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Failure of Iron Chelators to Protect Against Cerebral Infarction in Hypoxia-Ischemia

Published online by Cambridge University Press:  18 September 2015

V. MacMillan*
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.); and Departments of Biochemistry (I.F.) and Medicine (Neurology) (J.D.), Duke University, Durham, U.S.A.
I. Fridovich
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.); and Departments of Biochemistry (I.F.) and Medicine (Neurology) (J.D.), Duke University, Durham, U.S.A.
J. Davis
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.); and Departments of Biochemistry (I.F.) and Medicine (Neurology) (J.D.), Duke University, Durham, U.S.A.
*
Room 6366, Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S IA8
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Abstract:

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In this study the ability of iron chelators to attenuate hypoxic-ischemic brain damage was assessed in hyperglycemic rats that were exposed to 1% carbon monoxide and right carotid occlusion. The animals received deferoxamine (50 mg/kg), manganese-deferoxamine (50 mg/kg) or vehicle i.p. 0.5 h prior to hypoxemic-ischemic exposure and at 0.5, 3 and 24 h post-exposure; with subsequent histological examination of the brain at 7 days recovery. The area of cerebral infarction was measured at three levels using video imaging methods. The mean percentage of total hemisphere that was infarcted in the three groups was: vehicle — 28.5 ± 5.0; deferoxamine — 31.7 ± 12.1; and manganese deferoxamine — 30.6 ± 6.8 (p - n.s.). The results as obtained in this preliminary study indicate that aggressive pre- and post-treatment with iron chelators has no ability to attenuate cerebral infarction in this model.

Type
Research Article
Copyright
Copyright © Canadian Neurological Sciences Federation 1993

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