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Nancy R. Clendenon, PhD; Norman Allen, MD; Takashi Komatsu, MD; Leopold Liss, MD; Wanda A. Gordon, MT; Karl Heimberger

Arch Neurol. 1971;25(5):432-448.

Abstract
The combined effects of unilateral vascular occlusion and anoxia resulted in a high yield of cerebral infarctions in rats with clinical evidence of hemiplegia. Our data support the hypothesis of a complex, consecutive series of biochemical events, gradually developing and culminating in infarction. Accumulation of fluid was detected by 15 minutes and evidence for mitochondrial fragmentation by one hour following the anoxic-ischemic insult. Lysosomal enzyme release either was minimal or occurred after three hours and would not appear to be a decisive factor in the pathogenesis of cell injury in nervous tissue. Complex alterations in glycogen metabolism were demonstrated on the infarcted side and in the adjacent cortex of the contralateral hemisphere. Endothelial swelling was noted at the small arteriole and capillary level and may contribute to the development and the severity of the injury.

Author Affiliations
Columbus, Ohio

From the Neurochemistry Section, Division of Neurology, and departments of medicine (Drs. Clendenon, Allen, and Komatsu, Mrs. Gordon and Mr. Heimberger) and neuropathology (Dr. Liss), Ohio State University Hospitals, Columbus, Ohio.

Footnotes
Accepted for publication May 22, 1971.

Reprint requests to Division of Neurology, Department of Medicine, Ohio State University Hospitals, Columbus, Ohio 43210 (Dr. Clendenon).

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