Abstract
ABSTRACT
Intraocular pressure and facility of aqueous outflow were measured in adult cats after topical application of clorgyline, a selective inhibitor of type A monoamine oxidase (MAO), or deprenyl, a selective inhibitor of type B of the enzyme. Clorgyline produced a dose-related lowering of intraocular pressure which was associated with a dose-related increase in outflow facility. Sympathetic denervation markedly reduced both these effects of clorgyline. Both effects, on the other hand, persisted after death of the animals. Deprenyl did not lower intraocular pressure; in fact, a tendency toward pressure elevation was apparent 2 hours after its administration. Outflow facility was not significantly changed. These results suggest that an endogenous substrate of type A MAO, presumably norepinephrine, is responsible for the ocular tension lowering effect of clorgyline. Because cessation of circulation after death did not abolish the effect, it is assumed that the trabecular meshwork is the site of action and that sympathetic innervation normally supplies an adrenergic neurotransmitter to the meshwork area. The tendency toward rise in intraocular pressure produced by deprenyl is probably due to alteration of aqueous humor formation rather than to a change in outflow resistance.
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