A double-masked, randomized, 1-year study comparing the corneal effects of dorzolamide, timolol, and betaxolol. Dorzolamide Corneal Effects Study Group.

OBJECTIVE: To compare the long-term effects of dorzolamide hydrochloride (Trusopt, Merck and Co Inc, White-house Station, NJ), timolol maleate, and betaxolol hydrochloride on corneal endothelial cell density and corneal thickness. METHODS: This 1-year multicenter study was conducted in 298 patients with ocular hypertension or open-angle glaucoma who had a baseline central corneal endothelial cell density greater than 1500 cells/mm2 and central corneal thickness less than 0.68 mm in each eye. Patients were randomized to 0.5% betaxolol twice daily, 0.5% timolol twice daily, or 2.0% dorzolamide 3 times daily. Specular microscopy and ultrasonic pachymetry of the central cornea was performed at baseline and 6 and 12 months following institution of therapy. Endothelial cell densities were determined by a single masked observer. RESULTS: The mean percent changes from baseline for both outcome measures were similar in all 3 treatment groups at both 6 and 12 months. After 1 year of treatment, the mean percent loss in endothelial cell density from baseline was 3.6%, 4.5%, and 4.2% for the dorzolamide, timolol, and betaxolol groups, respectively. The mean percent change from baseline for corneal thickness was 0.47%, -0.25%, and 0.39% for the dorzolamide, timolol, and betaxolol groups, respectively. CONCLUSIONS: Dorzolamide is equivalent to timolol and betaxolol in terms of the change in central endothelial cell density and thickness after 1 year of therapy. All 3 treatments exhibit good long-term corneal tolerability in patients with normal corneas at baseline.

Characterization of retinal vascular abnormalities in lean and obese spontaneously hypertensive rats.

1. The obese SHR (Koletsky rat; SHR-k) is a unique animal model for the study of microvascular changes associated with genetic obesity, spontaneous hypertension, endogenous hyperlipidaemia, and hyperinsulinaemic, non-insulin dependent diabetes mellitus (Type II). 2. Lean and obese SHR-k exhibit retinal vascular changes which have not been previously characterized and are more severe than previously described in other animal models of experimental hypertension or non-insulin dependent diabetes. 3. Progressive retinal capillary dropout, capillary cell changes, vascular tortuosity and dilatation are severe. Vessels form elevated varicose vascular tortuosities which leak fluorescein dye and which are more frequent in the obese SHR-k. This study suggests that lean and obese SHR may be unique models for the study of multivariate factors in the pathogenesis of ischaemic neovascular proliferation.