Prostacyclin is a highly potent inhibitor of platelet aggregation and thrombus formation in the microcirculation, significantly more effective than prostaglandin E1.
Potent microcirculatory antithrombotic activity seen in animals; leaves open translation to human thrombosis prevention.
Isolated rings of hamster aorta produced an unstable substance which inhibited platelet aggregation in vitro and had the same characteristics as prostacyclin. Prostacyclin inhibited adenosine diphosphate (ADP)‐induced aggregation of hamster platelets in vitro. The effects of prostacyclin on ADP‐induced platelet thrombi in the microcirculation of the hamster cheek pouch were studied with a television microscope. Prostacyclin caused a dose‐dependent increase in the time of iontophoretic application of ADP which was required to induce platelet thrombi formation and embolization in venules (30 to 40 μm diameter). Prostacyclin caused a dose‐dependent reduction in the total time during which ADP‐induced thrombi were observed following local electrical damage to arterioles (40 to 80 μm diameter). Thrombus formation in venules and arterioles was abolished by 500 ng/ml prostacyclin in the Krebs solution superfusing the hamster cheek pouch. Prostacyclin was approximately twenty times more potent than prostaglandin E 1 in preventing thrombus formation in the microcirculation.
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Higgs et al. (1997) studied this question.
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