Paakkari I, Puurunen J
Eur J Pharmacol. 1984 Oct 15;105(3-4):223-8. doi: 10.1016/0014-2999(84)90613-7.
Prazosin at doses of 100 or 1000 nmol/kg i.v. induced bradycardia in urethane-anaesthetized rats. The bradycardia was completely abolished by atropine pretreatment or vagotomy. Prazosin also stimulated gastric acid secretion. This effect was completely abolished by vagotomy. The maximal hypotensive effect after prazosin i.c.v. occurred 10 min later than with i.v. administration. It is concluded that prazosin possesses vagal a stimulating property that may in part explain its modest tachycardiac effect seen in clinical use. The mechanism of vagal stimulation by prazosin remains unclear. The present findings suggest that prazosin does not exert any direct effects on central vagal structures accessible from the ventricular space.
静脉注射剂量为100或1000 nmol/kg的哌唑嗪可使氨基甲酸乙酯麻醉的大鼠出现心动过缓。预先给予阿托品或切断迷走神经可完全消除这种心动过缓。哌唑嗪还能刺激胃酸分泌。切断迷走神经可完全消除这种作用。脑室内注射哌唑嗪后的最大降压作用比静脉注射晚10分钟出现。结论是，哌唑嗪具有刺激迷走神经的特性，这可能部分解释了其在临床应用中出现的适度心动过速效应。哌唑嗪刺激迷走神经的机制尚不清楚。目前的研究结果表明，哌唑嗪对可从脑室空间进入的中枢迷走神经结构没有任何直接作用。
