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We evaluated the effects of alterations in fetal hematocrit on fetal oxygenation in 10 chronically catheterized fetal lambs. Hematocrit was varied from 10% to 55% by slow isovolemic exchange transfusions with plasma or packed red blood cells obtained freshly from donor fetuses. At each hematocrit studied, we measured umbilical blood flow (Qumb) and the oxygen concentrations in umbilical venous blood (CUVO2) and arterial blood (CAO2) and calculated fetal oxygen delivery (Qumb X CUVO2), oxygen extraction [(CUVO2 - CAO2)/CUVO2], and oxygen consumption [Qumb (CUVO2 - CAO2)]. Fetal oxygen delivery was maximal at a fetal hematocrit of 33% (mean oxygen delivery = 23 ml of oxygen per minute per kilogram of fetus) and decreased as hematocrit was raised or lowered from that value. Despite these reductions in oxygen delivery, fetal oxygen consumption was relatively stable (at about 7 ml of oxygen per minute per kilogram) at hematocrits ranging from about 16% to 48% because of compensatory increases in fetal oxygen extraction. Regardless of whether oxygen delivery decreased because of anemia or polycythemia, fetal oxygen consumption was maintained as long as oxygen delivery was greater than about 14 ml of oxygen per minute per kilogram of fetus. When oxygen delivery was less than 14 ml of oxygen per minute per kilogram, fetal oxygen consumption fell while arterial blood base deficit increased, indicating that oxygen supply was inadequate for fetal oxygen demands. These results indicate that fetal aerobic metabolism can be sustained over a wide range of fetal hematocrits. Furthermore, our data support the concept that the level of fetal oxygen delivery is an important determinant of the adequacy of fetal oxygenation.

The purpose of our experiments was to relate blood flow and oxygen delivery (blood flow x arterial blood oxygen concentration) to fetal organs as functions of fetal hematocrit. In 12 chronically catheterized fetal lambs, we observed two patterns of responses of fetal organs and tissues to isovolemic alterations in fetal hematocrit from 12% to 55%. In group 1 organs (brain, heart, adrenal glands), blood flows increased as hematocrit was either raised or lowered from normal such that oxygen delivery to these organs was stable over the entire range of hematocrits studied. In group 2 organs (gastrointestinal tract organs, spleen, kidneys, placenta, and carcass), blood flows varied little over the range of hematocrits from 12% to 40% or 45% but decreased at hematocrits greater than or equal to 40% to 45%. Because of these flow responses, oxygen delivery to these organs and tissues was maximal at hematocrits ranging from 32% to 38%. Our data indicate that the various organs of the unanesthetized fetal lamb respond in different ways to alterations in hematocrit. It is of particular interest that, in the great majority of the organs of the fetus, oxygen delivery is maximal at hematocrits considered normal for the fetal lamb in utero.