The effects of betamimetics and glucocorticoids on fetal vascular prostacyclin and platelet thromboxane synthesis in humans.

Since the vasodilatory, antiaggregatory prostacyclin (PGI2) and its antagonist thromboxane A2 (TxA2) evidently take part in the regulation of the fetoplacental blood flow, the influence of drugs commonly used during pregnancy, such as betamimetics (ritodrine and buphenine) and glucocorticoids (hydrocortisone and dexamethasone), on fetal PGI2 and TxA2 productions was investigated. Specimens of umbilical artery were superfused in vitro without (control) or with the drugs studied (10(-8) - 10(-3) mol/l) and the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable breakdown product of PGI2, was measured by radioimmunoassay. When studying TxA2 production, umbilical vein blood samples were allowed to clot in the absence and presence of the drugs studied, and the formation of thromboxane B2 (TxB2) a stable breakdown product of TxA2, was measured by radioimmunoassay. Ritodrine and buphenine had no influence on the production of either PGI2 or TxA2, but hydrocortisone and dexamethasone at concentrations of 10(-3) M/l inhibited umbilical PGI2 production to 5.5 +/- 1.4% (mean +/- SEM) and 69.9 +/- 5.0% of the control level, respectively, although they had no effect on TxA2 synthesis. It is concluded that if betamimetics alter the fetoplacental circulation, as suggested by some authors, they do not exert this effect through the fetal PGI2 or TxA2. In contrast, maternal glucocorticoid treatment may suppress fetal PGI2 generation, and thus perhaps reduce the fetoplacental blood flow.