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A Baethmann

Publications and source records attributed to A Baethmann.

169 records · Page 10Linked to original sources
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Molecular mechanisms of glial swelling in vitro.

The pathophysiological chain of events occurring during cerebral ischemia is still poorly understood on a molecular level. Therefore, an in vitro model to study glial swelling mechanisms, using C6 glial cells under controlled extracellular conditions, has been established. Flow cytometry serves to determine even small cell volume changes. In this report, the effects of anoxia and acidosis on glial swelling are summarized. Anoxia alone, or in combination with iodoacetate to inhibit anaerobic glycolysis, did not cause an increase of glial volume for up to 2 h. Acidification of the incubation medium below pH 6.8, on the other hand, was immediately followed by cell swelling to 115% of normal. Amiloride or the absence of bicarbonate and Na+ in the medium significantly reduced glial swelling. The data support the contention that swelling results from an activation of the Na+/H+-antiporter to control intracellular pH. It is suggested that swelling in an ischemic penumbra is promoted by this mechanism. Therapeutic approaches to control cerebral pH might be useful to protect brain tissue in cerebral ischemia.

Acidosis↗
PubMedDate not supplied

Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling.

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)

Cell Line↗