Normobaric oxygen worsens outcome after a moderate traumatic brain injury

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

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1137-1144
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Volume35
Issue number7
DOIs
StatePublished - Jul 1 2015

Keywords

  • MRI
  • TBI
  • mitochondria
  • normobaric oxygen
  • oxidative stress
  • vasogenic edema

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

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