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Xylazine‐induced mydriasis: possible involvement of a central postsynaptic regulation of parasympathetic tone
Author(s) -
HSU W. H.,
BETTS D. M.,
LEE P.
Publication year - 1981
Publication title -
journal of veterinary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.527
H-Index - 60
eISSN - 1365-2885
pISSN - 0140-7783
DOI - 10.1111/j.1365-2885.1981.tb00731.x
Subject(s) - mydriasis , xylazine , tone (literature) , neuroscience , postsynaptic potential , anesthesia , medicine , psychology , philosophy , ketamine , receptor , linguistics
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 μg/kg, i.v.) produced a slighdy greater mydriasis in the sympathectomized iris than in the parasympathectomized, physostigmine‐treated iris. The α 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 α‐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 die pretreated animals. The results suggest that pupillary dilation produced by i.v. xylazine is primarily die result of a central inhibition of parasympathetic tone to the iris. It also appears that xylazine produces this effect via postsynaptic α 2 ‐adrenergic mechanisms, while it produces bradycardia through a presynaptic α 2 ‐adrenergic mechanism.