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From the Brain Edema Clinical Research Center, Department of Neurology, University of California, School of Medicine, San Francisco.
We studied the cerebral effects of oxygen-derived free radicals generated from the xanthine oxidase/ hypoxanthine/ADP-Fej3+ system. Xanthine oxidase/hypoxanthine/ADP-Fe3+ solution (0.1 ml) was infused into caudate putamen, and brain was frozen rapidly in situ. Brain water and sodium content increased concomitant with decreased potassium content at 24 hours and 48 hours after the infusion. The degree of brain edema and injury depended on the dose of xanthine oxidase. Spongy neuropil and neuronal cytoplasmic vacuoles were seen at 2 hours, with an infiltration by polymorphonuclear leukocytes at 24 hours, followed by lipid-laden macrophages and reactive astrocytes. Leakage of fluorescent dye into neuropil was seen at 2 hours, but not later. These data suggest that oxygen-derived free radicals damage endothelial cells of the blood-brain barrier; the brain injury is characterized by edema and by structural damage of neurons and giia.
Address correspondence and reprint requests to Dr. Chan, Department of Neurology, M-794, University of California, School of Medicine, San Francisco, CA 94143.
This work was supported by NIH grant NS-14543. Dr. J.W. Schmidley is the recipient of a Clinician-Scientist Award from the American Heart Association.
Accepted for publication June 21, 1983.
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