THE demonstration that certain arteries and veins have the ability to generate from prostaglandin (PG) endoperoxides an unstable substance called prostacyclin (PGl2) (ref. 1), which will inhibit platelet aggregation2,3, should lead to a reappraisal of the homeostatic mechanisms preventing thrombosis. It has been suggested that the endothelium of these blood vessels contains an enzyme which is capable of converting PG endoperoxides from circulating platelets into an unstable substance, prostacyclin. This inhibits platelet aggregation and so prevents the initial step of thrombus formation within the vessel4. Damage to the endothelium of the vessel wall may prevent production of the enzyme PGI 2 synthetase, and the subsequent reduction in the local synthesis of prostacyclin could facilitate platelet aggregation in the area of damage. Maintenance of an adequate circulation within the placenta is critical to foetal well-being. This circulation is one both of low pressure and velocity and the presence of a substance which has a potent inhibitory effect on platelet aggregation would seem desirable for its maintenance. We demonstrate here the ability of normal placental tissue to generate a labile substance which has the ability to inhibit ADP-induced platelet aggregation. The properties exhibited by this substance are suggestive of it being PGI2.
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