A platelet procoagulant activity associated with platelet shape change.

PCA was measured for human PRP by determining recalcification times assayed in a minimal-dilution, controlled PH/PCO2 system in a siliconized cuvette, with the use of light transmission measurements (aggregometry). Platelet shape, aggregation, and plasma clotting end points were assayed photometrically, with platelet morphology and aggregation studied in parallel by light microscopy. With varying concentrations of ADP preincubated with PRP initially containing essentially disc-shaped platelets, it was found that induced shape change in the absence of an aggregation is necessary and sufficient for the development of PCA. This was consistently measurable as a shortening of recalcification times by approximately 50% for suspensions of shape-changed platelets vs. disc-shaped platelets. The pharmacologic inhibition of the endoperoxide pathway-mediated platelet secondary aggregation and release by aspirin administered in vivo does not impair the ability of human platelets to develop this PCA. Inhibition of shape change with amounts of 5'-adenosine monophosphate insufficient to affect coagulation tests in the absence of platelets leads to 80% to 90% inhibition of the ADP-induced PCA. This PCA is shown to be fully reversible, with morphologic reversion of shape-changed platelets to the discoid form, and is shown to be distinct from other PCAs previously described for platelets activated in different ways, such as PF3 activity. It is suggested that the binding of coagulation factors to the platelet membrane may be regulated concomitantly with shape change.