In the fetus, the functional equivalent of the alveolar-arterial blood PO2 difference is the uterine venous-umbilical venous blood PO2 difference. Generally, factors that affect one of the venous blood PO2s produce equivalent effects on the other. We previously showed that fetal anemia produces increases in umbilical venous blood PO2. To determine whether this increase was associated either with equivalent increases in uterine venous blood PO2 or with reductions in the uterine venous-umbilical venous PO2 difference, we studied eight chronically catheterized pregnant sheep and fetal lambs. Measurements of O2 gas tensions and O2 saturations, uterine and umbilical blood flows, and uterine, fetal, and placental O2 consumptions were made in animals with normal fetal hematocrits and during reductions in fetal hematocrit of 35% (moderate fetal anemia) or 60% (severe fetal anemia). Fetal anemia produced reductions in the uterine venous-umbilical venous blood PO2 difference; in some cases the PO2 difference was less than 2 mmHg (compared with normal values of 20 mmHg). The development of both moderate and severe fetal anemia had no effect on uterine and umbilical blood flows or placental O2 consumption but did reduce total uterine and fetal O2 consumption. These data indicate that fetal anemia induces changes in placental gas transport. These changes may be due to improvements in gas diffusion, reductions in perfusion mismatching, or reductions in vascular shunting. Our data further indicate that placental O2 consumption rate, which is high in normal pregnant sheep, plays no role in the maintenance of the uterine venous-umbilical venous blood PO2 difference in pregnant sheep.