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• W2884274311 abstract "Traumatic brain injury (TBI) is a leading cause of morbidity and mortality throughout the world. Despite improvements in medical care, the current clinical TBI treatment is mainly supportive and no specific neuroprotective drugs are available. TBI arises from external forces applied to the head, resulting in immediate and irreversible damage, or ‘primary injury’. In addition, early and long-lasting secondary injury cascades are triggered. Many of the debilitating functional impairments observed in patients result from the potentially preventable ‘secondary injury’. Over-activation of N-methyl-D-aspartate receptors is thought to play a key role in secondary injury. Xenon is a noble gas and general anaesthetic that is a competitive inhibitor of the N-methyl-D-aspartate receptor at the glycine binding site.1–3 Xenon has been shown to be neuroprotective in models of brain ischaemia. Much less is known about the xenon effect in the context of TBI. Our work focused on evaluating xenon’s neuroprotective efficacy in the reproducible controlled cortical impact animal model of blunt TBI, which includes elements found after moderate to severe TBI in humans, such as contusional lesion, brain oedema, elevated intracranial pressure, and neurological impairment. Adult C57BL/6 male mice (n=196) were fixed in a stereotactic frame under anaesthesia (sevoflurane 3.5% and buprenorphine s.c. 0.1 mg/kg) and underwent a right parietal cortical impact, delivered by a custom-made electropneumatic impactor with a 3-mm-diameter flat tip perpendicular to the brain surface. Impact velocity of 8 m s–1, impact duration of 150 ms, and brain-penetration depth of 1.0 mm were used. Throughout the procedure, the core body temperature was monitored and feedback controlled. The animals were randomly assigned to control (75% nitrogen:25% oxygen) and xenon treated (30%, 50%, or 75% xenon:25% oxygen, balanced with nitrogen) groups. Short-term and long-term outcomes, both functional and histological, were measured by researchers blinded to the treatment. The statistical significance was assessed with one-way and two-way analyses of variance with Bonferroni’s post hoc test. Our study showed 75% xenon significantly (P<0.05) reduced the contusion volume 24 h after injury, and significantly (P<0.05) improved the neurological outcome up to 4 days after injury and clinically relevant locomotor parameters 1 month after injury. Xenon treatment significantly (P<0.05) reduced the contusion volume when given up to 3 h after injury, and significantly (P<0.05) improved the neurological outcome when given up to 1 h after injury. Significant (P<0.05) reductions in the contusion volume and improvement in the neurological outcome 24 h after injury were also achieved with 30% and 50% xenon concentrations. Our results show in an animal model of TBI that xenon improves the functional outcomes and reduces the contusion volume. We demonstrated both a reduction in the development of secondary injury and an improvement in long-term translationally relevant motor outcomes. Our findings, including the demonstration of long-term neuroprotection and a clinically relevant therapeutic time window, support the idea that xenon may be of benefit as a neuroprotective treatment in TBI patients. 1.Armstrong SP, Banks P, McKitrick TJW, et al. Anesthesiology 2012; 117: 38–472.Dickinson R, Peterson BK, Banks P, et al. Anesthesiology 2007; 107: 756–673.Franks NP, Dickinson R, de Sousa SL, Hall AC, Lieb WR. Nature 1998; 396: 324" @default.
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• W2884274311 date "2018-08-01" @default.
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• W2884274311 title "Xenon treatment improves short-term and long-term outcomes in a rodent model of traumatic brain injury" @default.
• W2884274311 doi "https://doi.org/10.1016/j.bja.2018.05.022" @default.
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