We studied the effects of acute isovolemic maternal anemia on several variables of uterine and fetal oxygenation to answer these two questions: (1) Does maternal anemia cause reductions in oxygen delivery to the uterus, placenta, and fetus? (2) If so, what is the impact of such reductions on fetal oxidative metabolism? In 15 chronically catheterized pregnant sheep and fetal lambs, we measured uterine and umbilical blood flows and uterine and fetal oxygen deliveries, oxygen extractions, and oxygen consumptions at various, randomly selected maternal hematocrits ranging from 30% to 8%. We altered maternal hematocrit by performing isovolemic exchange transfusions with plasma or packed red blood cells. Uterine and umbilical blood flows were measured with the radionuclide-labeled microsphere technique, and the variables of oxygenation were calculated with modifications of the Fick principle. Decreases in maternal hematocrit led to linear reductions in oxygen delivery to the uterus, placenta, and fetus. Despite reductions in oxygen delivery of up to 50%, fetal oxygen consumption was maintained, because of compensatory increases in oxygen extraction. When hematocrit (and thus fetal oxygen delivery) was reduced by more than 50%, fetal oxygen consumption and the arterial blood base excess both decreased, indicating that, at these hematocrit levels, the supply of oxygen to fetal tissues was inadequate for the demands for oxygen by these tissues.