Evidence for free radical mechanisms of brain injury resulting from ischemia/reperfusion-induced events. J Neurotrauma 1992 Mar;9 Suppl 1:S157-63
Date
03/01/1992Pubmed ID
1588606Scopus ID
2-s2.0-0026573374 (requires institutional sign-in at Scopus site) 44 CitationsAbstract
Free radicals have been implicated in the injury that occurs to brain tissue in response to ischemia and reperfusion insults. Confirmatory in vivo studies have been limited by the difficulty in measuring free radicals in brain tissue. This review discusses potential mechanisms for free radical production in brain tissue and the evidence supporting the therapeutic efficacy of free radical scavengers. Free radicals may be produced during ischemia/reperfusion as a result of multiple mechanisms involving normal regulatory systems of intra-/extracellular metabolism. For example, metabolism of free fatty acids by the cyclo-oxygenase pathway and adenine nucleotides by xanthine oxidase has been proposed to produce free radical adducts during reperfusion. Therapeutic strategies aimed at decreasing brain injury from free radical production include administration of free radical scavengers at the time of reperfusion. Pharmacologic interventions for protection from free radical injury in brain are hindered because of limited access to the site of free production.
Author List
Kirsch JR, Helfaer MA, Lange DG, Traystman RJMESH terms used to index this publication - Major topics in bold
AnimalsBrain
Brain Injuries
Brain Ischemia
Deferoxamine
Free Radical Scavengers
Free Radicals
Leukocytes
Reperfusion Injury
Vitamin E
