Incorporation of [ 3H]Thmidine into myocardial capillary cells in streptozotocin-diabetic rats

Abstract

It was the aim of this study to test the hypothesis that abnormal thickening of capillary basal laminae in the diabetic organism may be due to postulated cycles of capillary cell turnover of increasing frequency. The accelerated cell turnover, it was theorized, may lead to laminar thickening through adhesion of basal laminae synthesized by regenerating cells with residual laminae of previously degenerated capillaries. Nine streptozotocin-diabetic rats and six nondiabetic controls were injected ip with tritiated thymidine, 1.0 μCi/g body weight. Three additional controls, for the purpose of identifying a potentially toxic action of streptozotocin which may affect the incorporation of thymidine into DNA, were treated in an identical manner. One hour postinjection, the animals were sacrificed, the heart was excised and sliced transversely. The tissue slices were fixed in 10% neutral buffered Formalin, dehydrated, and embedded in paraffin. Sections 6 μm thick were dipped in Kodak emulsion and were developed following an exposure of 4 weeks. Examination of the autoradiographs revealed distinctly labeled capillary endothelial cells in the myocardium of nondiabetic controls; labeling of these cells was strikingly reduced in the diabetic rats. These results indicate that proliferative activity of capillary endothelial cells is markedly retarded in the diabetic myocardium and that the reduced labeling can be ascribed genuinely to the diabetic environment. This finding does not provide support for the hypothesis that an accelerated cell turnover may be responsible for basal laminar thickning in the diabetic.