Prostacyclin is able to inhibit the development of platelet prothrombinase activity. This inhibition, which also occurs with dibutyryl cAMP, is presumably due to the ability of prostacyclin to prevent the formation of a negatively charged phospholipid surface at the exterior half of the platelet membrane. Generation of this procoagulant surface, as induced by platelet activation with collagen plus thrombin, does not depend on thromboxane A2 formation.