Calciumstabilizing Agents

Cell death cascades in ischemic stroke are mediated, in part, by excessive calcium influx resulting from activation of glutamate receptors and voltage-dependent calcium channels (VDCC). In addition, the function of Ca2+-ATPases is compromised, resulting in prolonged elevation of the intracellular calcium concentration. Drugs that block glutamate receptors (MK-801, for example) or VDCC (nimodipine and flunarazine, for example) have proven effective in rodent models of stroke. At least 14 clinical trials of nimodipine in ischemic stroke were conducted beginning in the mid 1980s. Nine trials found no effect, one trial found short-term worsened outcome with treatment, and four trials found positive outcomes (Danton and Dietrich, 2004). Clinical trials with flunarizine found no statistically significant improvement in outcome. Despite this discouraging analysis, dantrolene, which blocks ryanodine receptors, recently has been discussed for clinical trails as the result of beneficial effects in rodent stroke models (Zhang et al., 1993).

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