Abstract
The structure, properties, and range of therapeutic action of flunarizine are reviewed, and data from several studies are presented to support the general thesis that flunarizine in therapeutic doses acts to normalize damaged or abnormal brain tissue, but has little or no effect on normal brain tissue. When flunarizine was administered systemically in a single i.p. dose (40 mg/kg) or divided in oral doses (30 mg/kg preload, then 10 mg/kg) to 200–250 g male Wistar rats, the threshold for initiation of a spreading depression was increased by flunarizine treatment only in rats in which the cortex had been injured. When global ischemia was induced by cardiac arrest, the rise in extracellular potassium was delayed by both flunarizine and phenytoin. Flunarizine did not affect the release of potassium ion by repetitive electrical stimulation in normal cerebral cortex or the distribution of current-induced potassium translocation within normal cortex. These results support the designation of flunarizine as a “calcium overload blocker” that acts to protect damaged cells from excessive entry of calcium. Flunarizine may be a useful adjunct in the management of cerebral trauma.
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