The relative stability of AF volume in spite of large fluid shifts
suggests that control mechanisms exist. It is noteworthy that only
half of fetuses with esophageal atresia, and two-thirds of fetuses
with duodenal or proximal jejunal atresia develop polyhydramnios;
this suggests that other mechanisms besides swallowing are
involved in AF volume regulation. Compensation via the
intramembranous pathway is the best explanation for the
significant number of fetuses with upper intestinal atresia who do
not develop polyhydramnios. Compensation is evident in sheep
where ligation of the esophagus leads to increased absorption of AF
into the fetal circulation with no change in the total AF volume.
Intramembranous absorption occurs against a hydrostatic gradient
and had been assumed to be driven by passive diffusion due to an
osmotic gradient. More recent studies show that passive diffusion
accounts for only part of the intramembranous fluid absorption
and that many solutes diffuse in the opposite direction (from fetus
to AF). It is likely that much larger shifts of fluid and solutes occur
by bulk transfer of AF with all of its dissolved solutes into the fetal
circulation perhaps via a trans-cellular vesicular transport
mechanism.