Platelet adhesiveness and aggregation in relation to diabetic retinopathy

Abstract

Platelet adhesiveness, ADP-aetivated platelet a.ggregation and the activity of the ADP-splitting enzymes m blood and plasma have been studied in 22 diabetics with severe retinopathy, 22 long-duration diabetics with minimal or no retinopathy and 28 control subjects. The rate of platelet aggregation under the influence of 5, 3, 2 and t txM ADP, the maximum aggregation attained and the rate of disaggregation of these aggregates were measured. The platelets from actively deteriorating retinopaths were found to be more sensitive to the effect of low concentrations of ADP; a significant increase in the extent of aggregation and a decrease in the rate of disaggregation of platelet aggregates formed under the experimental conditions, in vitro were observed. If this should occur in vivo, then capillary occlusion might ensue. This increased sensitivity to ADP and inability to disaggregate, was not due to any differences in the activity of the ADP-splitting enzyme systems in blood. Significant differences in the parameters were not observed when the large diabetic groups were compared with the control subjects. Contrary to some reports, an increase in platelet adhesiveness was not apparent in either diabetic group.

Diabetic Patients Without Vascular Complications Display Enhanced Basal Platelet Activation and Decreased Antioxidant Status

“…First, our purpose was to define the level of platelet aggregation in such patients. Indeed, platelet hyperactivity has been reported in the literature, and this is supported by numerous studies in diabetic patients with vascular complications (10,24). Our present study shows an increased sensitivity to thrombin in diabetic patients, even in the absence of vascular complications.…”

Availability of endothelial von Willebrand factor and platelet function in diabetic patients infused with a vasopressin analogue

“…vWF could either leak from damaged endothelial cells, be more actively synthesized, or cleared more slowly from the circulation. Little is known about the possible relationships between the plasma levels of vWF and platelet adhesion and aggregation, which have been reported to be abnormal in diabetes by some investigators [2,4,8,9], but not by others [9][10][11][12]. vWF is necessary for platelet adhesion to subendothelial structures [13] and to glass surfaces [14].…”

Effect of gliclazide on prostaglandin I2 formation in normal and streptozotocin-induced diabetic animals.

“…Abnormalities of platelet functions in diabetic patients, especially in patients with microangiopathy (1,2), are known, and these abnormalities have been postulated to con tribute to the pathogenesis of diabetic micro angiopathy through their pivotal role in the thrombus formation and the proliferation of vascular connective tissue cells (3).…”