab. 2015 Jul;35(7):1137-44. doi: 10.1038/jcbfm.2015.18. Epub 2015 Feb 18.

DOI:10.1038/jcbfm.2015.18
PMID:25690469
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4640244/
Abstract

Traumatic brain injury (TBI) is a multifaceted injury and a leading cause of death in children, young adults, and increasingly in Veterans. However, there are no neuroprotective agents clinically available to counteract damage or promote repair after brain trauma. This study investigated the neuroprotective effects of normobaric oxygen (NBO) after a controlled cortical impact in rats. The central hypothesis was that NBO treatment would reduce lesion volume and functional deficits compared with air-treated animals after TBI by increasing brain oxygenation thereby minimizing ischemic injury. In a randomized double-blinded design, animals received either NBO (n = 8) or normal air (n = 8) after TBI. Magnetic resonance imaging (MRI) was performed 0 to 3 hours, and 1, 2, 7, and 14 days after an impact to the primary forelimb somatosensory cortex. Behavioral assessments were performed before injury induction and before MRI scans on days 2, 7, and 14. Nissl staining was performed on day 14 to corroborate the lesion volume detected from MRI. Contrary to our hypothesis, we found that NBO treatment increased lesion volume in a rat model of moderate TBI and had no positive effect on behavioral measures. Our results do not promote the acute use of NBO in patients with moderate TBI.

摘要

创伤性脑损伤(TBI)是一种多方面的损伤,是儿童、年轻人乃至退伍军人死亡的主要原因。然而,目前临床上尚无神经保护剂可用于对抗脑外伤后的损伤或促进修复。本研究调查了常压氧(NBO)在大鼠控制性皮质撞击后的神经保护作用。核心假设是,与空气处理的动物相比,NBO治疗将通过增加脑氧合从而使缺血性损伤最小化,来减少TBI后大鼠的损伤体积和功能缺陷。在随机双盲设计中,动物在TBI后接受NBO(n = 8)或正常空气(n = 8)处理。在对初级前肢体感皮层进行撞击后的0至3小时、1天、2天以及7天和14天进行磁共振成像(MRI)检查。在损伤诱导前以及在第2天、第7天和第14天进行MRI扫描前进行行为评估。在第14天进行尼氏染色,以证实从MRI检测到的损伤体积。与我们的假设相反,我们发现在中度TBI大鼠模型中,NBO治疗增加了损伤体积,并且对行为指标没有积极影响。我们的结果不支持在中度TBI患者中急性使用NBO。