Numerous agents have been administered in an attempt to achieve specific biochemical antiplatelet activity. A model of microsurgical trauma was utilized to create a nonocclusive thrombus, similar to what occurs in the postoperative period. Prostacyclin (PGI2) was given in a high intravenous dose which caused in vitro inhibition of platelet aggregation in rats and rabbits. Although hematological and cardiovascular side effects of PGI2 were tolerated, in vivo platelet thrombus formation persisted and constituted 25–75% of the postoperative thrombus. Even though platelets were inhibited by PGI2, other significant stimuli remained at the site of injury for activation and participation of platelets in the formation of a thrombus.
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