CONTINUED PLATELET INTERACTION WITH DEENDOTHELIALIZED AORTAE ASSOCIATED WITH SLOWER RE-ENDOTHELIALIZATION AND MORE EXTENSIVE INTIMAL HYPERPLASIA IN SPONTANEOUSLY DIABETIC BB WISTAR RATS

Diabetic patients are at increased risk for atherosclerosis and its co mplications. Platelets contribute to atherosclerosis through effects o f factors released from platelets which interact with injured vessels. Diabetic platelets are hypersensitive to agonists in vitro. If diabet ic platelets interact more extensively with injured vessels, they coul d contribute to increased vascular disease in diabetic patients. We ex amined the effect of spontaneous diabetes in BB Wistar rats on platele t accumulation and turnover, endothelial regeneration and intimal thic kening in rat aortae de-endothelialized with a balloon catheter. Cr-51 -labelled platelets were injected before or at different times after i njury, and platelet accumulation on the aortae was determined at vario us times after the injection. Platelets rapidly accumulate on the aort ae 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 a fter injury. After 4 days, aortae of control rats gradually lose their ability to attract new platelets; this phase is delayed in diabetic r ats. When Cr-51-platelets are injected 6 days after injury more radioa ctivity 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-endothelializat ion 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 contr ol and diabetic rats. The smooth-muscle-cell-rich neointima is thicker and more extensive in diabetic than in control rats 15 or 28 days aft er aortic injury. Diabetes in rats is associated with continued platel et interaction with de-endothelialized aortae, slower re-endothelializ ation, and the formation of a thicker and more extensive smooth-muscle -cell-rich neointima.