Differential inhibition by aspirin of vascular and platelet prostaglandin synthesis in atherosclerotic patients.
We studied the ability of a single oral dose of aspirin to inhibit prostacyclin synthesis by human arterial and venous tissue and to inhibit thromboxane A2 synthesis by platelets in 70 patients who were undergoing aortocoronary bypass. A dose of 40, 80, or 325 mg of aspirin was administered 12 to 16 hours before surgery. The generation of thromboxane in serum--which provides an estimate of platelet thromboxane production--was reduced from the control value by 77, 95, and 99 per cent after single doses of 40, 80, and 325 mg of aspirin, respectively. By contrast, prostacyclin production in aortic tissue that was removed at operation was reduced by only 35, 38, and 75 per cent, respectively, in response to these doses. Production of prostacyclin in saphenous-vein tissue (not tested after 40 mg of aspirin) fell only slightly and not significantly after 80 mg but was reduced by 85 per cent after 325 mg. These findings indicate that a low dose of aspirin (40 to 80 mg) can largely inhibit platelet aggregation and thromboxane synthesis but has much less effect on prostacyclin production in arterial and venous endothelium.
D000284:Administration, Oral; D000368:Aged; D001158:Arteries / Q000378:metabolism; D001161:Arteriosclerosis / Q000378:metabolism*; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D001808:Blood Vessels / Q000187:drug effects / Q000378:metabolism*; D046508:Culture Techniques; D011464:Epoprostenol / Q000096:biosynthesis; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D011453:Prostaglandins / Q000096:biosynthesis*; D013928:Thromboxane A2 / Q000096:biosynthesis; D014680:Veins / Q000378:metabolism
D011453:Prostaglandins; D013928:Thromboxane A2; D011464:Epoprostenol; D001241:Aspirin