Fetal recirculation of amniotic fluid arginine vasopressin

1986 ◽  
Vol 250 (3) ◽  
pp. E253-E258
Author(s):  
M. G. Ervin ◽  
M. G. Ross ◽  
R. D. Leake ◽  
D. A. Fisher

Amniotic fluid volume reflects a balance between fetal lung fluid and fetal urine production and fluid reabsorption via fetal swallowing. Arginine vasopressin (AVP) infusion decreases both fetal lung fluid and urine production and increases amniotic fluid osmolality and AVP concentration. In the present study we assessed the effect of amniotic fluid AVP injection on plasma AVP (n = 6) and renal function (n = 4) in chronically catheterized fetal lambs (X gestation = 130 days). Thirty minutes after addition of 25 micrograms of synthetic AVP into the amniotic cavity, mean +/- SE fetal plasma AVP increased from a base line of 2.7 +/- 0.2 to 14.6 +/- 3.4 pg/ml (P less than 0.01). One hundred and twenty minutes after injection, plasma AVP had increased to 26.9 +/- 5.7 pg/ml. Fetal urine volume did not change (0.78 +/- 0.01 ml/min) but significant increases in urine osmolality (169 +/- 19 to 315 +/- 25 mosm) and urine sodium (64 +/- 11 to 125 +/- 11 mueq/ml) were observed 120 min after AVP administration. In conclusion, amniotic fluid AVP levels can affect fetal plasma AVP concentration, and AVP absorbed from the amniotic fluid by the fetus remains biologically active.

1988 ◽  
Vol 255 (5) ◽  
pp. E674-E679 ◽  
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
R. Castro ◽  
J. Humme

Pregnant women may be exposed to exercise, thermal, or gastrointestinal (hyperemesis) water loss, all of which commonly induce a greater than 10 mosmol increase in plasma osmolality. Although fetal osmolality is dependent on maternal osmolality, the impact of maternal dehydration and subsequent maternal rehydration on the fetus has not been explored. Five pregnant ewes with singleton fetuses (136 +/- 1 day) were water deprived for 36 h resulting in a significant increase in plasma osmolality (298 +/- 3.4 to 313 +/- 5.0 mosmol). In response to maternal dehydration, fetal plasma osmolality (297.0 +/- 4.1 to 309.3 +/- 4.1 mosmol), arginine vasopressin (AVP) levels (1.5 +/- 0.2 to 7.9 +/- 1.0 pg/ml), hematocrit (35.1 to 38.6%), and urine osmolality (161.3 +/- 10.7 to 348.9 +/- 21.9 mosmol) significantly increased. Subsequently, ewes were rehydrated over 4 h with intravenously infused 0.45% saline (20 ml.kg-1.h-1). In response to maternal rehydration, maternal and fetal plasma osmolality decreased to basal values (298.9 +/- 3.2 and 300.1 +/- 3.8 mosmol, respectively) and fetal glomerular filtration rate (1.72 +/- 0.30 to 3.08 +/- 0.66 ml/min) and urine volume significantly increased (0.33 +/- 0.02 to 0.71 +/- 0.13 ml/min). However, fetal hematocrit (37.4%), plasma AVP (3.1 +/- 0.9 pg/ml), and urine osmolality (255.4 +/- 28.8 mosmol) did not return to basal levels during the observation period. These results demonstrate fetal hyperosmolality, blood volume contraction, AVP secretion, and altered urine production in response to maternal dehydration. Despite maternal rehydration and normalization of maternal and fetal plasma osmolality, fetal endocrine and fluid responses are prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 251 (4) ◽  
pp. E464-E469 ◽  
Author(s):  
M. G. Ross ◽  
M. G. Ervin ◽  
R. D. Leake ◽  
J. A. Humme ◽  
D. A. Fisher

Intravascular hemorrhage of the ovine fetus is a potent stimulus for arginine vasopressin (AVP) secretion. However, the method (acute, continuous) and rate of blood withdrawal may influence the fetal response. To determine the hemorrhage threshold for AVP secretion in response to slow continuous hemorrhage, five chronically catheterized ovine fetuses were continuously hemorrhaged (0.6% blood vol/min) to 24-30% blood volume withdrawal. Immediately after hemorrhage fetal blood was reinfused at an equivalent rate. In addition to AVP measurements by radioimmunoassay, fetal urinary responses were monitored as an index of fetal AVP secretion. Significant increases in plasma AVP occurred during hemorrhage (1.0 +/- 0.1 to 8.0 +/- 2.0 pg/ml). The fetal plasma AVP-hemorrhage threshold, as defined by regression analysis, occurred at withdrawal of 13.0% blood volume. Fetal urine volume significantly decreased from a mean basal rate of 0.59 +/- 0.03 to 0.21 +/- 0.06 ml/min at the completion of hemorrhage. Urinary sodium, potassium, and osmolar excretion also significantly decreased at the completion of hemorrhage. Urinary AVP excretion, urine osmolality, sodium, and potassium concentrations did not change significantly during the hemorrhage period but increased significantly during the reinfusion period; the delay a result of renal and catheter dead space. Reinfusion of blood resulted in a return of plasma AVP to basal levels. These results define a threshold for AVP secretion and demonstrate significant urinary effects in response to slow continuous hemorrhage.


1986 ◽  
Vol 250 (2) ◽  
pp. R235-R239
Author(s):  
L. L. Woods

The contribution of fetal urine to the increase in amniotic fluid osmolality during maternal hypertonicity was studied in chronically catheterized sheep of 130-135 days gestation. Nine percent NaCl was injected simultaneously into fetal and maternal veins, followed by a continuous infusion into the maternal vein. Maternal and fetal plasma osmolalities rose by 15 +/- 1 (SE) and 13 +/- 1 mosmol/kg, respectively, and remained constant for 4 h. Fetal urine osmolality rose significantly from 188 +/- 31 to 277 +/- 32 mosmol/kg within 1 h and remained constant thereafter. Fetal urine flow rose transiently, fell to normal within 10 min, and averaged 70% of normal beyond 1 h. Amniotic fluid osmolality rose by 10.8 +/- 2.8 mosmol/kg over 4 h. Following hypertonic injection into three fetuses blocked by the arginine vasopressin antagonist d(CH2)5D-tyr(Et)VAVP, urine osmolality did not change, and amniotic fluid osmolality rose by 2.7 +/- 0.3 mosmol/kg. Thus it appears that the increase in amniotic fluid osmolality during maternal hypertonicity may be due largely to an increased fetal urine osmolality coupled with a decreased flow of fetal urine into the amniotic space, rather than to bulk flow of fluid across the membranes and uterine wall.


1990 ◽  
Vol 259 (4) ◽  
pp. R745-R752 ◽  
Author(s):  
K. A. Dickson ◽  
S. B. Hooper ◽  
I. C. McMillen ◽  
R. Harding

Our aim was to determine fetal and maternal endocrine and fluid-balance responses to prolonged loss of amniotic and allantoic fluids in sheep. In seven sheep, amniotic and allantoic fluids were drained [379.1 +/- 20.1 (SE) ml/day] from 107 to 135.3 +/- 0.6 days of gestation (term: 145 days). The results from these sheep were compared with those from seven control sheep. Maternal water intake, urine production, and urine osmolality were not altered by fluid drainage, nor were fetal and maternal arterial blood gases, pH, or plasma osmolalities. Fluid drainage increased amniotic, but not allantoic, fluid osmolality. Maternal plasma cortisol concentration increased with fluid drainage, but maternal plasma concentrations of prolactin and arginine vasopressin were unchanged. Fluid drainage increased prolactin concentrations in fetal plasma and amniotic fluid, but fetal plasma concentrations of cortisol (hydrocortisone), arginine vasopressin, norepinephrine, and epinephrine were unchanged. Our results show that the fetus is capable of maintaining its plasma osmolality despite prolonged loss of fluid from its amniotic and allantoic sacs and that this is associated with alterations in the production rate and the composition of amniotic fluid.


2005 ◽  
Vol 289 (1) ◽  
pp. H146-H150 ◽  
Author(s):  
Job Faber ◽  
Debra Anderson ◽  
Roger Hohimer ◽  
Qin Yang ◽  
George Giraud ◽  
...  

Seven singleton 120-day fetal lambs were prepared with a shunt from the lung to the gastric end of the esophagus, a bladder catheter, and multiple amniotic fluid and vascular catheters. The urachus was ligated. Beginning 7 days later, amniotic fluid volumes were determined by drainage, followed by replacement with 1 liter of lactated Ringer (LR) solution. Urine flow into the amnion was measured continuously. In 14 of 27 experiments, amniotic fluid volumes were determined again 2 days after the inflow into the amnion had consisted of urine only and in 13 experiments after the inflow of urine had been supplemented by an intraamniotic infusion of LR solution. Intramembranous absorption was calculated from the inflows and the changes in volume between the beginning and end of each experiment. The relations between absorption rate and amniotic fluid volume, the “function curves,” were highly individual. Urine production during the infusion of LR solution did not decrease, fetal plasma renin activity decreased ( P < 0.001), and amniotic fluid volume increased by 140% [SE (27%), P < 0.005], but the increase in the amniochorionic absorption rate of 411% [SE (48%), P < 0.001] was greater ( P < 0.005) than the increase in volume. Each of the seven fetuses was proven capable of an average intramembranous absorption rate that exceeded 4.5 liters of amniotic fluid per day. During the infusion of LR solution, the increase in the rate of absorption matched the rate of infusion (both in ml/h), with a regression coefficient of 0.75 ( P < 0.001). Thus, even for large amniotic fluid volumes, volume is not limited by the absorptive capacity of the amniochorion, and, at least in these preparations, the position of the function curve and not the natural rate of inflow was the major determinant of resting amniotic fluid volume.


2012 ◽  
Vol 302 (7) ◽  
pp. L664-L678 ◽  
Author(s):  
Alana J. Westover ◽  
Stuart B. Hooper ◽  
Megan J. Wallace ◽  
Timothy J. M. Moss

Intra-amniotic (IA) lipopolysaccharide (LPS) induces intrauterine and fetal lung inflammation and increases lung surfactant and compliance in preterm sheep; however, the mechanisms are unknown. Prostaglandins (PGs) are inflammatory mediators, and PGE2 has established roles in fetal lung surfactant production. The aim of our first study was to determine PGE2 concentrations in response to IA LPS and pulmonary gene expression for PG synthetic [prostaglandin H synthase-2 (PGHS-2) and PGE synthase (PGES)] and PG-metabolizing [prostaglandin dehydrogenase (PGDH)] enzymes and PGE2 receptors. Our second study aimed to block LPS-induced increases in PGE2 with a PGHS-2 inhibitor (nimesulide) and determine lung inflammation and surfactant protein mRNA expression. Pregnant ewes received an IA saline or LPS injection at 118 days of gestation. In study 1, fetal plasma and amniotic fluid were sampled before and at 2, 4, 6, 12, and 24 h after injection and then daily, and fetuses were delivered 2 or 7 days later. Amniotic fluid PGE2 concentrations increased ( P < 0.05) 12 h and 3–6 days after LPS. Fetal lung PGHS-2 mRNA and PGES mRNA increased 2 ( P = 0.0084) and 7 ( P = 0.014) days after LPS, respectively. In study 2, maternal intravenous nimesulide or vehicle infusion began immediately before LPS or saline injection and continued until delivery 2 days later. Nimesulide inhibited LPS-induced increases in PGE2 and decreased fetal lung IL-1β and IL-8 mRNA ( P ≤ 0.002) without altering lung inflammatory cell infiltration. Nimesulide decreased surfactant protein (SP)-A ( P = 0.05), -B ( P = 0.05), and -D ( P = 0.0015) but increased SP-C mRNA ( P = 0.023). Thus PGHS-2 mediates, at least in part, fetal pulmonary responses to inflammation.


2002 ◽  
Vol 282 (3) ◽  
pp. H850-H854 ◽  
Author(s):  
J. Job Faber ◽  
Debra F. Anderson

Swallowing of amniotic fluid and lung fluid inflow were eliminated in 10 chronically instrumented fetuses. The urachus was ligated, and fetal was urine drained to the outside. At the beginning and the end of 21 experiments of 66 ± 5 (SE) h duration, all amniotic fluid was temporarily drained to the outside for volume measurement and sampling. Amniotic fluid osmolalities and oncotic pressures were experimentally controlled. Amniochorionic absorption of amniotic fluid depended strongly on the osmolality difference between amniotic fluid and fetal plasma ( P< 0.001), but at zero osmolality difference there still was a mean absorption rate of 23.8 ± 4.7 (SE) ml/h ( P < 0.001). Absorption was unaffected by the protein concentration difference between amniotic fluid and fetal plasma, but infused bovine albumin in the amniotic fluid was absorbed at a rate of 1.8 ± 0.4 g/h ( P < 0.001), corresponding to a volume flow of fluid of 33.8 ± 6.1 ml/h ( P < 0.001). Fluid absorption in the amniochorion is driven in part by crystalloid osmotic pressure, but about 25 ml/h is absorbed by a path that is permeable to protein. That path has the physiological characteristics of lymphatic drainage, although no anatomic basis is known to exist for a lymphatic system in the amniochorion.


1995 ◽  
Vol 7 (5) ◽  
pp. 1311 ◽  
Author(s):  
EM Wintour ◽  
R Riquelme ◽  
C Gaete ◽  
C Rabasa ◽  
E Sanhueza ◽  
...  

Samples of maternal and fetal plasma, fetal urine, and amniotic fluid were collected from 8 chronically cannulated pregnant llamas, in the last third of gestation. The samples were obtained for up to 18 days post-surgery. Osmolality, sodium (Na), potassium (K), chloride (Cl), and urea were measured on 40 samples collected on days 1, 2, 3, 4-5, 6-7, 8-9, and 10-19. The osmolalities of maternal and fetal plasma, fetal urine and amniotic fluid, averaged over these 7 time periods, were, respectively, 312 +/- 2, 311 +/- 1, 484 +/- 14, and 317 +/- 1 mosmol kg-1. Values are given as mean +/- s.e. The major differences from fetal fluid values in the ovine fetus (from previously published values) were the higher osmolality and urea concentration of llama fetal urine. Urine flow rate measured in 6 fetuses, 4.5-6.5 kg body weight, was 5.8 +/- 0.4 mliter h-1; urea clearance rate was 55.5 +/- 11.8 mliter h-1. Glomerular filtration rate (GFR), measured with 51Cr-EDTA in 5 fetuses on 1-4 occasions, was 111.4 +/- 23.3 mliter h-1. Fractional reabsorptions (FR) of Na, K and Cl were 97.9 +/- 1, 75.9 +/- 13.5 and 97.7 +/- 0.4% respectively. The GFR (25 mliter kg-1 h-1) and urine flow rate (1 mL kg-1 h-1) were less than half and about one-tenth the respective values in ovine fetuses. As Na reabsorption is the major oxygen-consuming activity of the kidney, the llama fetal kidney requires only half the oxygen needed by the ovine fetal kidney to reabsorb the filtered sodium load. The reason for the formation of hypertonic, rather than hypotonic, urine in the fetal llama may be due to both greater morphological maturity of the kidney and the excretion of as yet unidentified osmotically active organic substances.


1996 ◽  
Vol 81 (6) ◽  
pp. 2588-2594 ◽  
Author(s):  
Stephanie E. Mann ◽  
Mark J. M. Nijland ◽  
Michael G. Ross

Mann, Stephanie E., Mark J. M. Nijland, and Michael G. Ross.Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. J. Appl. Physiol. 81(6): 2588–2594, 1996.—Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-d-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 ± 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-μg) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 ± 13 to 253 ± 21 mosmol/kg) and remained elevated at 72 h (400 ± 13 mosmol/kg). Urinary sodium (33.0 ± 4.5 to 117.2 ± 9.7 meq/l) and chloride (26.0 ± 2.8 to 92.4 ± 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 ± 3 to 299 ± 4 mosmol/kgH2O), although there was no change in fetal plasma osmolality (294 ± 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 ± 0.03 to 0.05 ± 0.02 ml ⋅ kg−1 ⋅ min−1at 2 h and 0.06 ± 0.01 ml ⋅ kg−1 ⋅ min−1after 72 h), AF volume did not change (693 ± 226 to 679 ± 214 ml). There were no changes in fetal arterial blood pressures, pH,[Formula: see text], or[Formula: see text] after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.


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