Stroke, Vol 18, 623-628, Copyright © 1987 by American Heart Association
O Kempski, M Zimmer, A Neu, F von Rosen, M Jansen and A Baethmann
Volume regulation of C6 glial cells was studied in anoxia in vitro to
improve the understanding of ischemic cell swelling in the brain. Contrary
to in vivo conditions, anoxia or anoxia plus iodoacetate for additional
inhibition of anaerobic energy metabolism did not induce glial swelling.
However, intracellular K+ was markedly decreased while intracellular Na+
increased. Induction of energy failure by anoxia plus iodoacetate was found
to prevent the regulatory volume decrease on hyposmotic exposure of the
cells, which is regularly observed in normoxic control conditions.
Hyposmotic exposure in anoxia plus iodoacetate led only to an initial
tendency of cell volume normalization followed by secondary cell swelling.
This was associated with a net increase of intracellular Na+ that may
explain the failure of volume regulation under these circumstances.
Maintenance of a normal glial cell size during complete energy deprivation
by anoxia plus iodoacetate in isotonic medium strongly indicates that
energy failure per se does not suffice to induce cell swelling. Cell
swelling in cerebral ischemia in vivo thus is likely to require additional
mechanisms, most likely an increase of membrane permeability to Na+, which
may be caused by release and accumulation of excitotoxins such as glutamate
or by an extracellular release of K+. Such a mechanism would hardly
influence the extracellular homeostasis in vitro due to the large
medium-to-cell volume ratio. The findings demonstrate, nonetheless, the
significance of a competent energy metabolism to support cell volume
regulation. This is concluded from the failure of regulatory volume
decrease of hypotonically suspended glial cells in anoxia plus
iodoacetate.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling
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