Maternal ingestion of acetylsalicylic acid inhibits fetal and neonatal prostacyclin and thromboxane in humans.

Small doses of maternal acetylsalicylic acid have proved to prevent preeclampsia. To study the mechanism of this action of acetylsalicylic acid, healthy women ingested 100 mg (n = 13) or 500 mg (n = 14) of acetylsalicylic acid during labor at term. The fetal prostacyclin synthesis, as assessed by the production of 6-ketoprostaglandin F1 alpha (a metabolite of prostacyclin) by the umbilical artery, was reduced from 21.3 +/- 1.6 ng/gm/min of dry weight in the controls (n = 25, mean +/- SE) to 7.8 +/- 1.1 ng/ml/min (p less than 0.001) in infants of mothers receiving 500 mg of acetylsalicylic acid, but it was unchanged in infants with mothers receiving 100 mg of acetylsalicylic acid (19.5 +/- 2.3 ng/gm/min). Maternal ingestion of 500 mg of acetylsalicylic acid also was accompanied by reduced (p less than 0.10) urinary excretion of 6-ketoprostaglandin F1 alpha in neonates during the first 3 days of life. The fetal platelet thromboxane A2 synthesis, as assessed by the release of thromboxane B2 (a metabolite of thromboxane A2) during spontaneous clotting of the umbilical blood (63.4 +/- 4.2 pg/10(5) platelets, n = 22), was inhibited in infants born to mothers given 100 mg (14.0 +/- 3.7 pg/10(5) platelets, p less than 0.001) or 500 mg of acetylsalicylic acid (6.1 +/- 3.5 pg/10(5) platelets, p less than 0.001). The thromboxane B2 release by the umbilical artery (1.1 +/- 0.1 ng/gm/min, n = 13) also was decreased in infants of mothers receiving 500 mg of acetylsalicylic acid (0.57 +/- 0.1 ng/gm/min, n = 7, p less than 0.01). Thus a small dose of maternal acetylsalicylic acid (100 mg) inhibits only the fetoplacental thromboxane A2 but leaves prostacyclin production unaffected.