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Article
May 1947

RELATIVE DEFICIENCY OF PARASYMPATHOMIMETIC ACTIVITY IN AQUEOUS OF EYES WITH CHRONIC SIMPLE GLAUCOMA

Author Affiliations

NEW YORK
From the Ophthalmological Service and the Laboratories of the Mount Sinai Hospital.

Arch Ophthalmol. 1947;37(5):608-617. doi:10.1001/archopht.1947.00890220625007
Abstract

THE STUDIES of Loewi, Dale, Cannon and others have firmly established the validity of the concept of the chemical mediation of nerve impulses. It is now generally accepted that the effects of the somatic and parasympathetic nervous systems are produced by the liberation at the nerve endings of acetylcholine. This substance is quickly destroyed by cholinesterase, an enzyme present in the blood and tissue fluids. The effects of postganglionic sympathetic nerve impulses are the result of the liberation at the nerve terminals of epinephrine. The clinical implications of these findings are emphasized by the fact that in at least one disease, namely, myasthenia gravis, the primary dysfunction may be attributed to interference with the mechanism of acetylcholine activity.

The possible relation of these studies to the problem of glaucoma was suggested by several facts. Since the time of Laqueur, who in 1876 demonstrated the therapeutic effect of physostigmine on the

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