Abstract

Evidence is presented that stimulation of the cervical sympathetic nerve or of its end-plates can produce in the corresponding eye a slight but significant dilatation of the pupil previously constricted to a slit by ergotoxine. Furthermore, this dilatation occurs more frequently if faradization immediately follows elimination of parasympathetic control of the sphincter by atropine. Since ergotoxine constriction is produced by paralysis of the motor sympathetic terminations in the dilator pupillae and by direct muscular action on the sphincter, dilatation under sympathomimetics or by faradization of the cervical sympathetic nerve can be explained either on the supposition that incomplete occlusion of motor sympathetic impulses had been produced by the dosage of ergotoxine employed, or on the supposition that this nerve exhibits an inhibitory effect on the iris sphincter.

From the data presented, the latter supposition seems most plausible. Thus, explanation of mydriasis under sympathomimetic agents necessitates the inclusion of inhibitory sympathetic innervation of the sphincter as well as motor sympathetic innervation of the dilator muscles of the iris.