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A Study of Biochemical and Structural Alterations

Kiyoshi Sato, MD; Michio Yamaguchi, MD; Sean Mullan, MD; Joseph P. Evans, MD; Shozo Ishii, MD

Arch Neurol. 1969;21(4):413-424.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

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).

Footnotes
Submitted for publication March 27, 1969; accepted April 14.

Read in part before the annual meeting of the American Neurological Association, Washington, DC, June 17, 1968.

Reprint requests to Division of Neurological Surgery, University of Chicago Hospitals, 950 E 59th St, Chicago 60637 (Dr. Evans).

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