Citation

Katayama Y, Mori T, Maeda T, Kawamata T. Acta Neurochir. Suppl. 1998; 71: 289-292.

Affiliation

Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.

Copyright

(Copyright © 1998, Holtzbrinck Springer Nature Publishing Group)

DOI

unavailable

PMID

9779210

Abstract

The non-hemorrhagic mass effect of cerebral contusions is commonly attributed to vasogenic edema and/or cytotoxic edema (cellular swelling). We propose that a marked increase in osmolality within the contusion necrosis proper, in which the cellular elements uniformly undergo shrinkage, disintegration and homogenation, represents an important and unique mechanism underlying the contusion edema. The present study demonstrates in a rat model of cerebral contusion, that 1) the osmolality of the contused brain tissue increases rapidly, 2) the increase in osmolality is not caused by changes in inorganic ion contents, suggesting a metabolic production of osmoles or release of idiogenic osmoles, and 3) the contused brain tissue strongly attracts water, provided that blood supply is maintained. We suggest that the primary driving force of water accumulation into contused brain tissue is the elevated colloid osmotic potential of contusion necrosis.

Language: en