Maternal plasma hypo-osmolality: Effects on spontaneous and stimulated ovine fetal swallowing

Fetal swallowing is a major route of amniotic fluid resorption, and thus swallowing activity may alter amniotic fluid volume. Near-term ovine fetal swallowing increases in response to plasma and/or cerebrospinal fluid hypertonicity. As maternal hydration status alters amniotic fluid volume, we hypothesized that maternal plasma hypotonicity may alter fetal swallowing activity. Pregnant ewes (130 ± 1 d; n = 6) were chronically prepared with maternal and fetal vascular catheters, a fetal esophageal flow probe, and fetal thyrohyoid and nuchal and thoracic esophagus electromyogram electrodes. Spontaneous fetal swallowing and hypertonic saline thresholds for stimulated swallowing were determined prior to and following maternal hypotonicity induced with water loading and intravenous DDAVP (arginine vasopressin V2 agonist). Fetal swallowing thresholds were determined with intracarotid injections (0.15 ml/kg) of increasing sodium chloride concentrations (0.15-1.2 M) at 2-min intervals. Maternal DDAVP infusion significantly decreased mean (±SEM) maternal and fetal plasma osmolalities (298 ± 2-284 ± 3; 295 ± 2-278 ± 3 mOsm/kg, respectively) and sodium concentrations (1473 ± 0.4-137.5 ± 0.9; 142.7 ± 0.8-133.5 ± 1.0 mEq/l, respectively), suppressed spontaneous swallowing activity and volume (1.1 ± 0.2-0.6 ± 0.1 swallows/min; 0.7 ± 0.2-0.5 ± 0.1 ml/min, respectively) and significantly increased the osmotic threshold for swallowing stimulation (0.77 ± 0.08-1.03 ± 0.09 M NaCl). We conclude that: (1) maternal, and thus fetal, plasma hypotonicity results in suppression of spontaneous fetal swallowing activity and a decrease in volume swallowed, suggesting that spontaneous fetal ingestive behavior results, in part, from tonic dipsogenic stimulation, and (2) under hypotonic conditions, the intracarotid NaCl injection concentration for swallowing stimulation increases. These results suggest that the reset (lower) maternal plasma osmolality during human pregnancy may serve to minimize fetal ingestive and perhaps arginine vasopressin-mediated antidiuretic responses to acute maternal hypertonicity.