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Compdon-induced brain edem

Modification by prior depletion and supplementation of vitamin E

Cerebral Vascular Disease Research Center and the Department of Neurology, University of Miami School of Medicine (Drs. Yoshida, Ginsberg, Abe, Martinez, Watson, and Scheinberg, and Mr. Busto), Miami, FL, and the Analytical Research Laboratory, Eisai Company (Dr. Abe), Ltd, Tokyo, Japan.

We studied the degree of edema resulting from focal brain compression in rats raised on vitamin E-deficient, -normal, or -supplemented diets. After release of 24 hours of epidural compression, edema developed ipsilaterally and was characterized by extravasation of serum protein, increased water and sodium content, and little change in potassium. The degree of swelling and increase of sodium in the previously compressed area were most pronounced in the vitamin E-deficient group and mildest in the vitamin E-supplemented group. Degradative processes of biomembranes seem to participate in the pathogenesis of brain edema; vitamin E may stabilize membranes by physicochemical interactions between the phytyl side chain and polyunsaturated phospholipids, or vitamin E may disrupt chains of free radical reactions.

Address correspondence and reprint requests to Dr. Yoshida, Department of Neurology (D4-51, University of Miami School of Medicine, Miami, FL 33101.

Presented in part at the thirty-fourth annual meeting of the American Academy of Neurology, Washington, DC, April 1982.

This work was supported by USPHS Grant No. NS 05820.

Accepted for publication June 15, 1982

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