Ontogeny of CA 125 antigen in pregnancy: immunoradiometric determination in amniotic fluid and immunohistochemical localization in fetal membranes

CA 125 antigen was measured in amniotic fluid, maternal blood, cord blood, and fetal urine by a commercially available immunoradiometric assay kit. The amniotic fluid was obtained from 99 normal pregnancies at various gestational ages. The mean antigen levels were 29,676, 3350, and 1680 U/ml in amniotic fluid of the first, second, and third trimesters, respectively. In maternal blood, 12.5% of pregnant women in the first trimester of pregnancy showed elevated levels of CA 125 (65 to 100 U/ml). Late in gestation, CA 125 levels in cord blood and fetal urine were always less than 65 U/ml. Immunohistochemical study of CA 125 in fetal membranes, placenta, and decidua showed the presence of antigen only in the amnion. These results suggest that CA 125 is shed into amniotic fluid directly from the amniotic membrane.     

Amniotic fluid composition changes during urine drainage and tracheoesophageal occlusion in fetal sheep.

OBJECTIVE: Recently an intramembranous pathway was reported in the ovine fetus as a route for the rapid exchange of water, ions, and molecules between the amniotic fluid and the fetal blood that perfuses the fetal surface of the placenta and the fetal membranes. Our study was designed to test the hypothesis that the amniotic fluid composition would gradually equilibrate with fetal plasma when the major flows to and from the amniotic compartment were eliminated. STUDY DESIGN: Eleven near-term fetal sheep underwent ligation of the urachus to eliminate the allantoic fluid. An inflatable cuff was placed around the esophagus and trachea, and catheters were placed in the fetal urinary bladder, fetal circulation, and maternal circulation. At > or = 5 days after surgery the animals were subjected to either a control experiment or a continuous urine drainage plus tracheoesophageal occlusion for 8 hours. RESULTS: During the urine drainage plus occlusion study, amniotic fluid osmolality (p < 0.0001), Na+ (p < 0.0001), K+ (p < 0.01) Cl- (p < 0.001), and lactate (p < 0.001) increased compared with the control experiment. These corresponded to 50% reductions in the gradients for osmolality and Na+ between fetal plasma and amniotic fluid; the K+ gradient increased, and the Cl- gradient reversed. The percentage increases in amniotic Na+, K+, Cl-, and lactate were all 10% at 8 hours. CONCLUSION: These observations suggest that water is absorbed from the amniotic fluid through the intramembranous pathway into the fetal circulation at a rate of 1.25% of the total amniotic volume per hour or approximately 240 ml/day.     

表皮生长因子与胎儿宫内发育迟缓关系的研究

探讨表皮生长因子与胎儿宫内发育迟缓的关系。方法用放射免疫分析,测定８６例妊娠晚期妇女血清,羊水和脐静脉血ＥＧＦ浓度;根据新生儿出生体重,将研究对象分成对照组５４例,大于胎龄儿组１８例和ＩＵＧＲ组１４例。对照组中有１１例同时测定脐动脉血清ＥＧＦ浓度,比较各组间羊水和孕妇,脐血清ＥＧＦ水平及脐动,静脉血清间ＥＧＦ水平的差异。     

Fluoride concentration in amniotic fluid and fetal cord and maternal plasma

Fluoride concentrations were determined in plasma of 50 pregnant women, 44 samples of amniotic fluid and fetal cord blood of 29 fetuses at various stages of normal pregnancies, from an area with a relatively low water fluoride (less than 0.5 ppm) content. The mean concentrations of fluoride from maternal plasma, cord plasma and amniotic fluid (+/- S.D.) were 0.033 +/- 0.003, 0.028 +/- 0.005 and 0.017 +/- 0.003 ppm, respectively. Maternal and fetal plasma fluoride concentrations did not differ significantly. In the older age group fetal cord plasma fluoride concentration was significantly lower than maternal plasma levels (0.012 +/- 0.08 ppm vs. 0.023 +/- 0.001, respectively; p less than 0.05). Amniotic fluid fluoride levels were significantly higher at term than in midtrimester pregnancy, 0.017 +/- 0.0018 vs. 0.010 +/- 0.009 ppm (P less than 0.05), respectively. This higher concentration may imply higher fetal urinary excretion of fluoride at term due to the lower sequestration of fluoride as the process of bone calcification is more complete.     

Maternal-fetal transfer and amniotic fluid accumulation of lamivudine in human immunodeficiency virus-infected pregnant women

OBJECTIVE: The purpose of this study was to investigate placental transfer and amniotic fluid concentrations of lamivudine in human immunodeficiency virus-infected women who received the agent during pregnancy. STUDY DESIGN: Mothers in the study were receiving antiretroviral therapy that included lamivudine in a clinical setting. Maternal blood, cord blood, and amniotic fluid samples were obtained simultaneously at the time of delivery from 57 mother-infant pairs. RESULTS: At a median of 8.5 hours after the last maternal oral 150-mg dose of lamivudine, median maternal and fetal plasma concentrations were 302 and 240 ng/mL, respectively. Individual maternal and fetal concentrations were strongly correlated (r2 = 0.36; P < 10(-4)), and their median ratio was about 1. The median concentration in the amniotic fluid was 5 times higher than that in maternal plasma (upper range of ratio, 133). CONCLUSION: Lamivudine appeared to cross the placenta by simple diffusion and is concentrated in the amniotic fluid. High amniotic fluid levels of lamivudine may carry both benefits and risks for the child.     

Amniotic fluid insulin,C peptide concentrations,and fetal morbidity in infants of diabetic mothers

Glucose, insulin, C peptide, and insulin antibody concentrations were measured in amniotic fluid collected under basal conditions and 2 hours after an arginine challenge from 61 insulin-treated diabetic women (12 basal and 49 after arginine challenge) and 31 nondiabetic pregnant women in late gestation (23 basal and eight after arginine challenge). The insulin, C peptide, and glucose concentrations were significantly higher in diabetic pregnant women than in nondiabetic pregnant women in each case. In the amniotic fluid obtained after arginine challenge in diabetic pregnant women, C peptide concentration was correlated with both insulin concentration (r = 0.61) and birth weight (r = 0.53). The insulin and C peptide concentrations were significantly higher (p < 0.025) in samples from diabetic pregnancies associated with fetal morbidity than from diabetic pregnancies without fetal morbidity. Basal amniotic fluid insulin and C peptide concentrations were slightly greater in overweight infants of diabetic mothers compared to those of normal weight, whereas the differences for insulin and C peptide concentrations in the amniotic fluid obtained after arginine challenge were highly significant (p < 0.0125 and p < 0.0005, respectively). Finally insulin and C peptide concentrations in the amniotic fluid obtained after arginine challenge in diabetic pregnant women showed a correlation with maternal metabolic control but not with the degree (White classification) of maternal diabetes. No or negligible interference of insulin antibody in the radioimmunoassay of insulin in amniotic fluid was observed.     

Fetal absorption of intra-amniotic aldosterone: effects on urine composition.

OBJECTIVES: Amniotic fluid (AF) volume and composition are maintained by a balance of fetal fluid production and resorption. Ovine fetal resorption of peptide hormones (e.g., arginine vasopressin) from the amniotic cavity has been demonstrated, with resultant effects on fetal urine production. The present study was undertaken to determine whether intra-amniotically administered steroid hormones could be absorbed from the amniotic cavity into fetal plasma and whether intra-amniotic aldosterone administration would affect fetal renal sodium and potassium excretion. METHODS: Seven singleton fetuses (132 +/- 2 days) were prepared with bladder, vascular, and amniotic cavity catheters. After a 5-day recovery period, a bolus of aldosterone was injected into the amniotic cavity. Fetuses were monitored for an additional 24 hours during which time maternal, fetal, and AF samples were collected at timed intervals. RESULTS: After intra-amniotic aldosterone injection, AF aldosterone concentrations increased at 30 minutes and remained elevated for 4 hours after the aldosterone bolus. In response to increased AF aldosterone, fetal plasma aldosterone levels significantly increased by 30 minutes, peaked at 1 hour (17 +/- 4 to 758 +/- 160 pg/mL), and remained elevated for a minimum of 4 hours. Fetal urine sodium excretion significantly decreased and potassium excretion increased. Maternal plasma aldosterone levels increased significantly (25 +/- 10 to 401 +/- 56 pg/mL) but to levels below fetal values. Amniotic fluid and fetal and maternal aldosterone concentrations and fetal urine sodium and potassium excretion returned toward basal levels by 24 hours. CONCLUSION: The steroid hormone aldosterone can be absorbed from the amniotic cavity into the fetal circulation and can alter fetal urine electrolyte excretion. These results suggest that the amniotic cavity is a potential route of in utero pharmacologic fetal therapy.     

Transfer and dynamics of uric acid in the pregnant rhesus monkey. II. A mathematical model.

The objective of the present study was to develop a mathematical model of the dynamics of uric acid between fetal and maternal compartments in the term pregnant rhesus monkey. In 3 different animals 14C-labeled uric acid was injected into the fetal circulation, the amniotic fluid and the maternal circulation, respectively. In one experiment no uric acid was administered and the fetus was deliberately killed at the beginning of the experiment. Samples of fetal and maternal blood, maternal urine and amniotic fluid were collected at regular intervals. Semilogarithmic time-activity curves were constructed and time constants were determined. An open four-compartment model (fetal-placental plasma, fetal-placental interstitial space, amniotic fluid and maternal plasma) was applied to describe the intercompartmental dynamics of uric acid. Transplacental clearance was approx. 1 ml X min-1 in both directions, maternal renal clearance was about 17 ml X min-1. These results and the calculated values of the other intercompartmental clearances support earlier results, obtained with the steady infusion method. Uric acid concentrations in amniotic fluid and fetal plasma appeared to increase significantly during the experiments. The rise in amniotic fluid levels can only be explained by accepting a yet undefined compartment in which uric acid is produced and cleared directly into the amniotic cavity. It is speculated that this additional compartment could be the fetal lung.     

P-type inositol phosphoglycans in serum and amniotic fluid in active pre-eclampsia

OBJECTIVES: Abnormal secretion of P-type inositol phosphoglycans (IPG-P) has been described in maternal urine of pre-eclamptic women. The aim of this study was to determine the origin of production of IPG-P. We examined the IPG-P content of maternal and fetal serum, maternal urine and amniotic fluid in both normal pregnancy and pre-eclampsia. DESIGN: Established extraction and bioactivity assay techniques were used to compare total IPG-P levels in serum samples, and a polyclonal-antibody-based ELISA to assay the amniotic fluid and urine samples in matched pairs of women. SUBJECTS: Eleven women with pre-eclampsia requiring caesarean section (subjects), 11 pregnant women requiring elective caesarean section for reasons other than pre-eclampsia (controls). RESULTS: Our data confirm the abnormal level of IPG-P in maternal urine during pre-eclampsia. Moreover, IPG-P levels were higher in umbilical sera than in maternal sera samples. Amniotic fluid as well as urine ELISA results were significantly higher in the pre-eclamptic group compared with normal controls. Total IPG-P bioactivity in serum did not vary between serum compartments in normal pregnancy. Uterine vein IPG-P levels were lower in pre-eclampsia when compared with normal pregnancy. A possible correlation was observed between urine and amniotic fluid levels in normal women. No correlation was observed between measured blood levels and those in urine and amniotic fluid. CONCLUSIONS: It is hypothesized that steady state equilibrium of IPG-P in serum in normal pregnancy is disrupted in pre-eclampsia. Additionally, an abnormal IPG-P sub-fraction, detectable in urine and amniotic fluid, may be present and involved in the pathophysiology of the syndrome, although sites of production of this abnormal form remain unclear.     

Disposition of ethanol in maternal blood,fetal blood,and amniotic fluid of third-trimester pregnant ewes

The disposition of ethanol in maternal arterial blood, fetal arterial blood, and amniotic fluid of nine conscious, cannulated pregnant ewes (128 to 137 days' gestation) was determined for 1-hour maternal intravenous infusion of ethanol, 1 gm/kg maternal body weight. The maternal arterial blood and fetal arterial blood ethanol concentration-time curves were virtually superimposable up to 14 hours. The apparent zero-order ethanol elimination rates for maternal arterial blood and fetal arterial blood were similar. There was a time lag in the transfer of ethanol into amniotic fluid relative to fetal arterial blood, and the peak ethanol concentration in amniotic fluid was significantly lower than the concentrations in maternal arterial blood and fetal arterial blood. The apparent zero-order ethanol elimination rate for amniotic fluid was slower, but not significantly so, compared with the ethanol elimination rates for maternal arterial blood and fetal arterial blood. Ethanol-derived acetaldehyde was found in maternal arterial blood, fetal arterial blood, and amniotic fluid at concentrations at least 1000-fold lower than the respective ethanol concentrations. The data indicate that, for administration of this ethanol dosage regimen to the third-trimester pregnant ewe, there is rapid, bidirectional placental transfer of ethanol; elimination of ethanol from the fetus is regulated primarily by maternal elimination of ethanol; the amniotic fluid may serve as a reservoir for ethanol in utero; and there is appreciable acetaldehyde-metabolizing capacity.     

Fetal death: A condition with a dissociation in the concentrations of soluble vascular endothelial growth factor receptor-2 between the maternal and fetal compartments

Objective.?An anti-angiogenic state has been implicated in the pathophysiology of preeclampsia, fetal growth restriction and fetal death. Vascular endothelial growth factor (VEGF), an indispensible angiogenic factor for embryonic and placental development exerts its angiogenic properties through the VEGF receptor (VEGFR)-2. A soluble form of this protein (sVEGFR-2) has been recently detected in maternal blood. The aim of this study was to determine if fetal death was associated with changes in the concentrations of sVEGFR-2 in maternal plasma and amniotic fluid.

Study Design.?Maternal plasma was obtained from patients with fetal death (n?=?59) and normal pregnant women (n?=?134). Amniotic fluid was collected from 36 patients with fetal death and the control group consisting of patients who had an amniocentesis and delivered at term (n?=?160). Patients with fetal death were classified according to the clinical circumstances into the following groups: (1) unexplained; (2) preeclampsia and/or placental abruption; (3) chromosomal and/or congenital anomalies. Plasma and amniotic fluid concentrations of sVEGFR-2 were determined by ELISA. Non-parametric statistics and logistic regression analysis were applied.

Results.?(1) Patients with a fetal death had a significantly lower median plasma concentration of sVEGFR-2 than normal pregnant women (p?<?0.001). The median plasma concentration of sVEGFR-2 in patients with unexplained fetal death and in those with preeclampsia/abruption, but not that of those with congenital anomalies, was lower than that of normal pregnant women (p?=?0.006, p?<?0.001 and p?=?0.2, respectively); (2) the association between plasma sVEGFR-2 concentrations and preterm unexplained fetal death remained significant after adjusting for potential confounders (OR: 3.2; 95% CI: 1.4–7.3 per each quartile decrease in plasma sVEGFR-2 concentrations); (3) each subgroup of fetal death had a higher median amniotic fluid concentration of sVEGFR-2 than the control group (p?<?0.001 for each); (4) the association between amniotic fluid sVEGFR-2 concentrations and preterm unexplained fetal death remained significant after adjusting for potential confounders (OR: 15.6; 95% CI: 1.5–164.2 per each quartile increase in amniotic fluid sVEGFR-2 concentrations); (5) among women with fetal death, there was no relationship between maternal plasma and amniotic fluid concentrations of sVEGFR-2 (Spearman Rho: 0.02; p?=?0.9).

Conclusion.?Pregnancies with a fetal death, at the time of diagnosis, are characterized by a decrease in the maternal plasma concentration of sVEGFR-2, but an increase in the amniotic fluid concentration of this protein. Although a decrease in sVEGFR-2 concentration in maternal circulation depends upon the clinical circumstances of fetal death, an increase in sVEGFR-2 concentration in amniotic fluid seems to be a common feature of fetal death. It remains to be determined if the perturbation in sVEGFR-2 concentrations in maternal and fetal compartments observed herein preceded the death of a fetus.     

Acute maternal rehydration increases the urine production rate in the near-term human fetus

OBJECTIVE: We sought to investigate the effect of a decrease of maternal plasma osmolality produced by hypotonic rehydration on the fetal urine production rate in normal near-term human fetuses. STUDY DESIGN: Twenty-one healthy pregnant women attending the clinic for antenatal care were studied between 37 and 40 weeks' gestation. The fetal urine production rate was assessed by serial measurements of 3 diameters of the fetal bladder. The hourly fetal urine production rate was determined by linear regression analysis of the calculated bladder volumes versus time and was initially determined after a period of 4 hours of fluid deprivation. Thereafter, the women were asked to drink 1 L of water, and the hourly fetal urine production rate was assessed again. The hourly fetal urine production rate was only studied during behavioral state 1F because it is dependent on the behavioral state. The fetal behavioral state was determined by assessment of fetal heart rate, fetal eye movements, and fetal body movements. RESULTS: Successful recordings were obtained in 10 of the 21 women. The hourly fetal urine production rate increased significantly after hypotonic rehydration (P <.02). Compared with the initial hourly fetal urine production rate after 4 hours of fluid deprivation, the hourly fetal urine production rate showed an increase of 63.2% after hypotonic rehydration, from 38.2 +/- 16.3 mL/h to 62.4 +/- 34.6 mL/h (mean +/- SD). After rehydration, the baseline fetal heart rate fell significantly, from 141 +/- 6 to 132 +/- 8 beats/min (mean +/- SD; P =.005). CONCLUSION: The fetal urine production rate is augmented after acute maternal oral hypotonic rehydration after 4 hours of fluid deprivation. The current findings demonstrate that the near-term human fetus can handle such acute changes in fluid osmolality by increasing the urine production rate to maintain its fluid homeostasis. This mechanism implies that changes in maternal plasma osmolality and volume probably play an important role in determining amniotic fluid volume. Therefore the application of maternal hydration for the treatment of oligohydramnios should be further investigated.     

The missing link in amniotic fluid volume regulation: intramembranous absorption

Although fetal urine output and swallowing are major contributors to amniotic fluid regulation, other pathways for fluid movement must be involved in the regulation of amniotic fluid volume because many studies report fetal urine output to be greater than swallowing. This study was designed to examine the possibility of fluid transfer between the amniotic cavity and the fetal blood that perfuses the fetal membranes and surface of the placenta in the ovine fetus. We injected warmed distilled water into the amniotic fluid in three groups of chronically catheterized fetal sheep. In normal fetuses, there was rapid absorption of the water into the fetal circulation, resulting in highly significant decreases in fetal osmolality, plasma electrolytes, and heart rate as well as increases in arterial pressure and fetal hemolysis. Concomitantly, there was a small, delayed fall in maternal osmolality. In a second group of fetuses with ligated esophagi, these same responses occurred except that the fetal osmolality and electrolyte changes occurred earlier and were significantly greater. In a third group of fetuses killed just before the water injection, maternal osmolality was unchanged. These data suggest the intramembranous pathway as a major route of amniotic fluid absorption in the ovine fetus. In addition, esophageal ligation appears to augment the conductance of this pathway, as evidenced by a significantly greater estimated filtration coefficient and rate of water absorption in the ligated animals than in controls. Finally, the transmembranous pathway directly to the mother does not appear to be a major route.     

Cell-free foetal DNA in maternal plasma does not appear to be derived from the rich pool of cell-free foetal DNA in amniotic fluid

Background: Large quantities of cell-free foetal DNA have been detected in amniotic fluid, and it has been proposed that this material may contribute to the pool of cell-free foetal DNA in maternal plasma. Methods: Twelve maternal blood samples were obtained from pregnant women about to undergo an amniocentesis. Cell-free DNA was extracted from the maternal plasma samples and the matched amniotic fluid samples. The amount of cell-free foetal DNA was quantified by real-time PCR assays for the SRY and RHD genes. Results: Amniotic fluid was found to contain vast quantities of cell-free DNA (median concentration = 3,978 copies/ml amniotic fluid). The concentration of cell-free foetal DNA in maternal plasma was much lower (median concentration = 96.6 copies/ml maternal plasma). No significant correlation could, however, be determined between these two pools of cell-free foetal DNA. Conclusions: Our data confirm that amniotic fluid contains prodigious quantities of cell-free foetal DNA, but as no relationship exists between this material and that in the maternal circulation, it is unlikely that the amnion contributes to the presence of cell-free foetal DNA in maternal plasma.     

Amniotic fluid glucose values in normal and abnormal pregnancies

Glucose values were determined in 102 urine samples of newborn infants and in 2295 amniotic fluid (AF) samples of women between the 14th and 42nd week of pregnancy. One thousand, six hundred fifty-five of the AF samples derived from normal pregnancies, 50 from pregnancies with fetal malformations, 115 from cases of hydramnios, 246 from pregnant women with an abnormal oral glucose tolerance test, and 230 from insulin-dependent diabetics. Mean AF glucose concentration rises slightly between the 14th and 17th week of pregnancy, decreasing from 46 to about 16 mg% at the end of pregnancy. In cases of fetal malformations, 68% of the glucose levels was below the tenth percentile of normal values. Hydramnios showed no deviation from normal values. In patients with abnormal glucose tolerance, AF glucose increased by a total of 42% and by 67% in fetal hyperinsulinism. Insulin-dependent diabetics had glucose values elevated by a total of 77% and by 106% in fetal hyperinsulinism. The AF glucose profile reflects the level of maternal blood glucose that is transported to the fetus and excreted in the fetal urine as a major source of glucose in AF.     

Folate and vitamin B12 concentrations in maternal and fetal blood, and amniotic fluid in second trimester pregnancies complicated by neural tube defects.

OBJECTIVE: To investigate maternal and fetal folate and vitamin B12 concentrations in pregnancies affected by neural tube defects (NTD). DESIGN: Measurement of folate and vitamin B12 concentrations in amniotic fluid, fetal blood and maternal blood samples in midgestation. SUBJECTS: 32 women undergoing termination of pregnancy at 14-21 weeks gestation for social reasons (n = 24) or for fetuses with neural tube defects (n = 8). INTERVENTIONS: Fetoscopy before intra-amniotic injection of prostaglandins. RESULTS: In normal pregnancies there was a positive correlation between maternal and fetal serum folate, and the fetal serum and red blood cell folate concentrations were higher than the maternal. There were no differences in amniotic fluid, maternal blood or fetal blood folate concentrations between pregnancies with NTD and normal pregnancies. Although amniotic fluid vitamin B12 was lower in pregnancies with NTD, maternal serum vitamin B12 concentration was not reduced. CONCLUSION: In this small group of pregnancies with NTD at mid-gestation there is no evidence to suggest folate or vitamin B12 deficiency.     

Biological fate of methenamine in man. Absorption, renal excretion and passage to umbilical cord blood, amniotic fluid and breast milk.

Methenamine hippurate was administered orally as tablets or granules to healthy volunteers. Plasma concentrations of methenamine reached a maximum 1--2 hours after a single dose and then declined with a half-life of about 4 hours. The apparent distribution volume was similar to that of total body water. Renal clearance of methenamine was somewhat lower than that of creatinine. In cross-over experiments over six days, methenamine recovered in the urine corresponded to about 80 per cent of the dose given per 12 hours, slightly lower values being obtained from granules than from tablets. The efficient renal elimination of methenamine was confirmed in similar studies on patients post-operatively. Methenamine hippurate was also given to healthy pregnant women during labor, a few hours before expected delivery. Methenamine was found to pass the placental barrier. The concentration of methenamine in umbilical cord plasma was low but reached the level in maternal plasma after about 4 hours. In amniotic fluid the methenamine con centration was low and varying. No correlation was obtained to the maternal or umbilical cord plasma levels. The methenamine concentration in breast milk was of the same magnitude as in maternal plasma. It is concluded that methenamine may be safely given to pregnant and lactating women with respect to the ellbeing of the child.     

Amniotic fluid and fetal urinary responses to severe placental insufficiency in sheep

OBJECTIVE: Our purpose was to test the hypothesis that severe placental insufficiency leads to reductions in fetal urine production and amniotic fluid volume in late-gestation fetal sheep. STUDY DESIGN: At 0.85 of gestation, chronically catheterized fetal sheep with ligated urachus were either embolized for 5 days by repeated injection of boluses of 15-microm microspheres into the common fetal umbilical artery until fetal arterial oxygen content was reduced by 50% (n = 6) or were infused with saline solution (n = 6). Amniotic fluid volume was measured daily before embolization by means of an indicator dilution technique and by drainage at autopsy. Fetal urine production, heart rate, and mean arterial blood pressure were measured continuously for 1 hour before embolization and 1 hour after embolization each day. Fetal arterial blood gases, oxygen content, electrolytes, and osmolality were also monitored. RESULTS: Five days of placental insufficiency, which reduced fetal arterial oxygen content by 50% and arrested fetal growth, resulted in a reduced amniotic fluid volume without a reduction in fetal urine production. Compared with that of controls, amniotic fluid volume was reduced over the 5-day period by 547 +/- 144 mL (-62%, P <.01). Amniotic fluid composition was also altered, with a significant increase in lactate and sodium concentrations and osmolality on days 4 to 5. On days 2 to 5, there was a progressive increase in amniotic fluid osmolality above that of controls, which paralleled the changes in amniotic fluid sodium concentration (P <.05). Fetuses became hypertensive on days 2 to 4 of embolization, although this response was attenuated by day 5. CONCLUSIONS: Chronic severe placental insufficiency caused a reduction in amniotic fluid volume not attributable to reduced fetal urine production. Changes in amniotic fluid composition induced by placental insufficiency suggest an excess intramembranous absorption of amniotic fluid water, in relation to solutes, into the fetal and maternal compartments, which may lead to the development of oligohydramnios.     

Comparative study of proteinase inhibitors in human amniotic fluid and maternal serum

Serum and amniotic fluid samples from five pregnant women were analyzed for different proteinase inhibitors by ion-exchange chromatography on DEAE-cellulose. Alpha-2 macroglobulin was found to be absent in amniotic fluid. Even though alpha-1 antichymotrypsin was identified in amniotic fluid, its concentration gradient between serum and amniotic fluid (20--60) was much higher than that of alpha-1 antitrypsin (8--20). Two forms of alpha-1 antitrypsin were identified in both the fluids. In pregnancy, the ratio of the two forms was altered in favour of the less anionic form compared to normal sera. The contribution of the heat stable proteinase inhibitor for total antitryptic activity in amniotic fluid was more than in serum. The observation that urine samples from immature infants had higher heat stable inhibitory activity than urine samples from normal infants suggests that the heat stable inhibitor in amniotic fluid may arise from fetal kidney.