Neuroprotective Effects of Magnesium and Tirilazad in Rats Subjected to Transient Focal Cerebral lschemia

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.