Fischer Wolfgang, Kittner Holger, Regenthal Ralf, De Sarro Giovambattista
Rudolf-Boehm-Institute of Pharmacology and Toxicology, University of Leipzig, Leipzig, Germany.
Basic Clin Pharmacol Toxicol. 2004 Feb;94(2):79-88. doi: 10.1111/j.1742-7843.2004.pto940205.x.
The present study will summarize our findings concerning the anticonvulsant properties of the Ca2+ channel blocker flunarizine in a variety of experimental models of epilepsy. Flunarizine exhibits anticonvulsant effects against tonic seizures induced by electroshock or various chemoconvulsants in mice, however, did not protect against pentylenetetrazol-induced clonic seizures. In the MES test, the efficacy of clinically established antiepileptics was increased by co-medication. In the rotarod test, a minimal "neurotoxic" dose (TD50) of 18.0 mg/kg intraperitoneally was determined. In models of complex partial seizures like the hippocampal stimulation and the amygdala kindling in rats, flunarizine showed only a moderate activity. Thus, it can be suggested that the anticonvulsant potency of flunarizine in various screening tests is lower than that of standard antiepileptics such as carbamazepine and phenytoin. Concerning the possible mode of action, whole-cell patch-clamp experiments with cultured neonatal rat cardiomyocytes showed that flunarizine depressed the fast inward Na+ current in a concentration- and frequency-dependent manner well comparable with the action of phenytoin. It is concluded that the use-dependent inhibition of voltage-dependent Na+ channels may essentially contribute to the anticonvulsant activity of flunarizine in models for generalized tonic-clonic seizures. The clinical efficacy as add-on therapy is critically discussed in view of the present data.
本研究将总结我们关于钙离子通道阻滞剂氟桂利嗪在多种癫痫实验模型中的抗惊厥特性的研究结果。氟桂利嗪对电休克或各种化学惊厥剂诱导的小鼠强直性惊厥具有抗惊厥作用,然而,对戊四氮诱导的阵挛性惊厥没有保护作用。在最大电休克(MES)试验中,联合用药可提高临床已确立的抗癫痫药物的疗效。在转棒试验中,确定腹腔注射的最小“神经毒性”剂量(TD50)为18.0mg/kg。在大鼠海马刺激和杏仁核点燃等复杂部分性发作模型中,氟桂利嗪仅表现出中等活性。因此,可以认为氟桂利嗪在各种筛选试验中的抗惊厥效力低于卡马西平和苯妥英等标准抗癫痫药物。关于其可能的作用方式,对培养的新生大鼠心肌细胞进行的全细胞膜片钳实验表明,氟桂利嗪以浓度和频率依赖性方式抑制快速内向钠电流,这与苯妥英的作用相当。得出的结论是,电压依赖性钠通道的使用依赖性抑制可能在很大程度上促成了氟桂利嗪在全身强直-阵挛性发作模型中的抗惊厥活性。鉴于目前的数据,对其作为附加疗法的临床疗效进行了批判性讨论。