Li Q, Li B H
Department of Pharmacology, Jiangxi Medical College, Nanchang, China.
Zhongguo Yao Li Xue Bao. 1991 Sep;12(5):468-71.
The potentiation of motor activity caused by ephedrine (Eph) in mice was inhibited by prazosin but not by sulpiride. This potentiation effect caused by apomorphine (Apo) was not inhibited by prazosin. Apo produced stereotyped behavior (including sniffing, licking, and biting) in rodents, but Eph was ineffective except at the toxic dose (400 mg.kg-1 in mice, 200 mg.kg-1 in rats). Apo antagonized haloperidol-induced catalepsy in mice whereas Eph had no such effect. Severe vomiting was evoked by Apo in dogs, but not by Eph even when lethal dose (20 mg.kg-1) was used. Palpebral ptosis induced by prazosin was abolished by intracerebroventricular injection of Eph in mice, but not affected by Apo. The results suggest that the central stimulating action of Eph is mediated by alpha 1-adrenoceptors and not by dopamine receptors.
麻黄碱（Eph）引起的小鼠运动活性增强可被哌唑嗪抑制，但不被舒必利抑制。阿扑吗啡（Apo）引起的这种增强作用不被哌唑嗪抑制。Apo在啮齿动物中产生刻板行为（包括嗅、舔和咬），但Eph除了在中毒剂量（小鼠400 mg.kg-1，大鼠200 mg.kg-1）外无效。Apo可拮抗氟哌啶醇诱导的小鼠僵住症，而Eph没有这种作用。Apo可引起犬严重呕吐，但即使使用致死剂量（20 mg.kg-1）的Eph也不会引起呕吐。小鼠脑室内注射Eph可消除哌唑嗪诱导的睑下垂，但不受Apo影响。结果表明，Eph的中枢刺激作用是由α1-肾上腺素能受体介导的，而不是由多巴胺受体介导的。
