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The Role of a Factor in Brain Supernatant in the Prevention of Edema

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

Arch Neurol. 1970;22(6):521-527.

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

IT HAS BEEN suggested in a previous paper¹ that the biological function of the mitochondria in brain tissue decreases in association with the initiation and the development of brain edema. The mechanism of the impairment in mitochondrial function has been partially elucidated by many workers in the general biochemical field. It has also been found that the long-chain, free, fatty acids present in various tissues under physiological conditions can serve as a strong uncoupler in oxidative phosphorylation. Some investigators, on the other hand, have claimed that decay of mitochondrial function occurs independently, with an accumulation of free fatty acids.

We, therefore, undertook a more detailed study of this phenomenon in the hope of gaining information concerning the cause and the mechanism of swelling of brain tissue.

Tightly coupled mitochondria were isolated from fresh rat brain and were aged in vitro at 30 C in order to simplify the . . . [Full Text PDF of this Article]

Author Affiliations
Chicago; Tokyo

From the Division of Neurological Surgery, University of Chicago Hospitals, Chicago, and the Department of Neurosurgery, Juntendo University School of Medicine, Tokyo (Dr. Ishii).

Footnotes
Submitted for publication Aug 5, 1969; accepted Oct 25.

Read in part before the 93rd annual meeting of the American Neurological Association, Washington, DC, June 17, 1968.

Reprint requests to Division of Neurological Surgery, University of Chicago Hospitals, Chicago 60637 (Dr. Evans).

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