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  • Title: Maternal ingestion of acetylsalicylic acid inhibits fetal and neonatal prostacyclin and thromboxane in humans.
    Author: Ylikorkala O, Mäkilä UM, Kääpä P, Viinikka L.
    Journal: Am J Obstet Gynecol; 1986 Aug; 155(2):345-9. PubMed ID: 3526896.
    Abstract:
    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.
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