Abstract
Ischemic brain damage is seen as a common feature in many pathological conditions such as ischemic stroke, subarachnoid hemorrhage, head injury, and prolonged seizures [1]. A number of animal studies have shown that there is a marked increase in the extracellular concentrations of glutamate under such conditions [2–7]. The neuroprotective effects of glutamate antagonists have also been demonstrated in the animal models of ischemia and head injury [1, 8], and thus it has been suggested that these conditions share a common injury mechanism, that is, glutamate neurotoxicity.
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© 1995 Springer-Verlag Tokyo
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Fujisawa, H., Landolt, H., Bullock, R. (1995). Glutamate Neurotoxicity As a Mechanism of Ischemic Brain Damage: A Basic Study Using a New In Vivo Model. In: Tsubokawa, T., Marmarou, A., Robertson, C., Teasdale, G. (eds) Neurochemical Monitoring in the Intensive Care Unit. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68522-7_2
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DOI: https://doi.org/10.1007/978-4-431-68522-7_2
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