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Neuroprotective FK506 Does Not Alter In Vivo Nitric Oxide Production During Ischemia and Early Reperfusion in Rats
Author(s) -
Thomas J. K. Toung,
Anish Bhardwaj,
Valina L. Dawson,
Ted M. Dawson,
Richard J. Traystman,
Patricia D. Hurn
Publication year - 1999
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.30.6.1279
Subject(s) - medicine , neuroprotection , anesthesia , microdialysis , ischemia , nitric oxide , nitric oxide synthase , reperfusion injury , in vivo , infarction , saline , pharmacology , central nervous system , myocardial infarction , biology , microbiology and biotechnology
Previous studies have demonstrated that the immunosuppressant FK506 provides neuroprotection in experimental brain injury and suggest that this action may be mediated by suppression of neuronal nitric oxide synthase activation that occurs after ischemic depolarization. We sought to determine whether FK506 reduces histological injury after middle cerebral artery occlusion (MCAO) in the rat and whether the neuroprotective effect is mediated via suppression of in vivo nitric oxide (NO) production during ischemia or early reperfusion.

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