Indomethacin modifies the fetal hemodynamic response induced by percutaneous umbilical blood sampling

Percutaneous umbilical blood sampling induces a marked decrease of impedance to flow in the umbilical artery. Because these changes are believed to be the result of the release of prostanoids, we conducted a study to determine whether indomethacin administration before percutaneous umbilical blood sampling affects the hemodynamic response induced by this procedure.

Percutaneous umbilical blood sampling was performed in 20 singleton pregnancies that were treated for 3 days before the procedure with indomethacin (25 mg orally 6 hours apart) as tocolytic agent and in 22 untreated pregnancies. All the procedures were uncomplicated, and sampling of the umbilical vein was confirmed by blood pressure measurement at the time of the procedure. The umbilical artery pulsatility index and the fetal heart rate were measured immediately before and after the procedure. The first and last aliquots of umbilical vein plasma obtained at the beginning and closing of the procedure were assayed for endothelin-1, 6-keto-prostaglandin F1 alpha and thromboxane B2.

In untreated pregnancies percutaneous umbilical blood sampling induced a decrease of the umbilical artery pulsatility index (p < 0.0001) and an increase in 6-keto-prostaglandin F1 alpha (p < 0.001) and endothelin-1 levels (p = 0.001), whereas no significant changes were present in fetal heart rate and thromboxane B2 levels. In pregnancies treated with indomethacin, 6-keto-prostaglandin F1 alpha, and thromboxane B2, concentrations at the beginning of the procedure were both significantly less (p < 0.0001) than those found in untreated pregnancies. In pregnancies treated with indomethacin percutaneous umbilical blood sampling did not affect umbilical artery pulsatility index, and 6-keto-prostaglandin F1 alpha and thromboxane B2 levels did not vary during the procedure. However, endothelin-1 (p < 0.001) and fetal heart rate (p < 0.0001) increased after the procedure.

Indomethacin affects the fetal hemodynamic response to percutaneous umbilical blood sampling by inhibiting the release of prostanoids and the fall in umbilical artery pulsatility index. Under this condition the fetus adapts to the procedure by increasing the heart rate.