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* * * 迷路：半规管、前庭、耳蜗 外淋巴液：在骨迷路与膜迷路之间 内淋巴液：膜迷路内 * * 在我们临床常用的 Acta Otolaryngol Suppl. 1988;460:42-9. Cerebral antivasoconstrictive effects of flunarizine. Van Nueten JM, Janssens WJ. Janssen Research Council, Beerse, Belgium. Abstract Flunarizine is a selective Ca++-antagonist with weaker H1-histaminergic antagonistic properties. Flunarizine reduces vasospasm caused by an exaggerated Ca++-influx in depolarized arteries and by vasoactive substances released from aggregating platelets. This Ca++-antagonist also antagonizes the mutual amplification of the vasoconstrictor action of the platelet products. Flunarizine is particularly effective in the cerebral blood vessels, also when they are hyperreactive because of hypoxia. The compound does not interfere with normal arteriolar autoregulation or heart function. Thus flunarizine may be particularly effective in preventing vasospasm without lowering blood pressure or inducing a steal phenomenon. * Anesthesiology. 1986 Feb;64(2):215-24. Flunarizine, a calcium entry blocker, ameliorates ischemic brain damage in the rat. Deshpande JK, Wieloch T. Abstract The effects of flunarizine, a calcium entry blocker, were evaluated in a long-term survival model of ischemia in rats. One group of animals received the drug orally at 24 and 4 h prior to the insult (40 mg X kg-1 X dose-1). Another group was given flunarizine following the insult, intravenously at 5 min (0.1 mg X kg-1), and orally at 8 and 24 h (40 mg X kg-1 X dose-1). A third group received the solvent for the oral suspension on the same schedule as the pretreated group. Six animals from each group were subjected to 9 min ischemia and recovery of 7 days, at which time the brains were harvested for histologic study. In another six animals from each group, cortical metabolites and fatty acids were determined during early recirculation. Local cerebral blood flow was measured at 60 min recirculation in a third set of animals. Flunarizine significantly improved histological outcome