• The Korean Journal of Physiology
• /
• v.27 no.1
• /
• pp.13-25
• /
• 1993

To study the regulation of amniotic fluid volume and electrolyte concentration by the Membranes surrounding the amniotic fluid, the rate of $Li^+$ disappearance from amniotic sac of expired fetuses were examined while increasing the amniotic volume and osmolarity in rabbits. After intraamniotic injection of 1 ml isosmotic saline (about 20% of the amniotic fluid volume) containing 15 mM LiCl and 0.5 g/L Censored, the time courses of $Li^+$ and Censored disappearance were determined. From there the $Li^+$ clearance through the extrafetal routes was estimated and compared with that obtained from living fetuses. The volume, $Na^+$ concentration and osmolarity of amniotic fluid were measured and their relationships with $Li^+$ disappearance were evaluated. The fellowing results were obtained: 1. The rate of disappearance from amniotic fluid of living fetuses during the first 30 minutes was strikingly higher for $Li^+$ than for Censored, suggesting that extrafetal routes exist. At 60 and 90 minutes, however, the disappearance rate of $Li^+$ was less than that of Censored, suggesting the possibility of $Li^+$ reentry through fetal urination. 2. The disappearance of $Li^+$ from the amniotic fluid of the expired fetus was substantial, although lower than that of living fetuses, throughout the experimental period. 3. The $Na^+$ concentration and the osmolarity of the amniotic fluid of expired fetus measured 30 minutes after an intraamniotic injection of isoosmotic saline showed wide variation, but thereafter they changed gradually towards the normal extracellular fluid level. 4. When the amniotic fluid was iso- or hyposmolar, the rate of $Li^+$ disappearance from the amniotic fluid of the expired fetuses showed little variation. However, when the amniotic fluid was hyperosmolar, the rate at 30 minutes was markedly lower than those of isosmotic or hyposmotic amniotic fluid. At 90 minutes, the rate of $Li^+$ disappearance in hyperosmolar fluid reached a similar level to the rate in isosmolar fluid. 5. The intraamniotic injection of 400 mOsm/L saline solution decreased the disappearance rate of $Li^+$ from expired fetuses, while the injection of mannitol into the maternal vein induced no significant change. From these results it is concluded that: 1) a significant amount of $Li^+$ may leave the amniotic fluid via filtration through the membranes surrounding the amniotic fluid, 2) during hyperosmolar challenge to amniotic fluid, osmotic bulk flow might counteract the filterable loss, and 3) $Li^+$ disappearance might continue even after the volume and osmolarity of the amniotic fluid have recovered to control values.

• The Korean Journal of Physiology
• /
• v.29 no.1
• /
• pp.81-89
• /
• 1995

The effects of prolactin and vasopressin on the regulation of amniotic fluid (AF) volume and its $Na^{+}$ concentration $([Na^{+}])$ through the membrane surrounding the AF during increase in AF volume due to fetal urination were studied. About 70% of AF volume was replaced with normal isotonic saline solution. Isotonic saline solution (0.5 ml) containing Censored and LiCl was introduced into each amniotic sac. Vasopressin (25 ng/ml) or prolactin (1 mg/ml) of AF was then injected into experimental amniotic sac. The concentrations of Congored, $Li^{+}$, and $Na^{+}$ were measured at 30 and 60 min intervals after injection. Af samples with decreased Censored concentration ([CR]) during the period of 30 - 60 min were analyzed. The percentage change of $[Na^{+}]$ and the rate of $Li^{+}$ movement during this period were calculated, and the effects of vasopressin and prolactin on them were evaluated. Fellowing results were obtained: 1. The rate of reduction of [CR] in the AF was retarded by vasopressin or prolactin injection. 2. The rate of reduction of $[Li^{+}]$ in the AF was also retarded by vasopressin or prolactin injection. 3. The rate of reduction of $[Li^{+}]$ in the AF was less retarded by vasopressin than that of [CR]. 4. $[Na^{+}]$ changed to approach to the normal level, but this was markedly retarded by prolactin injection. 5. Direction of $Li^{+}$ movement was correlated with the change in $[Na^{+}]$ but it always moved out of the amniotic sac even when the $[Na^{+}]$ increased in vasopressin injected AF. From the above results, it is suggested that vasopressin in the AF triggers the fetus to urinate, and then the membranes surrounding the AF regulate osmolarity by efflux of $Na^{+}$. We suggest that prolactin facilitates water outflow across the amniotic membrane during increase in AF volume, in contrast to a constant volume, whereas regulation of $[Na^{+}]$ is partly restricted by prolactin.

• The Korean Journal of Physiology
• /
• v.28 no.1
• /
• pp.79-90
• /
• 1994

The objective of the present study is to assess the contribution of bulk flow to the regulatory mechanism of amniotic fluid volume and its ionic concentration in the membranes surrounding the amniotic fluid. For quantitative assessment, we prepared 4 kinds of artificial amniotic fIuids (isotonic isovolumetric, hypotonic isovolumetric, isotonic hypervolumetric and hypotonic hypervolumetric ones) by replacing 70% of amniotic fluid of pregnant rabbits with water or normal Tyrode solutions. Isoosmotic saline of 0.5 ml volume containing 0.05% Censored and 15 mM/l LiCl was administered initially into amniotic sacs of all subject animals. Samples of amniotic fluid were collected in after 30 and 90 minute intervals; the concentrations of Censored, $Na^+\;and\;Li^+$ were determined and compared. Followings are the results obtained. 1. from isovolumetric and increased Congcord group, we couldn't find significant change in $Li^+\;and\;Na^+$ concentration in isotonic amniotic fluid. However, $Na^+$ concentration increased significantly as well as a striking increase in Censored concentration in hypotonic amniotic fluid. 2. In isovoIumetric and decreased Censored group, the rate of $[Li^+]$ decrement and the rate of $[Na^+]$ increment were much higher in hypotonic amniotic fluid than in isotonic. 3. In hypervolumetric and increased Censored group, the rate of $Na^+$ efflux increased proportionately with the increment of Censored concentration up to 0.98, which was higher than the rate of $Li^+$ efflux in isotonic amniotic fluid. However, the increment of $Na^+$ concentration was rather related with the initial $Na^+$ concentration in hypotonic amniotic fluid, showing inverse relationship. $Li^+$ concentration increased only when there was a marked increase in Censored concentration and approached near a maximum value or 1. 4. For hypervolumetric and decreased Censored group, the observations were identical to isovolumetric and decreased Censored group. From these results the following conclusions could be made: 1) There is no net movement of water or monovalent cations across the membranes surrounding amniotic fIuid in isotonic isovolumetric condition. In contrast, there is a net efflux of amniotic fluid by osmotic bulk flow, resulting in elevation of $Na^+$ concentration in hypotonic isovolumetric condition. 2) In hypervolumetric conditions, there is a massive efflux of amniotic fluid or solvent drag through the surrounding membranes by fiItrative bulk flow, where the rate of $Na^+$ efflux has a linear relationship with that of water efflux. This is assumed to be carried out through enlarged and newly opened intercellular spaces resulting from increased intraamniotic pressure. 3) Once increasing intraamniotic pressure reaches a point allowing $Li^+$ to pass through during osmotic bulk flow in hypotonic amniotic fIuid, $Na^+$ influx seems to occur by diffusion simultaneously or immediately thereafter, too.

• The Korean Journal of Physiology
• /
• v.24 no.1
• /
• pp.27-37
• /
• 1990

The extrafetal transfer of $Li^{+}$ in amniotic fluid was studied in 45 pregnant rabbits. LiCl solution was administered either intravenously to mother or directly into the amniotic sac and monitored the appearance and disappearance of $Li^{+}$ in the amniotic fluid, then calculated the transfer rate of $Li^{+}$ of extrafetal origin. To study the transplacental $Li^{+}$ transfer, a solution of 150 mM LiCl was infused continuously via maternal vein (initial dose: 0.7 mmol/kg, maintaining dose: 0.03 mmol/kg/min) and the $Li^{+}$ concentration was measured in maternal blood and amniotic fluid after 60 and 120 minutes of infusion. Change in the volume of aminotic fluid was determined by Congo red dilution method at the same time. Effects of duration of gestation was not considered in this study. Extrafetal transport of $Li^{+}$ into the amniotic fluid was estimated by comparing the $Li^{+}$ concentration and volume of amniotic fluid determined before and after ligating the placental vessels. Extrafetal $Li^{+}$ transport from the amniotic fluid was determined by observing the time dependent disappearance of $Li^{+}$ and Congo red in amniotic fluid after injecting 0.5 ml solution of 15 mM or 90 mM LiCl and 50 mg/ml Congo red. Following are the results obtained: 1) During infusion of LiCl through maternal vein the ratio of the aminotic $Li^{+}$/maternal plasma $Li^{+}$ increased significantly along with the increment of fetal weight. 2) The volume of amniotic fluid of larger fetuses than 20.5 gm increased significantly during administration of LiCl while that of smaller fetuses did not change. 3) After umbilical cord ligation the $Li^{+}$ concentration of amniotic fluid of larger fetuses than 20.5 gm was decreased to $59.9{\pm}10.3%$ and $56.9{\pm}42.9%$ $(mean{\pm}S.D.)$ of those of control group after 60 and 120 minutes of LiCl infusion respectively. In amniotic fluid of smaller fetuses than 20.5 gm, there was no significant difference between control and ligation groups. 4) The disappearance rate of Congo red in the amniotic fluid was $45.2{\pm}8.2%/hr$. 5) The disappearance rate of $Li^{+}$ after intraamniotic injection of LiCl depended on the amount injected. On injecting $7.5\;{\mu}mol$ LiCl, $Li^{+}$ disappeared rapidly from the amniotic fluid and the rates after 60 min and 90 min were $97.0{\pm}2.8,\;98.5{\pm}2.0%$ respectively. On injecting $45\;{\mu}mol$ LiCl, the rates were $56.0{\pm}15.4,\;78.9{\pm}14.5%$ at 60 and 90 min. 6) From the above results it was concluded: a) $Li^{+}$ transfer into the amniotic fluid increased along with the fetal growth and one half of $Li^{+}$ influx is through the extrafetal route even after the maturation of fetal kidney. b) One half of the $Li^{+}$ transfer from the amniotic fluid was through swallowing of fetus, while the remaining half was transfered rapidly through amniotic membrane, which was concentration limited.

• Development and Reproduction
• /
• v.22 no.3
• /
• pp.263-273
• /
• 2018

Aquaporin (AQP) 3, a facilitated transporter of water and glycerol, expresses in placenta and fetal membranes, but the detailed localization and function of AQP3 in placenta remain unclear. To elucidate a role of AQP3 in placenta, we defined the expression and cellular localization of AQP3 in placenta and fetal membranes, and investigated the structural and functional differences between wild-type and AQP3 null mice. Gestational sacs were removed during mid-gestational period and amniotic fluid was aspirated for measurements of volume and composition. Fetuses with attached placenta and fetal membranes were weighed and processed for histological assessment. AQP3 strongly expressed in basolateral membrane of visceral yolk sac cells of fetal membrane, the syncytiotrophoblasts of the labyrinthine placenta and fetal nucleated red blood cell membrane. Mice lacking AQP3 did not exhibit a significant defect in differentiation of trophoblast stem cells and normal placentation. However, AQP3 null fetuses were smaller than their control litter mates in spite of a decrease in litter size. The total amniotic fluid volume per gestational sac was reduced, but the amniotic fluid-to-fetal weight ratio was increased in AQP3 null mice compared with wild-type mice. Glycerol, free fatty acid and triglyceride levels in amniotic fluid of AQP3 null mice were significantly reduced, whereas lactate level increased when compared to those of wild-type mice. These results suggest a role for AQP3 in supplying nutrients from yolk sac and maternal blood to developing fetus by facilitating transport of glycerol in addition to water, and its implication for the fetal growth in utero.

• Journal of Animal Reproduction and Biotechnology
• /
• v.35 no.2
• /
• pp.177-182
• /
• 2020

The present study aimed to investigate the conceptus-related changes during early pregnancy in the Black Bengal breed of goat. A total of 22 gravid genitalia of the Black Bengal goats were collected from local slaughterhouses. The crown-rump lengths (CRL) of the conceptuses were determined to estimate the gestational age (GA). The length and diameter of uterine horn and amniotic sac were measured, and volume of amniotic and allantoic fluid formed by individual conceptus were recorded. The results reveal that the CRL is positively correlated with GA of the conceptus (R² = 0.89, p < 0.05); however, CRL was not influenced by number of conceptus. Both the left and the right uterine horn gradually increased in size with the advancement of pregnancy irrespective of conceptus number present in the horn. The size of the amniotic sac of conceptus gradually increased with the conceptus age but maintained spherical shape from 5 to 7 weeks of pregnancy. The amniotic fluid formed by individual conceptus rapidly increased from 5 weeks (3.4 ± 0.3 mL) to 7 weeks (21.0 ± 2.0 mL) and 9 weeks (111.5 ± 4.0 mL). The volume of allantoic fluid formed by individual conceptus was steadily increased until 7 weeks (60.0 ± 5.0 mL) and began to decline slowly thereafter (50.0 ± 5.0 mL at 9 weeks). Notably, there was no effect of conceptus number per pregnancy on individual amniotic and allantoic fluid volume. The cotyledons have first appeared on the allanto-chorionic surface from 4 to 5 weeks of pregnancy. The closed eye, nostril and hooves of the conceptus became visible at 7 weeks of pregnancy. The present study has shown the basic information on conceptus-related developmental changes during early pregnancy up to 9 weeks in Black Bengal goat.