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Am J Physiol Heart Circ Physiol 257: H734-H738, 1989;
0363-6135/89 $5.00
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AJP - Heart and Circulatory Physiology, Vol 257, Issue 3 734-H738, Copyright © 1989 by American Physiological Society

ARTICLES

Fetal neuromuscular blockade: effect on oxygen demand and placental transport

R. B. Wilkening, D. W. Boyle and G. Meschia
Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.

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 less than 0.05). Umbilical blood flow increased 6% (P less than 0.05), whereas uterine blood flow did not change significantly. Fetal arterial oxygen saturation increased markedly (54.8-60.9%; P less than 0.001). There were also significant increases in umbilical vein oxygen saturation (83.6-86.9%; P less than 0.01), uterine vein oxygen saturation (70.7-72.2%; P less than 0.01), umbilical vein PO2 (29.4-32.1 Torr; P less than 0.001), and uterine vein PO2 (49.4-50.7 Torr; P less than 0.01). The uterine-umbilical venous PO2 difference decreased significantly (20.0-18.6 Torr; P less than 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 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.


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