Abstract

The possibility was investigated that previously described changes in the pharmacologic behavior of the iris of the anti-ChE-treated eye are due to sympathetic inhibition of the sphincter muscle. Sympathetic influence was eliminated by sympathetic decentralization of one or both eyes prior to anti-ChE (anticholinesterase) treatment and/or by systemic administration of reserpine (cats) or chlorpromazine (cats and rabbits) or by intravitreal injection of guanethidine (rabbits) after prolonged treatment of the eyes with anti-ChE. Sympathetic decentralization of the eye did not prevent redilatation of the pupil during anti-ChE treatment. Sympathetic decentralization or the sympatholytic agents used did not inhibit light reflexes or reverse the anti-ChE-induced insensitivity of the iris to pilocarpine or carbachol. These results show that neither the sympathetic nervous system nor sympathetic neurotransmitters play a detectable role in anti-ChE-induced alterations in the pharmacologic behavior of the iris. it is concluded that, in the case of the iris, the site or sites of the anti-ChE-induced changes are the cholinergic receptors and/or the parasympathetic nerve terminals of the sphincter muscle.