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October 1969

Brain Edema: A Study of Biochemical and Structural Alterations

Author Affiliations

Chicago; Tokyo
From the Division of Neurological Surgery, Pritzker School of Medicine of the University of Chicago, Chicago (Drs. Sato, Yamaguchi, Mullan, and Evans); and the Department of Neurological Surgery, Juntendo University School of Medicine, Hongo, Tokyo (Dr. Ishii).

Arch Neurol. 1969;21(4):413-424. doi:10.1001/archneur.1969.00480160085010

THE SEARCH for the fundamental factors responsible for the rapid deterioration of cerebral function and for the development of cerebral edema following brain injury is now subject to investigation from the viewpoint of bioenergetics. This has been made possible to a large extent by the discovery of a technique for isolating brain mitochondria with tightly coupled oxidative phosphorylation.1 The examination of brain edema from this viewpoint should be illuminating, since the greater part of the energy available for cellular processes, including the maintenance of the membrane function so vital for intercellular and intracellular fluid control, is supplied by adenosine triphosphate (ATP) generated in oxidative phosphorylation.2,3

In the present study, biochemical changes associated with the in vivo and in vitro development of brain edema, ie, the impairment of oxidative phosphorylation and the alterations in fatty acid metabolism, have been carefully examined and correlated with structural changes in the