Summary
Potential involvement of neuroexcitatory mechanisms was studied in: 1) repetitive forebrain ischaemia in gerbils, 2) global cerebral ischaemia in rats and 3) cryogenic injury to the cerebral cortex in rats and gerbils. Uptake of 45Ca was used as a marker of injury, whereas ultrastructural localization of calcium was assessed with an oxalate-pyroantimonate method. The blood-brain barrier was evaluated with immunostaining for serum albumin. Changes in extracellular glutamate were estimated by microdialysis and an enzymatic cycling assay. Changes in water content were assessed by specific gravity measurements.
Repetitive ischaemia of 3 × 5 min carotid occlusions produced a cumulative effect with regard to development of oedema and neuronal injury. This was associated with several-fold increments in glutamate release after repeated insults, whereas there was no apparent correlation with energy metabolism disturbances. Other studies revealed in all models a development of secondary foci distant to the primary impact of ischaemia or cold lesions, which were characterized by calcium accumulation in swollen dendrites, chronic neuronal changes and intraneuronal uptake of serum proteins, all of these changes being potentially compatible with involvement of neuroexcitatory mechanisms.
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© 1990 Springer-Verlag
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Saito, N. et al. (1990). Role of Neuroexcitation in Development of Blood-Brain Barrier and Oedematous Changes Following Cerebral Ischaemia and Traumatic Brain Injury. In: Reulen, HJ., Baethmann, A., Fenstermacher, J., Marmarou, A., Spatz, M. (eds) Brain Edema VIII. Acta Neurochirurgica, vol 51. Springer, Vienna. https://doi.org/10.1007/978-3-7091-9115-6_63
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DOI: https://doi.org/10.1007/978-3-7091-9115-6_63
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