| Abstrakt: |
Since 1954, when acetazolamide ( Diamox) * became available as an additional therapeutic agent for the management of glaucoma, several reports dealing with longterm acetazolamide therapy in chronic glaucoma have been published.1-8 A variety of hypotheses have been advanced concerning the mode of action of this drug.9-15 At the present time, all that can be said with certainty is that acetazolamide is a specific carbonic anhydrase inhibitor, that it lowers intraocular pressure of human and animal eyes, and that it does so by a partial inhibition of aqueous humor formation. The mechanism of action of this drug as well as its exact locus of action still remains to be demonstrated. Since carbonic anhydrase is known to be present in lens epithelium, ciliary body, and retina, it became of immediate interest to study two main problems: (a) Does long-term administration of acetazolamide interfere with the metabolic processes of ocular tissues? (b |
