Enhanced ocular hypotensive response to timolol in rabbits with prior dexamethasone treatment.

The purpose of this study was to determine glucocorticoid modulation of ocular pressure to timolol applied topically to rabbit eyes that were pretreated with dexamethasone. Rabbits were pretreated with five applications of topical 0.007% of dexamethasone (0.01% dexamethasone phosphate) or saline drops, administered at ten min intervals. The eyes were then treated with timolol maleate drops at concentrations of free base of 0.00007%, 0.0007%, 0.007% and 0.07%. An additional group of rabbits received dexamethasone pre-treatment only. Intraocular pressure was measured for the next four hr. Enhanced lowering of intraocular pressure was observed with dexamethasone pretreatment. Rabbits receiving the smaller dose of timolol had the least decrease in pressure. The most significant decreases in pressures occurred at 45 min after the administration of timolol with an average difference of 4.8 mm Hg between the timolol- and dexamethasone/timolol-treated eyes for the three largest concentrations of timolol. This synergism between glucocorticoids and beta-adrenergic blockers in lowering IOP may be potentially useful in the therapy of ocular hypertension and glaucoma.

Enhanced ocular hypotensive response to epinephrine in rabbits with prior dexamethasone treatment.

The purpose of this study was to determine glucocorticoid modulation of ocular pressure to epinephrine applied topically to rabbit eyes that were pretreated with dexamethasone. Rabbit eyes were pretreated with five applications of topical 0.07% dexamethasone (0.1% dexamethasone phosphate) or saline drops, administered at ten minute intervals. The eyes were then treated with epinephrine bitartrate drops at concentrations of free base epinephrine of 1.1%, 0.27%, 0.05%, 0.027%, 0.005% or 0.0005%. An additional group of rabbits received dexamethasone pretreatment only. Intraocular pressure (IOP) was measured for the next four hours. Enhanced lowering of intraocular pressure was observed with dexamethasone pretreatment. Rabbits receiving the smaller dose of epinephrine with dexamethasone had the largest decrease in IOP at 135 minutes after instillation of the epinephrine drops (0.005% epinephrine, mean difference +/- standard error of mean = 5.4 +/- 1.1 mmHg). Similarly, the duration of significant decrease of the IOP was prolonged in the groups receiving the lower concentrations of epinephrine (0.005% epinephrine, 255 minutes after administration of epinephrine). The synergism between glucocorticoids and adrenergic agonists in lowering IOP may be potentially useful in the therapy of ocular hypertension and glaucoma.

Relationship between corneal edema and topography.

We found that corneal edema can occur without significant concomitant changes in central and peripheral corneal topography. We examined the relationship between corneal edema and corneal topography in 10 subjects with normal ocular examinations. Baseline pachymetry and topographic measurements for both eyes of each patient were obtained. The right eye of each subject was exposed to an anoxic environment for 2 hours using a nitrogen chamber goggle. The left eye served as control. Optical pachymetry and computerized corneal topographic measurements were taken for both eyes immediately after removal of the nitrogen chamber goggle. All corneas exposed to the nitrogen chamber were thickened in all areas after removal of goggles. Average percent thickening per area was: 16.4% centrally, 6.3% nasally, 6.0% temporally, 6.3% superiorly, and 9.2% inferiorly. Corneas exposed to the nitrogen chamber demonstrated no significant topographic changes, except in the nasal area where the corneal power lessened. Furthermore, there was no significant correlation between corneal thickening in any area measured and changes in corneal topography. Control corneas did not thicken or demonstrate significant topographic changes.