To study mechanisms by which variations in fetal oxygen demand alter fetal oxygen saturation and PO2, we measured uterine and umbilical blood flow and transplacental oxygen diffusion rate in eight chronically prepared pregnant ewes before and during fetal neuromuscular blockade with pancuronium bromide (0.2 mg/kg). Uterine and umbilical blood flows were measured by applying the steady-state method using ethanol as the test substance. Fetal oxygen uptake decreased 7.5% (P < 0.05). Umbilical blood floow increased 6% (P < 0.05), whereas uterine blood flow did not change significantly. Fetal arterial oxygen saturation increased markedly (54.8-60.9%; P < 0.001). There were also significant increases in umbilical vein oxygen saturation (83.6-86.9%; P < 0.01), uterine vein oxygen saturation (70.7-72.2%; P < 0.01), umbilical vein PO2 (29.4-32.1 Torr; P < 0.001), and uterine vein PO2 (49.4-50.7 Torr; P < 0.01). The uterine-umbilical venous PO2 difference decreased significantly (20.0-18.6 Torr; P < 0.001), whereas there was no significant change in the uterine-umbilical venous PCO2 difference or in the umbilical ethanol shunt. The data indicate that the relatively large increase in fetal arterial oxygen saturation that follows a small decrease in fetal oxygen demand is caused by two aspects of placental oxygen transport: 1) umbilical and uterine blood flow do not react homeostatically to prevent the rise of PO2 in the placental circulation, and 2) the decrease in oxygen flux from placenta to fetus is associated with a decrease in the transplacental PO2 gradient.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)