title: Early and sustained alterations in cerebral metabolism after traumatic brain injury in immature rats.
abstract: Although studies have shown alterations in cerebral metabolism after traumatic brain injury (TBI), clinical data in the developing brain is limited. We hypothesized that post-traumatic metabolic changes occur early (<24 h) and persist for up to 1 week. Immature rats underwent TBI to the left parietal cortex. Brains were removed at 4 h, 24 h, and 7 days after injury, and separated into ipsilateral (injured) and contralateral (control) hemispheres. Proton nuclear magnetic resonance (NMR) spectra were obtained, and spectra were analyzed for N-acetyl-aspartate (NAA), lactate (Lac), creatine (Cr), choline, and alanine, with metabolite ratios determined (NAA/Cr, Lac/Cr). There were no metabolic differences at any time in sham controls between cerebral hemispheres. At 4 and 24 h, there was an increase in Lac/Cr, reflecting increased glycolysis and/or decreased oxidative metabolism. At 24 h and 7 days, there was a decrease in NAA/Cr, indicating loss of neuronal integrity. The NAA/Lac ratio was decreased ( approximately 15-20%) at all times (4 h, 24 h, 7 days) in the injured hemisphere of TBI rats. In conclusion, metabolic derangements begin early (<24 h) after TBI in the immature rat and are sustained for up to 7 days. Evaluation of early metabolic alterations after TBI could identify novel targets for neuroprotection in the developing brain.
authors.affiliation: Department of Pediatrics, University of Maryland School of Medicine, 22 South Greene Street, Baltimore, MD 21201, USA.
authors.forename: Paula A
authors.initials: PA
authors.lastname: Casey
authors.forename: Mary C
authors.initials: MC
authors.lastname: McKenna
authors.forename: Gary
authors.initials: G
authors.lastname: Fiskum
authors.forename: Manda
authors.initials: M
authors.lastname: Saraswati
authors.forename: Courtney L
authors.initials: CL
authors.lastname: Robertson
mesh_terms: D000375:Aging / Q000378:metabolism*; D000409:Alanine / Q000032:analysis / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000032:analysis / Q000378:metabolism; D001921:Brain / Q000254:growth & development / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D019069:Cell Respiration; D002794:Choline / Q000032:analysis / Q000378:metabolism; D003401:Creatine / Q000032:analysis / Q000378:metabolism; D018450:Disease Progression; D004734:Energy Metabolism; D006019:Glycolysis; D019344:Lactic Acid / Q000032:analysis / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology; D010085:Oxidative Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline; D000409:Alanine