Smith S E, Lekieffre D, Sowinski P, Meldrum B S
Department of Neurology, Institute of Psychiatry, Denmark Hill, UK.
Neuroreport. 1993 Sep 30;4(12):1339-42. doi: 10.1097/00001756-199309150-00013.
BW619C89 (4-amino-2-(4-methylpiperazin-l-yl)-5-(2,3,5-trichlorophenyl) pyrimidine) was evaluated for cerebroprotection after focal or global ischaemia. BW619C89, as the mesylate dihydrate salt, 20 mg kg-1, i.v. for 10 min immediately, or with a 1 h delay after permanent middle cerebral artery occlusion in Fischer rats reduces cortical infarct volume (visualized with (2,3,5-triphenyltetrazolium) by 49% (p < 0.05) or by 61% (p < 0.001) and improves neurological deficit. Administration of BW619C89 with a 2 h delay is ineffective. BW619C89, given i.p. 0 and 4 h after 20 min of transient bilateral common carotid artery occlusion in vertebral artery-occluded Wistar rats reduces glutamate release and neuronal cell loss in the hippocampal CA1 sector (p < 0.01) and striatum (p < 0.05). BW619C89 resembles BW1003C87 (5-(2,3,5-trichlorophenyl)-2,4-diaminopyrimidine) in inhibiting veratrine-induced glutamate release and protecting against ischaemic brain damage.
对BW619C89（4-氨基-2-(4-甲基哌嗪-1-基)-5-(2,3,5-三氯苯基)嘧啶）在局灶性或全脑缺血后的脑保护作用进行了评估。BW619C89以甲磺酸盐二水合物盐的形式，20mg/kg静脉注射10分钟，在Fischer大鼠永久性大脑中动脉闭塞后立即给药或延迟1小时给药，可使皮质梗死体积（用(2,3,5-三苯基四氮唑)可视化）减少49%（p<0.05）或61%（p<0.001），并改善神经功能缺损。延迟2小时给药则无效。在椎动脉闭塞的Wistar大鼠双侧颈总动脉短暂闭塞20分钟后0小时和4小时腹腔注射BW619C89，可减少海马CA1区（p<0.01）和纹状体（p<0.05）的谷氨酸释放和神经元细胞丢失。BW619C89在抑制藜芦碱诱导的谷氨酸释放和预防缺血性脑损伤方面与BW1003C87（5-(2,3,5-三氯苯基)-2,4-二氨基嘧啶）相似。
