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1 Departments of Anesthesia and Pharmacology, College of Medicine, State University of Iowa, Iowa City, Iowa
The mechanism of the sympathomimetic response of the cat's iris to nicotine was studied. Intracarotid injections of nicotine, 75 µg/kg, produced transient, ipsilateral mydriasis. This response was inhibited by phentolamnine, bretylium, tolazohine, phenoxybezamine, reserpine and guanethidine. Removal of the ciliary and superior cervical ganglia did not affect the mudriatic response to nicotine although, in this situation, it was inhibited by hexamethonium, tetramethylamonium and hemicholium.
The possibility of an underlying cholinergic mechanism was investigated. There was no pharmacological evidence for the presence of cholinergic fibers in the postganglionic sympathetic pathway to the iris. After acute removal of the superior cervical ganglion, atropine and neostigmine did not modify the response of the pupil to nicotine. Atropine inhibited the mydriatic response to nicotine after chronic removal of both superior cervical ganglia. This action of atropine may have been due to an ability of the drug to inhibit the response of the chronically denervated iris to norepineprine.
The sympathomimetic response to nicotine was dependent on the release of catecholamines from postganglionic sympathetic fibers supplying the iris. It is suggested that there may be ramifying sympathetic gamglia distal to the superior cervical ganglion. The excision of the latter structure may not have produced complete sympathectomy, and nicotine may have caused mydriasis by stimutation of these "ganglia."
Accepted on October 7, 1964