Indomethacin purportedly arrests premature labor by inhibiting the production of prostaglandins. Animal experimentation has demonstrated that prostaglandins are involved in the neonatal rerouting of the circulation. Experience with two neonates with disorders circulatory adjustment at birth following prenatal exposure to indomethacin indicates that indomethacin may interfere with these adjustments in man and favor the development of the serious oxygen dependency known as primary pulmonary hypertension of the newborn.
PIP: Indomethacin is used to prolong gestation by inhibiting prostaglandin production, but hemodynamic consequences in the fetus are still in question. Prostaglandins E and F are involved in regulating vascular resistance in the ductus arteriosus and pulmonary vascular bed as demonstrated in animal experiments; in sheep and rats, indomethacin produced constriction of closure of the ductus arteriosus. A possible consequence to the newborn is primary pulmonary hypertension due to elevated pulmonary vascular resistance. Until more information can establish the metabolic, hematologic, and hemodynamic effects of indomethacin on the fetus and newborn, its use should be limited to centers where the newborn can be promptly treated.