Xylazine-induced mydriasis: possible involvement of a central postsynaptic regulation of parasympathetic tone.

Abstract

Intravenous injection of xylazine (0.01-1 mg/kg) produced a dose-dependent mydriasis associated with a depression of tonic ciliary nerve activity in anesthetized cats. Xylazine-induced mydriasis was apparent in the sympathectomized iris but was absent in the parasympathectomized, physostigmine-treated iris. Epinephrine (30 micrograms/kg, i.v.) produced a slightly greater mydriasis in the sympathectomized iris than in the parasympathectomized, physostigmine-treated iris. The alpha 2-adrenergic blocking agent, yohimbine (0.5 mg/kg, i.v.) antagonized the pupillary dilation and reversed the depression of ciliary nerve activity induced by xylazine administration. In rats pretreated with reserpine (7.5 mg/kg, s.c., 20 h) and alpha-methyl-p-tyrosine (250 mg/kg, i.p., 5 h), intravenous injection of xylazine (0.01-1 mg/kg) resulted in mydriasis of similar magnitude as control animals. However, xylazine induced bradycardia in the control group but not in the pretreated animals. The results suggest that pupillary dilation produced by i.v. xylazine is primarily the result of a central inhibition of parasympathetic tone to the iris. It also appears that xylazine produces this effect via postsynaptic alpha 2-adrenergic mechanisms, while it produces bradycardia through a presynaptic alpha 2-adrenergic mechanism.