Maternal 1-deamino-8-D-arginine-vasopressin-induce sequential decreases inplasma sodium concentration: Ovine fetal renal responses

Citation
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
Citations number
19
Categorie Soggetti
Reproductive Medicine","da verificare
Journal title
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
ISSN journal
00029378 → ACNP
Volume
180
Issue
1
Year of publication
1999
Part
1
Pages
82 - 90
Database
ISI
SICI code
0002-9378(199901)180:1<82:M1SDI>2.0.ZU;2-3
Abstract
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.