To examine the effects of
vasopressin on fetal oxygenation the
hormone was infused intravenously for 1 h (1.4-3.5 mU X min-1 X kg
fetal weight-1) to chronically catheterized fetal lambs in utero (113-137 days gestation). Arterial pressure rose (48.3 to 59.6 mmHg) (1 mmHg = 133.322 Pa) and heart rate fell (185.3 to 141.0 beats/min) during the infusion. There was a significant increase in fetal arterial PO2 (20.0 to 23.1 mmHg) and significant declines in pH (7.414 to 7.381) and base excess. Umbilical blood flow rose, and the percentage increase in flow (23%) was identical to the proportional rise in arterial pressure. Accompanying the rise in umbilical blood flow was a rise in umbilical
oxygen delivery. But as there was no change in fetal oxygen consumption, fractional
oxygen extraction by the fetus fell significantly (0.31 to 0.25). These data indicate that the
vasopressin-induced rise in fetal vascular PO2 results from an increase in umbilical
oxygen delivery and concomitant fall in fractional extraction. Fetal
vasopressin levels are greatly elevated during
hypoxia, and under conditions of reduced
oxygen supply, the effects of the
hormone on umbilical
oxygen delivery and vascular PO2 could have definite survival value.