Platelet survival in rats with spontaneous diabetes mellitus.
The results from these studies show that platelet survival is prolonged in spontaneously diabetic rats. These results confirm those obtained in rats 4 weeks after they had been made diabetic by an injection of streptozocin. Platelet survival was also prolonged in the nondiabetic littermates (normoglycemic) of diabetic rats indicating that the effect on platelet survival may be unrelated to blood glucose concentrations. The mechanism responsible for this prolongation of platelet survival is unclear. Thus, under these experimental conditions in which rats do not have vascular disease, diabetes is associated with prolonged platelet survival. Vascular injury induced by indwelling aortic catheters shortened platelet survival to the same extent in diabetic rats, their nondiabetic littermates, and controls. There was a significantly greater accumulation of platelets on the damaged aortas of diabetic animals than on the aortas of nondiabetic littermates or controls. This could be a result of increased accumulation or decreased turnover of platelets on the vessel wall; macroscopic thrombi were not observed in any of the groups with indwelling aortic catheters. We conclude that the prolongation of platelet survival previously observed in rats with streptozocin-induced diabetes is attributable to the diabetic state and not to some other effect of the drug and that chronic diabetes in rats in the absence of vascular disease is not necessarily associated with shortened platelet survival.
D000818:Animals; D001011:Aorta / Q000293:injuries / Q000473:pathology; D001786:Blood Glucose / Q000378:metabolism; D001792:Blood Platelets / Q000502:physiology*; D002408:Catheters, Indwelling; D002470:Cell Survival; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D010976:Platelet Count; D051381:Rats; D011913:Rats, Inbred BB; D013927:Thrombosis / Q000209:etiology
D001786:Blood Glucose