作者: Charles Palmer , Sharon L. Menzies , Rebecca L. Roberts , Geno Pavlick , James R. Connor
DOI: 10.1002/(SICI)1097-4547(19990401)56:1<60::AID-JNR8>3.0.CO;2-A
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摘要: Iron can contribute to hypoxic-ischemic brain damage by catalyzing the formation of free radicals. The immature has high iron levels and limited antioxidant defenses. objective this study was describe early alterations in nonheme histochemistry following a (HI) insult neonatal rats. We induced HI right cerebral hemisphere groups 7-day-old Rats were anesthetized, then their brains perfused fixed at 0, 1, 4, 8, 24 hr, 2, 3 weeks recovery. Forty-micron-thick frozen sections stained for using intensified Perls stain. Increased staining first detected within cytoplasm cells with pyknotic nuclei 4 hr Staining increased rapidly over regions ischemic injury. By 7 days recovery, reactive glia cortical blood vessels also stained. gray matter persisted whereas white tracts had fewer iron-positive compared normal. increase could be caused an accumulation posthypoxicischemic injury or change from nonstainable heme stainable iron. Regardless source, our results indicate that there is available promote oxidant stress rat hypoxia-ischemia.