J Morales1, S M Brown, A S Abdul-Rahim, C E Crosson. 1. Department of Ophthalmology and Visual Sciences, Texas Tech University Health Sciences Center, Sixth and Flint, Lubbock, TX 79430, USA.
Abstract
OBJECTIVE: To determine the location of action of apraclonidine, an alpha-adrenergic receptor agonist that reduces aqueous production and lowers intraocular pressure (IOP). METHODS: The study cohort consisted of 6 patients with Horner syndrome (decreased or absent sympathetic innervation of 1 eye). We instilled 1% apraclonidine into the affected eye, and the changes in IOP and pupil diameter (PD) of both eyes were measured over 4 hours. In a separate session, apraclonidine was instilled into the normal eye and the measurements were repeated. RESULTS: The average baseline IOP was 16.3 mm Hg for affected eyes and 16.7 mm Hg for normal eyes. The average maximum ipsilateral reduction in IOP was 5.8 mm Hg in affected eyes and 5.2 mm Hg in normal eyes; this difference was not statistically significant. The average baseline PDs for affected and normal eyes were 3.2 mm and 4.2 mm, respectively. Instillation of apraclonidine into affected eyes produced mydriasis of 1.0 to 4.5 mm; baseline anisocoria reversed in all patients. There was no significant change in the PD of normal eyes after ipsilateral instillation of apraclonidine. CONCLUSIONS: Apraclonidine's major site of pharmacologic action for reduction of aqueous production is on postjunctional alpha(2) receptors in the ciliary body. The up-regulation of alpha receptors that occurs with sympathetic denervation unmasks apraclonidine's alpha(1) effect, which clinically causes pupil dilation. Apraclonidine may be a useful medication for the diagnosis of Horner syndrome. Arch Ophthalmol. 2000;118:951-954
OBJECTIVE: To determine the location of action of apraclonidine, an alpha-adrenergic receptor agonist that reduces aqueous production and lowers intraocular pressure (IOP). METHODS: The study cohort consisted of 6 patients with Horner syndrome (decreased or absent sympathetic innervation of 1 eye). We instilled 1% apraclonidine into the affected eye, and the changes in IOP and pupil diameter (PD) of both eyes were measured over 4 hours. In a separate session, apraclonidine was instilled into the normal eye and the measurements were repeated. RESULTS: The average baseline IOP was 16.3 mm Hg for affected eyes and 16.7 mm Hg for normal eyes. The average maximum ipsilateral reduction in IOP was 5.8 mm Hg in affected eyes and 5.2 mm Hg in normal eyes; this difference was not statistically significant. The average baseline PDs for affected and normal eyes were 3.2 mm and 4.2 mm, respectively. Instillation of apraclonidine into affected eyes produced mydriasis of 1.0 to 4.5 mm; baseline anisocoria reversed in all patients. There was no significant change in the PD of normal eyes after ipsilateral instillation of apraclonidine. CONCLUSIONS:Apraclonidine's major site of pharmacologic action for reduction of aqueous production is on postjunctional alpha(2) receptors in the ciliary body. The up-regulation of alpha receptors that occurs with sympathetic denervation unmasks apraclonidine's alpha(1) effect, which clinically causes pupil dilation. Apraclonidine may be a useful medication for the diagnosis of Horner syndrome. Arch Ophthalmol. 2000;118:951-954