Abstract
The intravenous injection of calcium exerts a pronounced effect upon the mechanism of pupilary constriction. The solution employed was m/8 CaCl2; this was injected slowly through the external jugular vein of rabbits; in some instances the ear veins were used. After 12 to 14 c.c. of the solution had run in, stimulation of the cervical sympathetic nerves no longer caused dilatation of the pupil. At the same time, the pupil appeared to be smaller than normal and reacted less readily to light. When 20 to 25 c.c. had entered, the pupils, as a rule, became almost pinpoint in size. If the infusion was now stopped, the pupils remained contracted for about thirty minutes, and usually about two hours elapsed before the pupils again reached their normal size. There were some exceptions in which a larger dose had to be infused before the pupil showed a distinct reaction to the calcium, and then the contraction did not become maximal. These exceptions seemed to occur when the rabbits were under profound ether anesthesia.
Atropin did not prevent this calcium myosis, but it retarded somewhat the onset of this myosis and hastened its disappearance after stoppage of the calcium infusion. Instillations of atropin into the conjunctival sac were a little more effective than intravenous injections. As far as we know calcium is the only substance which is able to overcome the full mydriatic effect of atropin.
What was said of atropin holds good, in general, also for cocaine; calcium overcomes the mydriatic effect of cocaine, but to a less extent than that of atropin. The mydriatic effect of the cocaine becomes especially active during the onset and the later period of the calcium myosis.
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