Tj. Roberts et al., Maternal 1-deamino-8-D-arginine-vasopressin-induce sequential decreases inplasma sodium concentration: Ovine fetal renal responses, AM J OBST G, 180(1), 1999, pp. 82-90
OBJECTIVE: Acute maternal plasma hypotonicity induces a reduced placental o
smotic gradient that contributes to augmented maternal-to-fetal water flow.
Subsequently, maternal plasma hyponatremia results in fetal plasma hyponat
remia, increased fetal urinary flow, and ultimately increased amniotic flui
d volume. We hypothesized that both the degree of reduction in the placenta
l osmotic gradient and the degree of fetal plasma hyponatremia influence fe
tal urinary diuretic responses. To differentiate the roles of these factors
, we determined fetal urinary responses to graded levels of plasma hyponatr
emia during a constant placental osmotic gradient. Furthermore, we sought t
o establish the minimum level of plasma hyponatremia necessary to facilitat
e an increase in fetal urine production.
STUDY DESIGN: Seven pregnant ewes (130 +/- 2 days) were prepared with mater
nal and fetal vascular catheters and a fetal bladder catheter. After 6 days
of recovery, fetal urinary flow and urine and plasma compositions were mea
sured during a 2-hour control period. At 2 hours, tap water (2 L, 38 degree
s C) with a 20-g bolus of 1-deamino-8-D-arginine-vasopressin was administer
ed to the ewe. Maternal plasma sodium concentration was decreased from cont
rol by 5 to 7, 10 to 12, and 15 to 17 mEq/L, and held at each level (levels
1, 2, and 3) for 60 minutes.
RESULTS: 1-Deamino-8-D-arginine-vasopressin administration induced sequenti
al decreases in maternal and fetal plasma sodium concentrations (control 14
6.9 +/- 0.5 mEq/L and 141.0 +/- 0.5 mEq/L, respectively) at level 1 (140.1
+/- 0.6 mEq/L and 136.7 +/- 0.7 mEq/L, respectively), level 2 (132.5 +/- 0.
7 mEq/L and 130.6 +/- 1.1 mEq/L, respectively), and level 3 (125.4 +/- 1.2
mEq/L and 123.0 +/- 1.5 mEq/L, respectively). The maternal-fetal placental
osmolality and sodium gradients were constant at each hypotonicity level. F
etal urinary flow significantly increased in association with the degree of
hyponatremia (from 0.17 +/- 0.03 mL/kg/min to 0.26 +/- 0.04 mL/kg/min, 0.3
3 +/- 0.05 ml/kg/min, and 0.38 +/- 00.5 mL/kg/min at levels 1,2, and 3, res
pectively).
CONCLUSIONS: These results indicate the following: (1) Sequential decreases
in maternal plasma tonicity result in parallel decreases in fetal plasma t
onicity. (2) The fetal urinary diuretic response is highly correlated with
the degree of fetal plasma hypotonicity, despite a constant placental osmot
ic gradient. A fetal therapeutic response (53% increase in fetal urine prod
uction) may be induced by a maternal plasma sodium concentration decrease o
f only 5 to 7 mEq/L.