• The Korean Journal of Physiology
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• v.28 no.1
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• pp.79-90
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• 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
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• v.29 no.1
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• pp.81-89
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• 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
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• v.27 no.1
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• pp.13-25
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• 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
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• v.18 no.1
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• pp.1-8
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• 1984

In order to determine the extent of the placental transfer of Lithium ion, pregnant rabbits at $27{\sim}29$ days of gestation, which has hemochorial placenta similar to the human placenta, received 2 mM/Kg of $Li^+$ in the form of LiCl intravenously. Maternal arterial blood, placental sinus blood, fetal blood, amniotic fluid and maternal urine were drawn two hours after the single dose of LiCl. Concentrations of $Li^+$, $Na^+$, $K^+$ and osmolarity were measured in plasma of collected bloods, amniotic fluid and urine. Followings are the results obtained. 1) Evident level of $Li^+$ was detected in fetal blood, although fetal plasma concentration of $Li^+$ found to be almost one third of maternal plasma. 2) Plasma concentration of $Li^+$ in placental sinus blood was higher than that in fetal plasma but lower than that in maternal plasma. It means that downward concentration gradient of $Li^+$ from mother to fetus was still remarkable two hours after the injection. 3) Significant level of $Li^+$ was also detected in amniotic fluid. It seemed likely that $Li^+$, at least in part, excreted by the fetal urinary tract. 4) There were no differences in $Na^+$ and osmolar concentration between fetal and maternal blood. 5) From above results, it was concluded that $Li^+$ may transfer across the placenta but limited passage capacity through placental barrier for $Li^+$ is significant, beacause net transfer assumed to be going on even at two hours, at which time maternal equlibrium has been reached.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.23-33
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• 1987

This study was carried out to investigate the characteristics of lithium concentration difference between maternal and fetal plasma and the effect of previous lithium loading on rapid transplacental transport of large amounts of lithium. Pregnant rabbits at $20{\sim}22\;days$ of gestation were divided into two groups: chronic $Li^+$ injection group and chronic plus acute $Li^+$ injection group. Small amounts of LiCl (1 mmol/kg per day) were given intraperitoneally to all rabbits of both group, for 5 days before sacrifice. The rabbits of chronic plus acute injection group, received additional intravenous injections of large amounts of LiCl (2 mmol/kg) one hour before sacrifice. Maternal arterial blood, placental sinus blood, fetal blood and amniotic fluid were drawn and analyzed for the plasma concentrations of $Li^+$, $Na^+$ and $K^+$ and for osmolartiy. Followings are the results obtained. 1) There was no difference in the $Li^+$ concentration between maternal plasma and placental sinus plasma in chronic lithium group, although the $Li^+$ concentration of placental sinus plasma was slightly lower than that of maternal arterial plasma in the chronic plus acute lithium group. 2) The $Li^+$ concentration of fetal plasma was much lower than that of placental sinus plasma in both groups, the ratio being $0.76{\pm}0.250$ ($mean{\pm}95%$ confidence interval) for the chronic $Li^+$ group and $0.78{\pm}0.366$ for the chronic plus acute $Li^+$ group. 3) The ratio of $Li^+$ concentration of fetal plasma to maternal arterial plasma was $0.71{\pm}0.196$ in the chronic group and $0.59{\pm}0.261$ in the chronic plus acute group. 4) $Li^+$ concentration of amniotic fluid was much higher than that of fetal plasma in the chronic $Li^+$ group but not significantly different in the chronic plus acute $Li^+$ group. 5) An acute loading of $Li^+$ did not produce any detectable changes in $Na^+$ and $K^+$ concentrations and osmolarity of the maternal plasma. The above results may suggest that: (a) The placental barrier maintains steady state lithium concentration gradient between placental sinus plasma and fetal plasma. (b) In rabbits chronically treated with $Li^+$ the steady state $Li^+$ gradient is established within one hour after an acute $Li^+$ loading, provided that the $Li^+$ concentration in the maternal plasma is less than 4 mmole/l.