Continued platelet interaction with de-endotheliazed aorta associated with slower re-endothelization and more extensive intimal hyperplasia in spontaneously diabetic BB Wistar rats
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Diabetic patients are at increased risk for atherosclerosis and its complications. Platelets contribute to atherosclerosis through effects of factors released from platelets which interact with injured vessels. Diabetic platelets are hypersensitive to agonists in vitro. If diabetic platelets interact more extensively with injured vessels, they could contribute to increased vascular disease in diabetic patients. We examined the effect of spontaneous diabetes in BB Wistar rats on platelet accumulation and turnover, endothelial regeneration and intimal thickening in rat aortae de-endothelialized with a balloon catheter. 51Cr-labelled platelets were injected before or at different times after injury, and platelet accumulation on the aortae was determined at various times after the injection. Platelets rapidly accumulate on the aortae 30 min after injury and the net accumulation is similar in control and diabetic rats. Platelets continue to interact to a similar extent with the aortae of control and diabetic rats up to 4 days after injury, but the extent of interaction is less than that observed initially after injury. After 4 days, aortae of control rats gradually lose their ability to attract new platelets; this phase is delayed in diabetic rats. When 51Cr-platelets are injected 6 days after injury more radioactivity accumulates in a 24-h period on aortae of diabetic (22,050 +/- 6290 plts/mm2) than of control rats (8030 +/- 670 plts/mm2, P < 0.05). Seven days after injury, the percentage of aortic re-endothelialization is less in diabetic (58.2 +/- 7.2) than in control rats (86.8 +/- 6.9, P < 0.01). By 28 days, re-endothelialization is complete in control and diabetic rats. The smooth-muscle-cell-rich neointima is thicker and more extensive in diabetic than in control rats 15 or 28 days after aortic injury. Diabetes in rats is associated with continued platelet interaction with de-endothelialized aortae, slower re-endothelialization, and the formation of a thicker and more extensive smooth-muscle-cell-rich neointima.
