摘要
双侧脑室注射普鲁卡因酰胺(每侧200或400μg/每只小鼠),可不同程度地减轻小鼠的士的宁(1.5mg/kg)、异烟肼(275mg/kg)、氨基脲(200mg/kg)所致惊厥的发作强度,并延缓药物性惊厥所致死亡的时间。侧脑室注射异搏停(每侧10μg)无效。结果提示抑制钠内流,使细胞膜稳定可能是普鲁卡因酰胺抗惊厥机制之一;也提示神经膜上钠通透性异常与癫痫发作有关。癫痫发作与膜的慢钙通道无直接关系。
Procainamide,blocker of membrane sodium channels,injected intra- cerebroventricularly (icy) (200 or 400 μg/mouse bilaterally) reduced the severity of seizures induced by strychnine (1.5mg/kg),isoniazid (275mg/ kg)and semicarbazide (200mg/kg) in mice and delayed their death ind- uced by seizure.But injecting Ca-antagonists (Verapamil and nifedipine) was not effective.These results suggest that blocking the Na inward current to cause membrane stabilization is possibly one of the anticon- vulsant mechanisms,and that epileptic seizure is related to alteration in neuronal permeability to sodium but not directly related to slow calsium channels.
出处
《江西医学院学报》
1989年第1期9-13,共5页
Acta Academiae Medicinae Jiangxi
关键词
药物性惊厥
普鲁卡因酰胺
异博停
抗惊厥药物
作用机制
动物实验
procainamids/antagonists & inhibitors
verapamil/antagonists & inhibitors
convulsions/drug therapy
strychnine
isoniazide
semicarbazides
animals
laboratry
mice