Effect of acute intravascular volume expansion on human fetal prostaglandin concentrations

Direct fetal intravascular transfusion is well tolerated by the human fetus. However, the rapid transfusion of high-hematocrit blood should increase vessel distention and the flow shear force. Each is known to stimulate the release of prostacyclin. We measured prostaglandins E2 and F2 alpha and the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha, by radioimmunoassay before, at the estimated midway point of, and at the completion of 40 umbilical venous transfusions performed because of immune hemolytic anemia. Umbilical venous pressures corrected for amniotic fluid pressure were measured at similar intervals during nine of the procedures. The mean (+/- SEM) length of gestation at transfusion was 29 +/- 1 week, opening hematocrit 23% +/- 1%, and total volume of 70% hematocrit red blood cells transfused 83 +/- 5 ml. 6-Keto-prostaglandin F1 alpha was the principal circulating fetal prostanoid and its concentration was unrelated to gestational age. Intravenous transfusion was associated with an 84% increase in 6-keto-prostaglandin F1 alpha (p = 0.03) and a 68% increase in prostaglandin E2 (p less than 0.05). The rise for each strongly correlated with the rise in the fetal umbilical venous pressure (6-keto-prostaglandin F1 alpha, r = 0.94, p = 0.0005; prostaglandin E2, r = 0.81, p less than 0.03). We conclude that 6-keto-prostaglandin F1 alpha is the principal circulating prostaglandin in the human fetus and that the release of venodilator prostaglandins may be one reason the human fetus can tolerate a large increase in intravascular volume without obvious sequelae.