We evaluated the circulation of the liver and ductus venosus, using the radionuclide-labeled mkrosphere technique, in 24 chronically prepared fetal lambs. We placed catheters in fetal descending aorta and inferior vena cava, and hi a carotid artery and an umbilical vein; in 11 fetuses, we aho Inserted a catheter hi a mesenteric vein that drained into the portal vein. After allowing 2-4 days for recovery from the stresses of anesthesia and operation, we measured blood flow to the fetal liver and hs various lobes and through the ductus venosus. Total Mood flow to the liver was 435 ± 122 ml/min per 100 g liver (mean ± SD), of which hepatic arterial flow represented 9%, portal venous flow 18%, and umbilical venous flow 73%. Hepatic arterial and umbilical venous flows were approximately equally divided between left and right lobes, although portal blood flow was directed almost exclusively to the right lobe. The right lobe received 40% more total blood flow than the left, even though the left lobe weighed more than the right. Approximately 53% of umbilical venous blood flow but less than 9% of portal venous blood flow entered the ductus venosus; umbilical venous flow therefore accounted for more than 98% of ductus venosus blood flow. Ductus venosus flow showed a strong linear correlation with umbilical blood flow. However, there was no relationship between ductus venosus flow and gestational age. The results suggest that the liver receives a large Mood flow primarily because of a large umbilical venous contribution. It is not dear whether the fetal liver requires this large flow and peculiar lobar distribution for normal function and growth. It is unlikely, however, that the ductus venosus functions actively to maintain a stable blood flow to the fetal liver.

In 16 chronically prepared fetal lambs we compared the systemic distribution of ductus venosus blood flow with that of abdominal inferior vena caval blood by simultaneously injecting microspheres labeled with different radionuclides into an umbilical vein and into the abdominal inferior vena cava. A significantly greater proportion of ductus venosus blood flow than of abdominal inferior vena caval blood flow supplied the brain, heart, and upper body; this resulted from streaming of ductus venosus blood flow within the thoracic inferior vena cava with preferential direction of that blood flow through the foramen ovale. Blood flows to upper and lower body structures and placenta calculated from umbilical venous microsphere injections and reference arterial blood samples did not differ from those computed fromabdominal inferior vena caval injections and reference samples. Thus, despite streamline blood flow within the fetal thoracic inferior vena cava, organ blood flows can be accurately measured with either an umbilical venous or an abdominal inferior vena caval injection of microspheres when either is combined with the appropriate reference arterial blood samples.

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In seven chronically catheterized fetal lambs, blood flow and oxygen consumption (VO2) in the combined small and large intestines were determined at various oxygen concentrations in fetal arterial blood (CaO2). Intestinal blood flow (Qi) was measured with the radioactive-microsphere technique; intestinal oxygen delivery (DO2 = Qi X CaO2), VO2 [Qi X C(a-v)O2, where oxygen extraction [C(a-v)O2/CaO2] were computed with the Fick equation. Compared with normally oxygenated fetuses (CaO2 greater than 6.6 ml/dl), moderately hypoxemic fetuses (CaO2 = 4.4-6.6 ml/dl) had decreased intestinal DO2, increased oxygen extraction, and no change in intestinal VO2, Qi, or mesenteric-venous pH and base excess. During severe fetal hypoxemia (CaO2 less than 4.4 ml/dl), DO2 decreased further while oxygen extraction increased substantially. Intestinal VO2 dropped, however, because the rise in oxygen extraction could no longer completely compensate for the reduced DO2. With severe hypoxemia, Qi and mesenteric-venous pH and base excess also fell. These data indicate that the fetal intestinal tract is able to meet its oxygen needs during hypoxemia until a critically low level of oxygenation is reached. Below this level intestinal oxygenation becomes inadequate, and anaerobic metabolism ensures.

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