Abstract
Neuronal death after cerebral ischemia is mediated by a massive release of excitatory amino acids and generation of free radicals. Calcium influx into cells is considered to be a crucial step of the deleterious cascade triggered by ischemia. Magnesium competes with calcium to reduce calcium entry into cells, blocks voltage-sensitive and N-methyl-d-aspartate-activated ion channels, and inhibits the release of excitatory amino acids. The 21-amino steroid tirilazad is a well-known antioxidant. We speculated that combined administration of these clinically available drugs might be superior to current monotherapy.
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© 1999 Springer-Verlag Berlin Heidelberg
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Schmid-Elsaesser, R., Hungerhuber, E., Zausinger, S., Baethmann, A., Reulen, HJ. (1999). Neuroprotective Effects of Magnesium and Tirilazad in Rats Subjected to Transient Focal Cerebral lschemia. In: Ito, U., Fieschi, C., Orzi, F., Kuroiwa, T., Klatzo, I. (eds) Maturation Phenomenon in Cerebral Ischemia III. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58602-6_43
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DOI: https://doi.org/10.1007/978-3-642-58602-6_43
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-65023-2
Online ISBN: 978-3-642-58602-6
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