| Summary: | This project was undertaken to increase the understanding of platelet function, with paticular emphasis on abnormal platelets in diabetes mellitus, and improving the quality of platelet concentrates for transfusion. {1} Potential platelet antagonists, including PGE1, verapamil, insulin and hirudin, were added to platelet concentrates in an attempt to improve the recovery and shelf-life of the concentrate. Each "preservative" caused some improvement in platelet concentrate quality, as measured by functional tests, and radio-immunoassay for the platelet activation marker, B- thromboglobulin. The best results were obtained with the addition of PGE1, which facilitated recovery of all samples to which it was added, suggesting a cheap way of ensuring consistently good platelet concentrates. {2} Various investigations were carried out regarding abnormal platelet function in diabetes mellitus. No significant differences were found in the responses of platelets from diabetics and age-matched controls to the calcium-channel blocking drug, Verapamil, in vitro. Similarly, the capacity of diabetic platelets to produce malondialdehyde, a by-product of thromboxane A2 synthesis, was not significantly different from control platelets. The use of insulin in aggregometry studies showed, surprisingly, that insulin could have a pro-aggregatory effect on platelets from diabetics, but not those from healthy controls. In addition, evidence for the existence of a platelet aggregation-enhancing factor in the plasma of diabetics and older controls was obtained. {3} Extensive tests to investigate the nature of spontaneous platelet aggregation (SPA) in whole blood have established the existence of two types of SPA, (i) ADP-dependent, and (ii) ADP-independent. The results obtained suggest a major role for erythrocytes in the development of inappropriate platelet aggregation.
|
|---|
