ELECTRORETINOGRAM IN SUCROSE-FED DIABETIC RATS TREATED WITH AN ALDOSEREDUCTASE INHIBITOR OR AN ANTICOAGULANT

To investigate the role of increased polyol pathway activity and hemod ynamic deficits in the pathogenesis of diabetic retinopathy in non-ins ulin-dependent diabetes mellitus (NIDDM), Otsuka Long-Evans Tokushima fatty (OLETF) rats, an animal model of human NIDDM, were given water w ith or without 30% sucrose and some of them were fed laboratory chow c ontaining 0.03% cilostazol, an anticoagulant, or 0.05% [5-(3-thienyl)t etrazol-1-yl] acetic acid monohydrate (TAT), an aldose reductase inhib itor, for a wk. Long-Evans Tokushima Otsuka (LETO) rats were used as n ondiabetic controls. The peak latencies of oscillatory potentials of t he electroretinogram in sucrose-fed OLETF rats were significantly prol onged compared with those in OLETF rats without sucrose feeding and LE TO rats. There was a marked increase in platelet aggregability and a s ignificant decrease in erythrocyte 2,3-diphosphoglycerate in sucrose-f ed OLETF rats. Cilostazol significantly improved these parameters with out changes in retinal levels of sorbitol and fructose. TAT, however, ameliorated all of these parameters. These findings confirm that the s ucrose-fed OLETF rat is a useful animal model of retinopathy in human NIDDM and suggest that cilostazol improved diabetic retinopathy by mod ifying vascular factors, not by altering polyol pathway activity.