scholarly journals Regulation of intramembranous absorption and amniotic fluid volume by constituents in fetal sheep urine

2013 ◽  
Vol 305 (5) ◽  
pp. R506-R511 ◽  
Author(s):  
Debra F. Anderson ◽  
Sonnet S. Jonker ◽  
Samantha Louey ◽  
Cecilia Y. Cheung ◽  
Robert A. Brace

Our objective was to test the hypothesis that fetal urine contains a substance(s) that regulates amniotic fluid volume by altering the rate of intramembranous absorption of amniotic fluid. In late gestation ovine fetuses, amniotic fluid volumes, urine, and lung liquid production rates, swallowed volumes and intramembranous volume and solute absorption rates were measured over 2-day periods under control conditions and when urine was removed and continuously replaced at an equal rate with exogenous fluid. Intramembranous volume absorption rate decreased by 40% when urine was replaced with lactated Ringer solution or lactated Ringer solution diluted 50% with water. Amniotic fluid volume doubled under both conditions. Analysis of the intramembranous sodium and chloride fluxes suggests that the active but not passive component of intramembranous volume absorption was altered by urine replacement, whereas both active and passive components of solute fluxes were altered. We conclude that fetal urine contains an unidentified substance(s) that stimulates active intramembranous transport of amniotic fluid across the amnion into the underlying fetal vasculature and thereby functions as a regulator of amniotic fluid volume.

2014 ◽  
Vol 306 (3) ◽  
pp. R185-R189 ◽  
Author(s):  
Robert A. Brace ◽  
Cecilia Y. Cheung ◽  
Debra F. Anderson

Intramembranous absorption increases during intra-amniotic infusion of physiological saline solutions. The increase may be due partly to the concomitant elevation in fetal urine production as fetal urine contains a stimulator of intramembranous absorption. In this study, we hypothesized that the increase in intramembranous absorption during intra-amniotic infusion is due, in part, to dilution of a nonrenal inhibitor of intramembranous absorption that is present in amniotic fluid. In late-gestation fetal sheep, amniotic fluid volume and the four primary amniotic inflows and outflows were determined over 2-day intervals under three conditions: 1) control conditions when fetal urine entered the amniotic sac, 2) during intra-amniotic infusion of 2 l/day of lactated Ringer solution when urine entered the amniotic sac, and 3) during the same intra-amniotic infusion when fetal urine was continuously replaced with lactated Ringer solution. Amniotic fluid volume, fetal urine production, swallowed volume, and intramembranous absorption rate increased during the infusions independent of fetal urine entry into the amniotic sac or its replacement. Lung liquid secretion rate was unchanged during infusion. Because fetal membrane stretch has been shown not to be involved and because urine replacement did not alter the response, we conclude that the increase in intramembranous absorption that occurs during intra-amniotic infusions is due primarily to dilution of a nonrenal inhibitor of intramembranous absorption that is normally present in amniotic fluid. This result combined with our previous study suggests that a nonrenal inhibitor(s) together with a renal stimulator(s) interact to regulate intramembranous absorption rate and, hence, amniotic fluid volume.


1997 ◽  
Vol 273 (3) ◽  
pp. R1094-R1102 ◽  
Author(s):  
M. L. Cock ◽  
R. Harding

We determined the effects of placental insufficiency induced by umbilicoplacental embolization on fetal renal function and amniotic fluid volume and composition. Pregnant ewes underwent surgery at 115 +/- 2 days after mating (term approximately 147 days) for implantation of fetal vascular, bladder, and amniotic sac catheters. We studied five fetuses from 120 to 140 days during umbilicoplacental embolization and six control fetuses. Umbilicoplacental embolization reduced fetal arterial partial pressure of oxygen from 24.1 +/- 0.5 mmHg (pretreatment) to 14.6 +/- 0.2 mmHg. Fetal body weights were reduced to 80% of control values. Urine production and glomerular filtration rate in treated fetuses were significantly lower than in controls at 135 days of gestation. Amniotic fluid volume was not different between embolized and control animals. Fetal urine production in treated fetuses, when adjusted for body weight, was not different from that in control fetuses. We conclude that, in fetal growth restriction, reduced kidney weight, rather than hypoxemia per se is responsible for reduced urine production, which, if severe and prolonged, may contribute to oligohydramnios.


1991 ◽  
Vol 165 (6) ◽  
pp. 1620-1626 ◽  
Author(s):  
Yuji Fujino ◽  
Connie L. Agnew ◽  
Peter Schreyer ◽  
M. Gore Ervin ◽  
Dan J. Sherman ◽  
...  

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.


2009 ◽  
Vol 36 (2) ◽  
pp. 191-195 ◽  
Author(s):  
S. M. Lee ◽  
J. K. Jun ◽  
E. J. Lee ◽  
J. H. Lee ◽  
C.-W. Park ◽  
...  

1993 ◽  
Vol 169 (4) ◽  
pp. 885-888 ◽  
Author(s):  
James E. Maher ◽  
John Owen ◽  
John Hauth ◽  
Robert Goldenberg ◽  
C.Richard Parker ◽  
...  

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