Glaucoma. Apraclonidine is used for pre&postlaser prophylaxis of intraocular pressure spikes.
To reduce the penetration of clonidine into the brain, a polar (hydrophilic)
analog, apraclonidine, was developed for ophthalmic use. As a single
drop, apraclonidine is a very effective ocular hypotensive agent. Maximal
pressure reduction in the treated eye was 37% (6.5 mmHg) and lasted up
to 12 hours. The dose-response curve for apraclonidine plateaus between
0.25% and 0.5%. Most of the unwanted effects of apraclonidine are local
and are related to α1-adrenoceptor stimulation. These include conjunctival
blanching, eyelid retraction, and mild mydriasis. Apraclonidine has a very
low potential for systemic effects.
Approved for use in the United States in 1996, brimonidine is similar to
clonidine in its relative α2-adrenoceptor agonism, lipophilicity, and relative
lack of α1-adrenoceptor agonism. Brimonidine achieves better penetration
of the cornea than apraclonidine, although it has a theoretical potential for
greater untoward effects such as sedation and systemic hypotension.
Decreased production and increased outflow of aqueous humor.
α2-adrenoceptor agonists and β-adrenoceptor antagonists reduce aqueous humor flow by reducing aqueous humor production. In contrast to apraclonidine, brimonidine also increases uveoscleral outflow as measured by fluorophotometry.
The most frequent adverse events associated with brimonidine are oral
dryness, ocular hyperemia, ocular discomfort, headache, and fatigue.
Less frequent effects include corneal staining and photophobia. Rare
events included lid crusting, abnormal taste, and depression.