Gherezghiher T, Koss M C
Eur J Pharmacol. 1979 Aug 1;57(2-3):263-6. doi: 10.1016/0014-2999(79)90376-5.
Pupillary responses to clonidine (3--100 micrograms/kg, i.v.) and epinephrine (1--30 micrograms/kg, i.v.) were observed in anesthetized rats. Clonidine caused a dose-dependent mydriasis which was effectively antagonized by pretreatment with yohimbine (1.5 mg/kg, i.v.). Pretreatment with phentolamine (5 mg/kg, i.v.) was less effective in antagonizing this clonidine-induced mydriasis. Phenoxybenzamine (2 mg/kg, i.v.) was almost without effect. In contrast, both phentolamine and phenoxybenzamine blocked the pupillary dilation produced by epinephrine while yohimbine pretreatment resulted in no antagonism of epinephrine-induced mydriasis. These results suggest that clonidine-induced mydriasis in the rat is mediated by a central adrenergic inhibitory mechanism.
在麻醉大鼠中观察了可乐定(3 - 100微克/千克,静脉注射)和肾上腺素(1 - 30微克/千克,静脉注射)对瞳孔的反应。可乐定引起剂量依赖性散瞳,预先静脉注射育亨宾(1.5毫克/千克)可有效拮抗这种散瞳作用。预先静脉注射酚妥拉明(5毫克/千克)对拮抗可乐定引起的散瞳作用效果较差。苯苄胺(2毫克/千克,静脉注射)几乎没有作用。相反,酚妥拉明和苯苄胺都能阻断肾上腺素引起的瞳孔扩张,而预先注射育亨宾对肾上腺素引起的散瞳没有拮抗作用。这些结果表明,大鼠中可乐定引起的散瞳是由中枢肾上腺素能抑制机制介导的。