Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury

D. S. DeWitt, L. W. Jenkins, D. S. Prough

Research output: Contribution to journalReview article

73 Scopus citations

Abstract

Both experimental traumatic brain injury and clinical traumatic brain injury appear to render the brain more vulnerable to a second ischemic insult. The mechanisms of enhanced vulnerability to subsequent ischemia appear to include a reduced ability to increase cerebral blood flow in response to hypotension, hypoxemia, or acute anemia and increased tissue sensitivity to ischemia. Although numerous mediators may be involved in increased tissue sensitivity, those that particularly merit investigation include oxygen free radicals, glutamate, arachidonate metabolites, calcium ions, and protein kinase C.

Original languageEnglish (US)
Pages (from-to)376-383
Number of pages8
JournalNew Horizons: Science and Practice of Acute Medicine
Volume3
Issue number3
StatePublished - Jan 1 1995

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Keywords

  • cerebral blood flow
  • cerebral metabolism
  • excitotoxicity
  • free radicals
  • glutamate
  • ischemic brain injury
  • protein kinase C
  • superoxide dismutase
  • traumatic brain injury

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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