Maternal DDAVP-induced hyponatremia preserves fetal urine flow during acute fetal hemorrhage

Abstract

. Maternal DDAVPinduced hyponatremia preserves fetal urine flow during acute fetal hemorrhage. Am J Physiol Regul Integr Comp Physiol 285: R373-R379, 2003. First published April 10, 2003 10.1152/ajpregu.00765.2002-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 Ϯ 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 g bolus, 4 g/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. rapid induction of hyponatremia; arginine vasopressin; amniotic fluid volume; pregnancy; sheep AMNIOTIC FLUID VOLUME is dependent on a balance of fluid secretion (fetal urine flow and lung liquid) and fluid resorption (fetal swallowing and, in sheep and perhaps humans, intramembranous flow) (4,8,21). Fetal urine is the principal source of amniotic fluid, with production rates in the near-term ovine or human fetus of ϳ1,000 ml/day (5, 14). Fetal endocrine responses to intrauterine stress, including increased AVP secretion, may reduce fetal urine flow rates and thus amniotic fluid volume (oligohydramnios) (23,24). Consequently, oligohydramnios may be a marker of fetal compromise and is associated with significant perinatal morbidity and mortality. In addition, oligohydramnios presents an ongoing risk of umbilical cord compression and fetal hypoxia.To address the risks of oligohydramnios, clinicians have increased amniotic fluid volume with infusions administered via transabdominal or transcervical catheters. Alternatively, amniotic fluid volume may be increased by a...

Central cholinergic mechanisms mediate swallowing, renal excretion, and c-fos expression in the ovine fetus near term

“…The present study demonstrates that central administration of carbachol increases fetal urine production and alters sodium, potassium, and chloride excretion. In fetuses, several investigations have shown that fetal renal functions (such as urinary flow rate, free water clearance, and urine osmolality) can be affected by hemorrhage and hyperosmotic mechanisms (6,11,29), indicating that volume and osmotic mechanisms in the control of the renal fluid-electrolyte excretion develop in utero.…”

“…Fetal renal fluid and electrolyte excretion also can be controlled by hemorrhage, osmotic, and vasopressin mechanisms (6,10,11,15,29). Nijland et al found anticholinergic suppression of ovine fetal swallowing (28).…”