Citation

DeWitt DS, Jenkins LW, Prough DS. New Horiz. 1995; 3(3): 376-383.

Affiliation

Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555-0591, USA.

Copyright

(Copyright © 1995, Williams and Wilkins and the Society)

DOI

unavailable

PMID

7496745

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.

Language: en