We operated on 14 singleton fetal sheep at 126 +/- 3 d gestation and p
roduced nonimmune anemia in 12 of them to study the mechanisms respons
ible for hydrops. Two fetuses served as controls. Partial exchange tra
nsfusions were performed daily to lower the hematocrit while we measur
ed arterial blood gas tensions; Hb concentration; oxygen saturation; a
rterial oxygen content; aortic, central venous, and umbilical venous p
ressures; heart rate; plasma protein concentration; and colloid osmoti
c pressure. Hydrops developed in six of the fetuses and did not develo
p 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had similar total amounts of blood withdrawn based on kilograms of dry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 beca
me 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 o
xygen content, plasma protein concentration, colloid osmotic pressure,
and aortic pressure were similar in both groups. At autopsy the hydro
pic fetuses had 78 +/- 47 mL of ascites and 20 +/- 26 mL of pleural fl
uid. The water content of the hydropic fetuses and of the hydropic fet
uses' placentas was greater than that of the nonhydropic fetuses. We c
onclude that a more rapid development of anemia is associated with hyd
rops in fetal sheep. The fetal sheep that became hydropic also had an
elevated central venous pressure.