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This study was designed to investigate myocardial abnormalities in general, and the extent of capillary basal laminar thickening (CBLT) in particular, in experimentally induced diabetic rats. For this purpose, buffered streptozotocin (70 mg/kg) was administered to 34 rats; control groups consisted of 18 rats, uninjected or buffer-injected only. Animals were sacrificed at monthly intervals up to 12 months and at 15 months following induction of the diabetes. Myocardial, renal, and skeletal muscular tissues, prepared for ultrastructural examination, were subjected to quantitative procedures, in order to obtain an index of CBLT. The results indicated that abnormal CBLT was present and relatable to the length of exposure to the hyperglycemia. Six months following induction, the increments in laminar thickening in diabetic rats significantly differed from those in normal maturing rats. In the diabetic myocardium CBLT represented the single, specific, and clearly identifiable strucutural abnormality. Increased CBLT was also observed within renal glomeruli and quadriceps in diabetic rats, to a more marked extent than that seen in the myocardium. Parenchymal changes in the three tissues under study were most pronounced in the kidneys of diabetic rats. These findings, paralleling previously published observations in human diabetics, fail to reveal morphologic evidence of an intrinsic diabetic cardiomyopathy and suggest that CBLT in experimentally diabetic rats is associated with the altered metabolic state in these animals.