Maternal administration of
DDAVP induces maternal and fetal plasma
hyponatremia, accentuates fetal urine flow, and increases amniotic fluid volume. Fetal
hemorrhage represents an acute stress that results in fetal AVP secretion and reduced urine flow rate. In view of the potential
therapeutic use of
DDAVP for pregnancies with reduced amniotic fluid volume, we sought to examine the impact of maternal hypotonicity during acute fetal
hemorrhage. Chronically catheterized pregnant ewes (130 +/- 2 days) were allocated to control or to
DDAVP-induced
hyponatremia groups. In the latter group, tap water (2,000 ml) was administered intragastrically to the ewe followed by
DDAVP (20 microg bolus, 4 microg/h) and a maintenance
intravenous infusion of 5%
dextrose water for 4 h to achieve maternal
hyponatremia of 10-12 meq/l. Thereafter, ovine fetuses from both groups were continuously hemorrhaged to 30% of estimated blood volume over a 60-min period.
DDAVP caused similar degree of reductions in plasma
sodium and osmolality in pregnant ewes and their fetuses. In response to
hemorrhage,
DDAVP fetuses showed greater reduction in hematocrit than control fetuses (14 vs. 10%). Both groups of fetuses demonstrated similar increases in plasma AVP concentration. However, the AVP-
hemorrhage threshold was greater in
DDAVP fetuses (22.5%) than in control (17.5%).
Hemorrhage had no significant impact on plasma osmolality,
electrolyte levels, or cardiovascular responses in either group of fetuses. Despite similar increases in plasma AVP,
DDAVP fetuses preserved fetal urine flow rates, with values threefold those of control fetuses. These results suggest that under conditions of acute fetal stress of
hemorrhage, maternal
DDAVP may preserve fetal urine flow and amniotic fluid volume.