Increased thromboxane biosynthesis in normal pregnancy is mainly derived from platelets.

Thromboxane biosynthesis was determined in normal pregnant subjects by measurement of its major urinary and plasma metabolites, 2,3-dinor-thromboxane B2 and 11-dehydro-thromboxane B2. Urinary 2,3-dinor-thromboxane B2 increased early in pregnancy (731 +/- 124 pg/mg creatinine) compared with nonpregnancy (less than 350 pg/mg creatinine; p less than 0.001) and the postpartum period (155 +/- 42 pg/mg creatinine, p = 0.015) and remained elevated throughout gestation. Similarly, plasma and urinary 11-dehydro-thromboxane B2 were increased in pregnancy. To determine the cellular origin of the increase in thromboxane biosynthesis in pregnancy, platelet cyclooxygenase was selectively inhibited with aspirin in a dose of 120 mg orally followed by 20 mg twice daily for 7 days (n = 4). Selectivity was confirmed by measurement of urinary 2,3-dinor-6-keto-prostaglandin F1 alpha, an index of prostacyclin biosynthesis. Coincident with a 97% inhibition of serum thromboxane B2, urinary 2,3-dinor-thromboxane B2 was almost completely inhibited and paralleled the recovery of platelet cyclooxygenase after withdrawal of aspirin. This study demonstrates that thromboxane biosynthesis is increased in pregnancy. The increase is mainly platelet derived and is consistent with increased platelet activation throughout pregnancy.