Glucose and oxygen metabolism after penetrating ballistic-like brain injury

Shyam Gajavelli, Shimoda Kentaro, Julio Diaz, Shoji Yokobori, Markus Spurlock, Daniel Diaz, Clayton Jackson, Alexandra Wick, Weizhao Zhao, Lai Y. Leung, Deborah Shear, Frank Tortella, Ross Bullock

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Traumatic brain injury (TBI) is a major cause of death and disability in all age groups. Among TBI, penetrating traumatic brain injuries (PTBI) have the worst prognosis and represent the leading cause of TBI-related morbidity and death. However, there are no specific drugs/interventions due to unclear pathophysiology. To gain insights we looked at cerebral metabolism in a PTBI rat model: penetrating ballistic-like brain injury (PBBI). Early after injury, regional cerebral oxygen tension and consumption significantly decreased in the ipsilateral cortex in the PBBI group compared with the control group. At the same time point, glucose uptake was significantly reduced globally in the PBBI group compared with the control group. Examination of Fluorojade B-stained brain sections at 24 hours after PBBI revealed an incomplete overlap of metabolic impairment and neurodegeneration. As expected, the injury core had the most severe metabolic impairment and highest neurodegeneration. However, in the peri-lesional area, despite similar metabolic impairment, there was lesser neurodegeneration. Given our findings, the data suggest the presence of two distinct zones of primary injury, of which only one recovers. We anticipate the peri-lesional area encompassing the PBBI ischemic penumbra, could be salvaged by acute therapies.

Original languageEnglish (US)
Pages (from-to)773-780
Number of pages8
JournalJournal of Cerebral Blood Flow and Metabolism
Volume35
Issue number5
DOIs
StatePublished - May 5 2015

Fingerprint

Brain Injuries
Oxygen
Glucose
Penetrating Head Injuries
Wounds and Injuries
Control Groups
Oxygen Consumption
Cause of Death
Age Groups
Traumatic Brain Injury
Morbidity
Brain
Pharmaceutical Preparations
Therapeutics

Keywords

  • 2-deoxy glucose
  • cerebral metabolism
  • Fluorojade B
  • glucose
  • neurodegeneration
  • oxygen

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Neurology

Cite this

Gajavelli, S., Kentaro, S., Diaz, J., Yokobori, S., Spurlock, M., Diaz, D., ... Bullock, R. (2015). Glucose and oxygen metabolism after penetrating ballistic-like brain injury. Journal of Cerebral Blood Flow and Metabolism, 35(5), 773-780. https://doi.org/10.1038/jcbfm.2014.243

Glucose and oxygen metabolism after penetrating ballistic-like brain injury. / Gajavelli, Shyam; Kentaro, Shimoda; Diaz, Julio; Yokobori, Shoji; Spurlock, Markus; Diaz, Daniel; Jackson, Clayton; Wick, Alexandra; Zhao, Weizhao; Leung, Lai Y.; Shear, Deborah; Tortella, Frank; Bullock, Ross.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 35, No. 5, 05.05.2015, p. 773-780.

Research output: Contribution to journalArticle

Gajavelli, S, Kentaro, S, Diaz, J, Yokobori, S, Spurlock, M, Diaz, D, Jackson, C, Wick, A, Zhao, W, Leung, LY, Shear, D, Tortella, F & Bullock, R 2015, 'Glucose and oxygen metabolism after penetrating ballistic-like brain injury', Journal of Cerebral Blood Flow and Metabolism, vol. 35, no. 5, pp. 773-780. https://doi.org/10.1038/jcbfm.2014.243
Gajavelli, Shyam ; Kentaro, Shimoda ; Diaz, Julio ; Yokobori, Shoji ; Spurlock, Markus ; Diaz, Daniel ; Jackson, Clayton ; Wick, Alexandra ; Zhao, Weizhao ; Leung, Lai Y. ; Shear, Deborah ; Tortella, Frank ; Bullock, Ross. / Glucose and oxygen metabolism after penetrating ballistic-like brain injury. In: Journal of Cerebral Blood Flow and Metabolism. 2015 ; Vol. 35, No. 5. pp. 773-780.
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