Objective—To determine effects of a topical formulation of an aldose reductase inhibitor (ARI) on the development of sugar cataracts in dogs fed a diet high in galactose.
Animals—Ten 6-month old Beagles.
Procedures—Dogs were fed a diet containing 30% galactose, and after 16 weeks, 6 dogs were treated topically with a proprietary ARI formulation and 4 dogs were treated with a placebo. Cataract formation was monitored by means of slit-lamp biomicroscopy and fundus photography. Dogs were euthanized after 10 weeks of treatment, and lenses were evaluated for degree of opacity, myo-inositol and galactitol concentrations, and concentration of the ARI.
Results—All dogs developed bilateral cortical opacities dense enough to result in a decrease in the tapetal reflex after being fed the galactose-containing diet for 16 weeks. Administration of the ARI arrested further development of cataract formation. In contrast, cataracts in the vehicle-treated dogs progressed over the 10-week period to the mature stage. Evaluation of the isolated lenses after 26 weeks of galactose feeding indicated that lenses from treated dogs were significantly less optically dense than lenses from control dogs. Lenticular myo-inositol concentration was significantly higher in the treated than in the control dogs.
Conclusions and Clinical Relevance—Results suggest that topical application of a proprietary ARI formulation may arrest or reverse the development of sugar cataracts in dogs fed a diet high in galactose. This suggests that this ARI formulation may be beneficial in maintaining or improving functional vision in diabetic dogs with early lens opacities.
OBJECTIVE To establish a study cutoff for evidence of glaucoma on the basis of IOP measurements from a large population of healthy dogs and to assess the effects of IV propofol administration on IOPs in premedicated and nonpremedicated dogs with and without glaucoma defined by this method.
DESIGN Prospective, descriptive study.
ANIMALS 234 client-owned dogs.
PROCEDURES IOPs measured in 113 healthy dogs (226 eyes) were used to calculate an IOP value indicative of glaucoma. The IOPs were measured in an additional 121 dogs (237 eyes) undergoing ophthalmic surgery. Midazolam-butorphanol was administered IV as preanesthetic medication to 15 and 87 dogs with and without glaucoma, respectively. A placebo (lactated Ringer solution) was administered IV to 8 and 11 dogs with and without glaucoma, respectively. Anesthesia of surgical patients was induced with propofol IV to effect. The IOPs and physiologic variables of interest were recorded before (baseline) and after preanesthetic medication or placebo administration and after propofol administration.
RESULTS An IOP > 25 mm Hg was deemed indicative of glaucoma. Compared with baseline measurements, mean IOP was increased after propofol administration in nonpremedicated dogs without glaucoma and unchanged in nonpremedicated dogs with glaucoma. Propofol-associated increases in IOP were blunted in premedicated dogs without glaucoma; IOP in affected eyes of premedicated dogs with glaucoma was decreased after preanesthetic medication and after propofol administration.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that preexisting IOP influences the response to anesthetic drugs, and administration of preanesthetic medication with muscle-relaxing properties may blunt or reduce propofol-induced increases in IOP. Further research with a larger number of dogs is needed to confirm our results in dogs with glaucoma.