HYDROPS IN FETAL SHEEP FROM RAPID INDUCTION OF ANEMIA

We operated on 14 singleton fetal sheep at 126 +/- 3 d gestation and produced nonimmune anemia in 12 of them to study the mechanisms responsible for hydrops. Two fetuses served as controls. Partial exchange transfusions were performed daily to lower the hematocrit while we measured arterial blood gas tensions; Hb concentration; oxygen saturation; arterial oxygen content; aortic, central venous, and umbilical venous pressures; heart rate; plasma protein concentration; and colloid osmotic pressure. Hydrops developed in six of the fetuses and did not develop in six others, although both groups were anemic to the same degree, had similar total amounts of blood withdrawn based on kilograms of dry weight, and had similar dry weights. The fetuses who had hydrops became anemic more rapidly than the nonhydropic fetus (5.2 +/- 1.9 veusus 8.3 +/- 2.7 d; p < 0.05) and had more blood exchanged each day (197 +/- 56 versus 113 +/- 28 mL/kg dry body wt/d; p 0.008). Umbilical venous pressures increased in both hydropic and nonhydropic fetuses, but the central venous pressure became elevated only in the hydropic fetuses. Changes in heart rate, arterial pH and blood gas tensions, arterial oxygen content, plasma protein concentration, colloid osmotic pressure, and aortic pressure were similar in both groups. At autopsy the hydropic fetuses had 78 +/- 47 mL of ascites and 20 +/- 26 mL of pleural fluid. The water content of the hydropic fetuses and of the hydropic fetuses' placentas was greater than that of the nonhydropic fetuses. We conclude that a more rapid development of anemia is associated with hydrops in fetal sheep. The fetal sheep that became hydropic also had an elevated central venous pressure.