[Venous prostacycline synthesis and plasma thromboxane B2 after low-dose aspirin].
It has been reported that low-dose aspirin inhibits prostaglandin synthesis of platelets, but not of endothelial cells. Whereas platelet prostaglandin synthesis is irreversibly inhibited by acetylation of cyclooxygenase, the nuclei-containing vascular wall cells are able to resynthesize this enzyme. The optimal optimal dosage in influencing vascular haemostatic regulation is still an open question in the literature. Hence, we examined the effect of a single dose of aspirin (50-500 mg), given to patients undergoing surgery for varicose veins, on venous wall PGI2 synthesis in a biopsy specimen and on plasma thromboxane B2 levels monitored continuously for up to 96 hours. Our findings demonstrate that a dose as low as 50 mg per day is able to inhibit thromboxane formation significantly. On the other hand, this dose does not influence vascular wall PGI2 synthesis. Based upon these data it is concluded that the optimal dosage to achieve a beneficial effect on haemostatic balance should not exceed 50 mg aspirin per day.
D000328:Adult; D001241:Aspirin / Q000008:administration & dosage*; D001792:Blood Platelets / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004727:Endothelium / Q000378:metabolism; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D007866:Leg; D008875:Middle Aged; D013929:Thromboxane B2 / Q000097:blood; D014680:Veins / Q000378:metabolism*
D013929:Thromboxane B2; D011464:Epoprostenol; D001241:Aspirin
Venöse Prostazyklinsynthese und Plasmathromboxan B2 nach Low-dose-Aspirin.