Effect of esophageal ligation on amniotic fluid volume and urinary flow rate in fetal sheep

2000 ◽  
Vol 182 (3) ◽  
pp. 699-705 ◽  
Author(s):  
Larry C. Matsumoto ◽  
Cecilia Y. Cheung ◽  
Robert A. Brace
1991 ◽  
Vol 165 (6) ◽  
pp. 1620-1626 ◽  
Author(s):  
Yuji Fujino ◽  
Connie L. Agnew ◽  
Peter Schreyer ◽  
M. Gore Ervin ◽  
Dan J. Sherman ◽  
...  

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.


2009 ◽  
Vol 200 (3) ◽  
pp. 313.e1-313.e6 ◽  
Author(s):  
Juanita K. Jellyman ◽  
Cecilia Y. Cheung ◽  
Robert A. Brace

1994 ◽  
Vol 266 (4) ◽  
pp. R1174-R1181 ◽  
Author(s):  
E. M. Wintour ◽  
D. Alcorn ◽  
A. McFarlane ◽  
K. Moritz ◽  
S. J. Potocnik ◽  
...  

Treatment of nine pregnant Merino ewes (64.0 +/- 0.4 days of gestation) with dexamethasone (D; 0.76 mg/h for 48 h) resulted in significant alterations in fetal fluids compared with eight saline-infused control animals (S; 63.0 +/- 0.9 days). There was a substantial increase in allantoic fluid volume (177 +/- 18 ml, D vs. 31 +/- 6, S) but no change in amniotic fluid volume (248 +/- 12 ml, D; 305 +/- 24, S). For allantoic fluid there was a significant decrease in osmolality (213 +/- 4 mosmol/kg water, D; 230 +/- 5, S) and alterations in composition. Amniotic fluid osmolality was unchanged (292 +/- 2 mosmol/kg water, D; 293 +/- 1, S), but amniotic fluid composition was affected. In four fetuses in which bladder and amniotic cannulas were inserted at gestational age 68-75 days, fetal urine flow rate increased from a mean of 4.1 +/- 1.1 to 13.8 +/- 2.6 ml/h after 24 h and 11.8 +/- 3.0 ml/h at 48 h for a similar maternal D infusion, whereas no such increase occurred in four control fetuses. All the fetal urine voided during a 3.5- to 4-h infusion of 51Cr-labeled EDTA into the fetal bladder was directed to the allantois. The results suggest that the increase in allantoic fluid volume resulted from increased fetal urine output into the allantoic compartment, although the composition of the excess allantoic fluid differed substantially from that of fetal urine. There was a greater incidence of abnormal cotyledons in the D-infused ewes.(ABSTRACT TRUNCATED AT 250 WORDS)


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.


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.


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