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pubmed:abstractText |
Ticlopidine, known to inhibit the primary wave of ADP-induced platelet aggregation and to increase the bleeding time, can modify platelet prostaglandin metabolism. The basal level of platelet PGE1 is enhanced by the drug. Ticlopidine does not decrease biosynthesis of prostaglandin endoperoxides from arachidonic acid but increases production of primary prostaglandins, cheifly prostaglandin D2, and causes a slight diminution of thromboxane B2 formation. The excess of prostaglandin endoperoxides not converted to primary prostglandins may escape from platelets and produce more prostacyclin if endothelial cell microsomes are present in the incubate.
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