• Lora Talley Watts, Justin Alexander Long, Venkata Hemanth Manga, Shiliang Huang, Qiang Shen, and Timothy Q Duong.
• 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.
• J. Cereb. Blood Flow Metab. 2015 Jul 1;35(7):1137-44.

AbstractTraumatic 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.

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