Key result
A single 100 mg aspirin dose reduced serum TXB2 and 6-keto-PGF1 alpha by >90%, while a 20 mg dose inhibited TXB2 more than 6-keto-PGF1 alpha with a longer duration of effect on TXB2.
Why the study?
Does a single low dose of aspirin (20 mg or 100 mg) reduce prostacyclin and thromboxane formation in healthy subjects?
Does a single low dose of aspirin (20 mg or 100 mg) reduce prostacyclin and thromboxane formation in healthy subjects?
A 20 mg dose of aspirin provides a more prolonged inhibition of thromboxane relative to prostacyclin synthesis compared to a 100 mg dose.
May support 20 mg aspirin for selective, prolonged TX inhibition; leaves open clinical outcome benefits versus standard dosing.
The effects of two low doses of aspirin (20 mg and 100 mg) on prostacyclin and thromboxane formation during whole blood clotting were studied in 8 healthy volunteers. A single 100 mg aspirin dose caused more than 90% reduction of both serum TXB2 and 6-keto-PGF1 alpha; a single 20 mg dose of aspirin inhibited serum TXB2 more than 6-keto-PGF1 alpha but effects on these two products could not be completely dissociated. However, the effect of a single 20 mg aspirin dose on serum TXB2, was of much longer duration than its inhibitory effect on PGI2 synthesis during whole blood clotting.
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Davı̀ et al. (1983) studied Healthy (n=8). Aspirin was evaluated on Prostacyclin and thromboxane formation during whole blood clotting (serum TXB2 and 6-keto-PGF1 alpha). A single 100 mg aspirin dose reduced serum TXB2 and 6-keto-PGF1 alpha by >90%, while a 20 mg dose inhibited TXB2 more than 6-keto-PGF1 alpha with a longer duration of effect on TXB2.
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