Amniotic Fluid Homeostasis Research Articles

The Stomach-Bladder Proximity Sign: What Does it Say?

AbstractFetal gastrointestinal tract (GIT) anomalies account for 7 to 8% of congenital malformations. There are no well defined protocols for examining fetal GIT, which is a dynamic system that plays a vital role in amniotic fluid homeostasis. We present four cases that highlight the importance of the relative positions of the stomach, small bowel, and bladder in the coronal plane of the fetal abdomen in the diagnosis/exclusion of certain anomalies.

Polyhydramnios, Transient Antenatal Bartter’s Syndrome, and MAGED2 Mutations

BackgroundThree pregnancies with male offspring in one family were complicated by severe polyhydramnios and prematurity. One fetus died; the other two had transient massive salt-wasting and polyuria reminiscent of antenatal Bartter’s syndrome.MethodsTo uncover the molecular cause of this possibly X-linked disease, we performed whole-exome sequencing of DNA from two members of the index family and targeted gene analysis of other members of this family and of six additional families with affected male fetuses. We also evaluated a series of women with idiopathic polyhydramnios who were pregnant with male fetuses. We performed immunohistochemical analysis, knockdown and overexpression experiments, and protein–protein interaction studies.ResultsWe identified a mutation in MAGED2 in each of the 13 infants in our analysis who had transient antenatal Bartter’s syndrome. MAGED2 encodes melanoma-associated antigen D2 (MAGE-D2) and maps to the X chromosome. We also identified two different MAGED2 mutations in two families with idiopathic polyhydramnios. Four patients died perinatally, and 11 survived. The initial presentation was more severe than in known types of antenatal Bartter’s syndrome, as reflected by an earlier onset of polyhydramnios and labor. All symptoms disappeared spontaneously during follow-up in the infants who survived. We showed that MAGE-D2 affects the expression and function of the sodium chloride cotransporters NKCC2 and NCC (key components of salt reabsorption in the distal renal tubule), possibly through adenylate cyclase and cyclic AMP signaling and a cytoplasmic heat-shock protein.ConclusionsWe found that MAGED2 mutations caused X-linked polyhydramnios with prematurity and a severe but transient form of antenatal Bartter’s syndrome. MAGE-D2 is essential for fetal renal salt reabsorption, amniotic fluid homeostasis, and the maintenance of pregnancy. (Funded by the University of Groningen and others.)

Involvement of HDL receptor SR-BI-mediated vitamin e uptake in murine neural tube closure

Involvement of HDL receptor SR-BI-mediated vitamin e uptake in murine neural tube closure

The expression and regulation of aquaporins in placenta and fetal membranes

Previous studies by our group as well as other researchers have found expression of Aquaporins (AQPs) 1, 3, 8, and 9 in human chorioamniotic membranes and placenta. Our previous study found that the alteration of the expression of AQPs 1, 3, 8, and 9 in placenta and fetal membranes was an adaptive response to maintain amniotic fluid homeostasis in case of abnormal amniotic fluid volume, which is likely to affect the intramembranous absorption and transport of water and solute from mother to fetus. However, the actual regulation mechanisms of intramembranous absorption and placental water flow are not yet clear, making it difficult to treat abnormal amniotic fluid volume effectively. Several studies found that many factors, including hormone levels, osmotic pressure, temperature, and oxygen concentration, regulate expression of AQPs in placenta, fetal membranes, and other mammalian organs through several signal transduction pathways, such as the cAMP, the MAPK, the PI3K/AKT, and the PKC pathways. These factors could provide potential therapeutic targets for the treatment of abnormal amniotic fluid volume.

Utilisations thérapeutiques des membranes fœtales et de leurs cellules dérivées

During all the pregnancy, the foetal membranes play several functions (mechanic, anti-infectious, hormonal, regulation of the amniotic fluid homeostasis…) fundamental for an optimal development and maternal-foetal physiology. After delivery, these amniotic membranes have regained for a few years, a new interest and a second “ex-utero” life due to their therapeutic use. This use was firstly initiated experimentally in ophthalmological pathologies, around 1950. The recent understanding of molecular and cellular mechanisms enables to explain scientifically these first empiric uses. They are an interesting solution in ocular aggressions like viral attacks, chemical or temperature burns. They also represent an attractive alternative in case of corneal grafts and a biological matrix for limb cells cultures used to regenerate the corneal lesions. An industrial engineering is now in place to boost the performances of these human membranes. The isolation and identification of stem cells (mesenchymal origin) in these amniotic membranes are promising in the field of cell therapy. Recently, the first results have been published demonstrating the clinical efficiency of the stems cell during pancreatic, cardiac, lung neuronal lesions.

Cellular and subcellular localization of aquaporins 1, 3, 8, and 9 in amniotic membranes during pregnancy in mice

The amniotic membrane encloses the amniotic fluid and plays roles in the regulation of amniotic fluid flux through the intramembranous pathway during pregnancy. Aquaporins (AQPs) 1, 3, 8, and 9 are expressed in amniotic membranes. AQPs are water channel proteins that facilitate the rapid flux of water or small molecules across the plasma membrane. Recently, additional roles of AQPs in facilitating cell migration, proliferation, and apoptosis have been suggested, with AQPs being distributed in the appropriate subcellular regions for their functions. The cellular and subcellular distributions of AQPs in the amniotic membrane however remain unclear. We have examined the cellular and subcellular localization of AQPs in amniotic membranes during pregnancy in mice. After embryonic day 12 (E12), AQP1 was distributed in the plasma membrane of finely branched cell processes in the amniotic fibroblasts. AQP3 was present in both epithelial cells and fibroblasts between E10 and E12. The distribution of AQP3 in the epithelial cells dynamically changed as follows: at E14 in the lateral membrane and apical junction; at E16 in the lateral membrane alone; at E17 in the lateral membrane and cytoplasm. AQP8 was expressed in the epithelial cells and complementarily localized in the apical junction and the lateral membrane. AQP9 was detected only in the apoptotic cells of the epithelium. These cellular and subcellular localizations of amniotic AQPs indicate that each AQP plays distinct functional roles, such as in water and urea transport, cell migration, cell proliferation, and apoptosis, for amniotic fluid homeostasis or tissue remodeling of amniotic membranes.

Gastric emptying cycles in the human fetus

Fetal swallowing contributes greatly to amniotic fluid homeostasis and fetal somatic development. Despite the absorption and recirculation of significant volumes of amniotic fluid, little is known about the rates of fetal gastric emptying or gastrointestinal absorption. We sought to determine the patterns of human fetal gastric emptying cycles across gestation. The gastric emptying cycle of 80 normal human fetuses at 12 to 39 weeks of gestation was studied. Real-time ultrasound examination of the fetal stomach (defined as the largest gastric area inclusive of the pylorus) was recorded continuously for a minimum of 1 hour (60-112 minutes). Images were replayed with measurements of gastric size every minute. The gastric area ratio was defined as the ratio of the fetal gastric area divided by the area of the fetal abdominal transverse section. The changes in gastric area ratio of all subjects were analyzed with the discrete Fourier transform method. The calculable maximum cycle was 60 or 112 minutes, and the minimum cycle was 2 minutes. The highest and second highest peaks of all power spectrum were recorded, and each cycle was converted from frequency of each peak. The gastric emptying cycles of the highest peak before 24 weeks of gestation were scattered between 30 and 100 minutes with low power. At 32 to 35 weeks of gestation, cycles were focused at approximately 40 minutes with increased power. At term, the cycles increased to >80 minutes. The gastric emptying cycles of the second highest peak were constant at 20 minutes, with stronger power after 24 weeks of gestation. Fetal gastric emptying cycles normalize during the early third trimester. The near-term evidence of delayed emptying may contribute to newborn infant feeding satiation.

Expression and localization of aquaporin 1 and 3 in human fetal membranes

Objectives: Aquaporins are a family of water-selective channels that facilitate fluid movement across cell membranes. Specifically, aquaporin 1 (AQP1) and aquaporin 3 (AQP3) have been found to be important in osmotic water movement across membranes. Our goal in this study was (1) to determine whether AQP1 or AQP3 messenger RNA are expressed in the chorioamniotic membrane and, if present, (2) to determine the precise membrane location of these aquaporins. Study Design: Placentas were collected from women with intact membranes not in labor who underwent elective cesarean sections at term (37-40 weeks). The membranes (amnion and chorion) directly overlying the placenta were sampled as well as the free-floating reflected membranes. RNA and protein were isolated from the amnion and chorion. Reverse transcriptase-polymerase chain reaction, Western analysis, and immunohistochemistry were used to determine expression and localization of AQP1 and AQP3. Results: AQP1 messenger RNA was found in amnion and chorion from both membrane locations. Western analysis also yielded positive results for amnion and chorion from both locations. Immunohistochemical localization of AQP1 showed it to be present on the apical aspect of the chorionic plate amnion. AQP3 protein was not found in the fetal membranes. Conclusions: AQP1 is present in the fetal membranes. AQP1 may play a role in water movement from the amniotic cavity across the placenta into the fetal circulation. Further studies are needed to clarify our understanding of the role of fetal membrane aquaporins in amniotic fluid homeostasis. (Am J Obstet Gynecol 2002;187:902-7.)

Effects of central angiotensin II receptor antagonism on fetal swallowing and cardiovascular activity

Objective: Fetal plasma angiotensin II levels are 10 times the levels found in adults. Despite these high levels, central injection of angiotensin II may stimulate fetal swallowing and increase fetal arterial blood pressure. We postulated that the high rate of spontaneous fetal swallowing and normal fetal pressor regulation may be dependent, in part, on central angiotensin II. In view of the potential dipsogenic role of both type 1 and type 2 angiotensin II receptors, we examined the central effect of the nonselective angiotensin II receptor antagonist saralasin on fetal swallowing and cardiovascular responses. Study Design: Six time-dated pregnant ewes and fetuses were chronically prepared with fetal vascular and intracerebroventricular catheters, electrocorticograms, and esophageal electromyogram electrodes and studied at 130 ± 1 days' gestation. After an initial 2-hour baseline period (0 to 2 hours), saralasin (1 mL, 64 μg) was injected intracerebroventricularly (2 to 4 hours). After 4 hours the dose of saralasin was repeated together with angiotensin II (1 mL, 6.4 μg), and the fetuses were monitored for a final 2 hours. Four fetuses also underwent an identical control study (on an alternate day) in which saralasin was replaced with artificial cerebrospinal fluid. Results: Blockade of central angiotensin II receptors by intracerebroventricular saralasin significantly reduced mean (± SEM) spontaneous fetal swallowing (1.3 ± 0.1 to 0.4 ± 0.1 swallows per minute; P <.001) but did not alter fetal mean blood pressure (50 ± 5 versus 56 ± 5 mm Hg). Intracerebroventricular angiotensin II, in the presence of saralasin, did not affect swallowing (0.6 ± 0.1 swallows per minute) or fetal blood pressure. In the control study, intracerebroventricular artificial cerebrospinal fluid did not change fetal swallowing (0.9 ± 0.1 versus 1.0 ± 0.1 swallows per minute), whereas intracerebroventricular angiotensin II significantly increased swallowing activity (1.0 ± 0.1 versus 2.0 ± 0.1 swallows per minute; P <.001) and fetal blood pressure (51 ± 2 to 59 ± 3 mm Hg; P =.003). Conclusions: Tonic activity of central angiotensin II receptor stimulation contributed to the high rate of basal ovine fetal swallowing but not fetal basal blood pressure. Angiotensin II–mediated fetal dipsogenic and pressor responses are a result of specific angiotensin II receptor binding in central brain regions. These results indicate that fetal exposure to angiotensin II antagonists or angiotensin-converting enzyme inhibitors may have adverse effects on fetal and amniotic fluid homeostasis. (Am J Obstet Gynecol 2001;185: 828-33.)

Plasma osmolality dipsogenic thresholds and c-fos expression in the near-term ovine fetus.

In ovine and human pregnancy, fetal swallowing contributes importantly to amniotic fluid homeostasis. Fetal dipsogenic responsiveness to short-term plasma hyperosmolality develops in late gestation, although fetal swallowing is not stimulated in response to long-term plasma osmolality increases (2 to 3%), which typically stimulate adult drinking behavior. To explore the near-term fetal plasma osmolality threshold for swallowing stimulation, we examined the effects of i.v. hypertonic saline-induced subacute increases in plasma hypertonicity on fetal swallowing behavior. Central sites of activation were examined by c-fos expression in putative dipsogenic nuclei. The results demonstrate that subacute 2 to 3% plasma osmolality increases do not stimulate near-term ovine fetal swallowing. However, fetal swallowing activity significantly increased (3 times) after plasma osmolality increased >6% above basal values. Consistent with a specific dipsogenic response, i.v. hypertonic saline induced c-fos expression in the anterior third ventricle region, a putative dipsogenic center, as well as in the fetal hindbrain. The stimulation of fetal swallowing under conditions of higher osmotic stimulation and the correlation with forebrain c-fos expression indicates that near-term fetal osmoregulation mechanisms are functional, although not completely mature. Reduced fetal dipsogenic responsiveness may result from altered osmoreceptor sensitivity, downstream neuronal or synaptic immaturity, or potentially inhibitory actions of stimulated hindbrain nuclei.

Regulation of hypothalamic arginine vasopressin messenger ribonucleic acid and pituitary arginine vasopressin content in fetal sheep: Effects of acute tonicity alterations and fetal maturation

Objective: Fetal arginine vasopressin contributes to fetal and amniotic fluid homeostasis by increasing water resorption in the kidney and, at higher plasma levels, circulatory homeostasis by vasopressor effects. In utero and neonatal exposure of rat pups to prolonged alterations in plasma osmolality may permanently alter (imprint) pituitary arginine vasopressin content and adult responses to osmotic challenges. Our objective was to investigate fetal developmental changes and the impact of maternal dehydration and maternal hyponatremia on fetal pituitary arginine vasopressin content and hypothalamic arginine vasopressin messenger ribonucleic acid expression. Study Design: Ten pregnant ewes with singleton fetuses (135 ± 1 day) were chronically prepared with maternal vascular catheters. Ewes were assigned to receive water deprivation (n = 4) [desamino, d -Arg8]-arginine vasopressin–induced plasma hyponatremia (n = 3), or 4 days of observation (n = 3). Three additional pregnant ewes with preterm (110 ± 1 day) singleton fetuses were also included for a study of maturational effects. Daily maternal blood samples were analyzed for determination of plasma arginine vasopressin, electrolytes, and osmolality. After the study protocol, fetuses were operatively delivered, umbilical blood samples obtained, and fetuses put to death for pituitary and hypothalamic tissues. Pituitary arginine vasopressin content was determined by radioimmunoassay, and hypothalamus arginine vasopressin messenger ribonucleic acid expression was detected by Northern blotting. Results: Dehydration significantly (P < .05) increased, and hyponatremia significantly decreased maternal plasma sodium concentration compared with controls. Fetal plasma sodium concentration significantly changed in parallel with maternal values (dehydration: 139 ± 1 to 150 ± 1 mEq/L; hyponatremia: 138 ± 1 to 128 ± 5 mEq/L). Fetal hypothalamic arginine vasopressin messenger ribonucleic acid expression and pituitary content did not change in relation to these relatively acute alterations in plasma tonicity. However, among all animals, arginine vasopressin messenger ribonucleic acid expression was significantly negatively correlated with pituitary arginine vasopressin content (r2 = 0.563; P = .02). Arginine vasopressin messenger ribonucleic acid expression was significantly lower in both preterm and near-term fetuses (P < .05) than that in the maternal ewe, although pituitary arginine vasopressin content (in micrograms per milligram of protein) was significantly greater in preterm fetuses (P < .01, vs maternal; P < .05, vs near term). Conclusions: The significant inverse relation between arginine vasopressin content and arginine vasopressin messenger ribonucleic acid suggests a dynamic arginine vasopressin synthesis–content feedback relationship is functional in the near-term fetus. Although relatively acute periods of maternal hypertonicity or hypotonicity do not alter fetal pituitary arginine vasopressin content or hypothalamic arginine vasopressin messenger ribonucleic acid expression, longer-term plasma tonicity alterations may potentially have an impact on the fetal arginine vasopressin hypothalamic-pituitary axis. (Am J Obstet Gynecol 1998;179:899-905.)

Mechanism of arginine vasopressin suppression of ovine fetal lung fluid secretion: lack of V2-receptor effect.

Fetal lung liquid production is essential for in utero pulmonary development, and the resorption of lung liquid at birth facilitates neonatal transition. Lung liquid also contributes importantly to amniotic fluid volume. Factors that influence lung liquid production/resorption may, therefore, impact fetal pulmonary growth and development as well as amniotic fluid homeostasis. Arginine vasopressin (AVP) inhibits fetal lung liquid production and facilitates lung liquid resorption. In view of studies administering fetal AVP or the V2 receptor agonist, 1 desamino 8-D AVP (dDAVP) for the regulation of amniotic fluid volume, we sought to determine the impact of AVP V2 receptor stimulation on fetal lung liquid production. Eight near-term ovine fetuses (130 +/- 2 d; term = 145 d) were prepared with hind limb vascular catheters, a bladder catheter, and a tracheal catheter. Each ewe received vascular and amniotic catheters. After 5 days of recovery, the animals were studied for a 2-hr control period and for 2 hr following intravenous dDAVP injection (1 ng/kg). Lung liquid and urine flow rates and plasma electrolyte and osmolality composition were determined at 30-min intervals. To confirm fetal lung liquid suppression in response to AVP, two animals received an intravenous injection of AVP (2 ng/kg) 24 hr after the first experiment. dDAVP administration had no effect on lung liquid production (3.4 +/- 0.4 ml/kg/h), electrolyte concentrations, or osmolality. Fetal urine electrolyte concentrations and osmolality (154 +/- 24-295 +/- 22 mOsm/kg H2O) increased in response to dDAVP, whereas urine flow decreased (9.4 +/- 2.5-4.2 +/- 1.5 ml/kg/h). In the fetuses exposed to AVP, lung liquid production decreased (3.3-1.6 ml/kg/h). As AVP, although not dDAVP, inhibited fetal lung liquid production, these results indicate that AVP effects on lung liquid are likely mediated via the AVP V1 receptor, not the V2 receptor. The use of fetal administration of dDAVP for the regulation of urine production and amniotic fluid volume will not adversely impact lung liquid production.

Mechanism of arginine vasopressin suppression of ovine fetal lung fluid secretion: Lack of V2‐receptor effect

Fetal lung liquid production is essential for in utero pulmonary development, and the resorption of lung liquid at birth facilitates neonatal transition. Lung liquid also contributes importantly to amniotic fluid volume. Factors that influence lung liquid production/resorption may, therefore, impact fetal pulmonary growth and development as well as amniotic fluid homeostasis. Arginine vasopressin (AVP) inhibits fetal lung liquid production and facilitates lung liquid resorption. In view of studies administering fetal AVP or the V2 receptor agonist, 1 desamino 8-D AVP (dDAVP) for the regulation of amniotic fluid volume, we sought to determine the impact of AVP V2 receptor stimulation on fetal lung liquid production. Eight near-term ovine fetuses (130 ± 2 d; term = 145 d) were prepared with hind limb vascular catheters, a bladder catheter, and a tracheal catheter. Each ewe received vascular and amniotic catheters. After 5 days of recovery, the animals were studied for a 2-hr control period and for 2 hr following intravenous dDAVP injection (1 ng/kg). Lung liquid and urine flow rates and plasma electrolyte and osmolality composition were determined at 30-min intervals. To confirm fetal lung liquid suppression in response to AVP, two animals received an intravenous injection of AVP (2 ng/kg) 24 hr after the first experiment. dDAVP administration had no effect on lung liquid production (3.4 ± 0.4 ml/kg/h), electrolyte concentrations, or osmolality. Fetal urine electrolyte concentrations and osmolality (154 ± 24–295 ± 22 mOsm/kg H2O) increased in response to dDAVP, whereas urine flow decreased (9.4 ± 2.5–4.2 ± 1.5 ml/kg/h). In the fetuses exposed to AVP, lung liquid production decreased (3.3–1.6 ml/kg/h). As AVP, although not dDAVP, inhibited fetal lung liquid production, these results indicate that AVP effects on lung liquid are likely mediated via the AVP V1 receptor, not the V2 receptor. The use of fetal administration of dDAVP for the regulation of urine production and amniotic fluid volume will not adversely impact lung liquid production. J. Matern.–Fetal Med. 7:177–182, 1998. © 1998 Wiley-Liss, Inc.

Mechanism of arginine vasopressin suppression of ovine fetal lung fluid secretion: Lack of V2-Receptor effect

Fetal lung liquid production is essential for in utero pulmonary development, and the resorption of lung liquid at birth facilitates neonatal transition. Lung liquid also contributes importantly to amniotic fluid volume. Factors that influence lung liquid production/resorption may, therefore, impact fetal pulmonary growth and development as well as amniotic fluid homeostasis. Arginine vasopressin (AVP) inhibits fetal lung liquid production and facilitates lung liquid resorption. In view of studies administering fetal AVP or the V2 receptor agonist, 1 desamino 8-D AVP (dDAVP) for the regulation of amniotic fluid volume, we sought to determine the impact of AVP V2 receptor stimulation on fetal lung liquid production. Eight near-term ovine fetuses (130 ± 2 d; term = 145 d) were prepared with hind limb vascular catheters, a bladder catheter, and a tracheal catheter. Each ewe received vascular and amniotic catheters. After 5 days of recovery, the animals were studied for a 2-hr control period and for 2 hr following intravenous dDAVP injection (1 ng/kg). Lung liquid and urine flow rates and plasma electrolyte and osmolality composition were determined at 30-min intervals. To confirm fetal lung liquid suppression in response to AVP, two animals received an intravenous injection of AVP (2 ng/kg) 24 hr after the first experiment. dDAVP administration had no effect on lung liquid production (3.4 ± 0.4 ml/kg/h), electrolyte concentrations, or osmolality. Fetal urine electrolyte concentrations and osmolality (154 ± 24–295 ± 22 mOsm/kg H2O) increased in response to dDAVP, whereas urine flow decreased (9.4 ± 2.5–4.2 ± 1.5 ml/kg/h). In the fetuses exposed to AVP, lung liquid production decreased (3.3–1.6 ml/kg/h). As AVP, although not dDAVP, inhibited fetal lung liquid production, these results indicate that AVP effects on lung liquid are likely mediated via the AVP V1 receptor, not the V2 receptor. The use of fetal administration of dDAVP for the regulation of urine production and amniotic fluid volume will not adversely impact lung liquid production.

Fetal Swallowing: Relation to Amniotic Fluid Regulation

In summary, fetal swallowing activity contributes importantly to fetal and amniotic fluid homeostasis, and fetal somatic and gastrointestinal development. Human and ovine fetal swallowing increases throughout gestational with fetal swallowed volumes markedly greater (relative to body weight) than adults. Although the regulation of swallowing activity in early gestation is unknown, intact central and systemic dipsogenic mechanisms have been shown during the last third of ovine gestation. Recent studies suggest that swallowing behavior may be modulated in accordance with neurobehavioral state changes and influenced by hypoxia, hypotension and plasma osmolality changes. Whether fetal swallowing also is regulated by the development of "hunger" sensation, salt appetite, or the development of taste is uncertain. Nevertheless, it is likely that, for species in which swallowing behavior develops in utero, there are potentially dramatic influences of the maternal-fetal pregnancy environment on the imprinting of regulatory mechanisms controlling ingestive behavior. Ultimately, the regulation of fetal swallowing may aid in the prevention and/or therapy of human amniotic fluid disorders.

Amniotic fluid volume response to esophageal occlusion in fetal sheep

Although ovine and human fetuses swallow considerable volumes of fluid, the impact of absence of fetal swallowing on amniotic fluid volume regulation is unclear. To study the role of fetal swallowing on urine production and amniotic fluid, seven ovine fetuses (126 ± 1 days) were chronically prepared with fetal bladder and vascular catheters, an esophageal flow probe, an inflatable esophageal cuff, and amniotic fluid catheters. In the five fetuses that underwent esophageal ligation after the control period, fetal swallowing averaged 0.27 ml/min before occlusion. In response to esophageal occlusion, significant increases were noted in fetal plasma arginine vasopressin (6.9 ± 2.6 to 16.6 ± 4.4 pg/ml) and urine osmolality (159 ± 1 to 324 ± 30 mOsm/kg), whereas urine volume (0.25 ml/min) did not change. Amniotic fluid volume increased nearly threefold after 3 days of esophageal occlusion (582 ± 180 to 1530 ± 271 ml). Amniotic fluid volume remained normal (334 to 419 ml) in the one fetus in which the occluder did not inflate. In the one fetus in which the esophagus was occluded at surgery, amniotic fluid volume was increased after the surgical recovery period (1489 ml). These data indicate an important role of fetal swallowing in amniotic fluid homeostasis and the potential interaction of swallowing with fetal urine production. (AM J OBSTET GYNECOL 1991;165:1620-6.)

Fetal plasma and renal responses to ruminal fluid

Amniotic fluid homeostasis is dependent on a balance of fetal fluid production and absorption. The fetal gastrointestinal tract is believed to resorb 500 to 1000 ml of amniotic fluid per day during 7 to 10 bouts of swallowing activity. However, the impact of ruminal fluid on fetal plasma composition and fluid homeostasis is largely unknown. Seven ovine fetuses (120 ± 1 day) received intraruminal infusions of 0.9% or 3% saline solution on alternate days. In response to successive 40-minute intraruminal infusions of 0.9% saline solution (0.5 and 1.0 ml/kg/min), there was no change from basal levels of fetal plasma osmolality (295.7 ± 2.9 mosm), plasma arginine vasopressin (1.45 ± 0.29 pg/ml), urine osmolality (150 ± 8 mosm), or urine volume (0.49 ± 0.10 ml/min). In response to the 3% saline solution infusion, significant increases were noted in fetal plasma osmolality (295.4 ± 3.1 to 302.6 ± 2.6 mosm), plasma arginine vasopressin (1.77 ± 0.31 to 4.84 ± 0.79 pg/ml), and urine osmolality (157 ± 13 to 342 ± 25 mosm), whereas fetal urine volume significantly decreased (0.35 ± 0.05 to 0.15 ± 0.06 ml/min). These results indicate that hypertonic, but not isotonic, saline solution infusion into the fetal gastrointestinal tract may affect fetal plasma composition and urine production. Under conditions of significant plasma to luminal osmotic gradients, fetal gastrointestinal water and electrolyte transfer may be more rapid than can be compensated by either fetal renal function or placental equilibration.

Perinatal fluid and electrolyte regulation: role of arginine vasopressin.

Not many years ago, the fetus was perceived to exert little impact on amniotic fluid homeostasis. It is now clear that the fetus plays an integral role in modulating fluid flux between the maternal, fetal, and amniotic fluid compartments. Moreover, fetal AVP secretion and the associated renal and cardiovascular responses represent important aspects of the potential to adapt to changes in the intrauterine environment. Although the physiologic significance of the increased AVP secretion observed in response to labor and delivery remain speculative, AVP regulation also is an essential aspect of neonatal adaptation. Still, many questions remain regarding both the regulation of fetal and neonatal fluid dynamics and the ontogeny of AVP receptor systems.