Rapid recovery of in vivo prostacyclin formation after inhibition by aspirin. Evidence from measurements of the major urinary metabolite of prostacyclin by GC-MS.
The effect of aspirin on the in vivo formation of prostacyclin and thromboxane A2 in normal healthy individuals was studied by measuring the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha and 2,3-dinor-TxB2 by gas chromatography-mass spectrometry. Administration of 500 mg aspirin twice daily caused a sustained reduction in the excretion of 2,3-dinor-TxB2 to 10-15% of the predose value, while the excretion of 2,3-dinor-6-keto-PGF1 alpha was reduced for only about 3 hours after the aspirin dose. The data demonstrate a considerable difference in the inhibitory effect of aspirin on the in vivo synthesis of thromboxane A2 and prostacyclin.
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D000328:Adult; D001241:Aspirin / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis* / Q000652:urine; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D006801:Humans; D008297:Male; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine; D013997:Time Factors
D011448:Prostaglandin Antagonists; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C028965:2,3-dinor-thromboxane B2; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D011464:Epoprostenol; D001241:Aspirin