The Increase in Local Cerebral Glucose Utilization Following Fluid Percussion Brain Injury is Prevented with Kynurenic Acid and is Associated with an Increase in Calcium

  • D. A. Hovda
  • A. Yoshino
  • T. Kawamata
  • Y. Katayama
  • I. Fineman
  • D. P. Becker
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)


Immediately following a lateral fluid percussion brain injury, the cerebral cortex and hippocampus ipsilateral to the percussion show a marked accumulation of calcium and a pronounced increase in glucose metabolism. To determine if this increase in glucose metabolism was related to the indiscriminate release of the excitatory amino acid (EAA) glutamate, kynurenic acid (an EAA antagonist) was perfused into the cerebral cortex through a microdialysis probe for 30 min prior to injury. The results show that adding kynurenic acid to the extracellular space prior to trauma prevents the injury-induced increase in glucose utilization. These results indicate that calcium contributes to the ionic fluxes that are typically seen following brain injury and supports the concept of an increased energy demand upon cells to drive pumping mechanisms in order to restore membrane ionic balance.


Middle Cerebral Artery Occlusion Glucose Utilization Excitatory Amino Acid Cereb Blood Flow Kynurenic Acid 
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Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • D. A. Hovda
    • 2
  • A. Yoshino
    • 1
  • T. Kawamata
    • 1
  • Y. Katayama
    • 1
  • I. Fineman
    • 1
  • D. P. Becker
    • 1
  1. 1.Division of Neurosurgery, UCLA School of MedicineUniversity of California at Los AngelesUSA
  2. 2.Division of Neurosurgery, UCLA School of Medicine, CHS 74-140University of California at Los AngelesLos AngelesUSA

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