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J. Lipid Res.
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A more recent version of this article appeared on September 1, 2008

Papers In Press, published online ahead of print May 23, 2008
J. Lipid Res., doi:10.1194/jlr.M800200-JLR200
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Submitted on April 22, 2008
Revised on May 22, 2008
Accepted on May 23, 2008

Formation of eicosanoids, E2/D2-isoprostanes and docosanoids following decapitation-induced Ischemia, measured in high-energy microwaved rat brain

Santiago E. Farias, Mireille Basselin, Lisa Chang, Kim A. Heidenreich, Stanley I. Rapoport, and Robert C. Murphy

Pharmacology, University of Colorado Denver, Aurora, CO 80045-0511

Corresponding Author: robert.murphy{at}uchsc.edu

Inflammatory lipid mediators derived from arachidonic acid (AA) and docosahexaenoic acid (DHA) modify the pathophysiology of brain ischemia. The goal of this work was to investigate the formation of eicosanoids and docosanoids generated from AA and DHA, respectively, during no-flow cerebral ischemia. Rats were subjected to head-focused microwave irradiation 5 min following decapitation (complete ischemia) or prior to decapitation (controls). Brain lipids were extracted and analyzed by reverse phase liquid chromatography/tandem mass spectrometry. After complete ischemia, brain AA, DHA and docosapentaenoic acid concentrations increased 18-, 5- and 4-fold compared to controls, respectively. PGE2 and PGD2 could not be detected in control microwaved rat brain, suggesting little endogenous PGE2/D2 production in the brain in the absence of experimental manipulation. Concentrations of TXB2, E2/D2-isoprostanes, 5-HETE, 5-oxo-ETE, and 12-HETE were significantly elevated in ischemic brains. In addition, DHA products such as mono-, di- and tri-hydroxy-DHA were detected in control and ischemic brains. Mono-hydroxy-DHA, identified as 17-hydroxy-DHA and thought to be the immediate precursor of neuroprotectin D1, was 6.5-fold higher in ischemic than control brain. The present study demonstrated increased formation Eicosanoids, E2/D2-isoprostanes and docosanoids following cerebral ischemia. A balance of these lipid mediators may mediate immediate events of ischemic injury and recovery.


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