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PubMed1979

Evaluation of two assays of functional surfactant in amniotic fluid: surface-tension lowering ability and the foam stability index test.

We characterize two assays of total amniotic fluid surfactant that are based on function: the surface-tension lowering ability of extracts of amniotic fluid lipid (I) and the foam stability index test (II). I is determined on chloroform extracts of amniotic fluid. II is defined as the highest ethanol volume fraction of an amniotic fluid-ethanol mixture that will permit a stable foam to form after 30 s of vigorous shaking. The relationship of I to disaturated phosphatidylcholine concentrations (after osmium tetroxide treatment of the amniotic fluid lipid extract) is in the expected theoretical form of a hyperbolic function. The relation between values for II and disaturated phosphatidylcholine concentrations showed a consistent bias, suggesting that components other than disaturated phosphatidylcholine contribute to stable foam formation. Phosphatidylclycerol concentrations did not appear to account for this bias. The relation between I to II values suggest that both assays measure total surfactant. I, II, and concentration of disaturated phosphatidyl choline are all excellent indicators of fetal pulmonary maturity. From a practical standpoint, the foam stability index test is the most efficient approach to routine assessment of fetal pulmonary status.

Amniotic Fluid↗
PubMed1992

Eradication of Ureaplasma urealyticum from the amniotic fluid with transplacental antibiotic treatment.

Ureaplasma urealyticum was isolated from the amniotic fluid of a patient with preterm premature rupture of membranes at 24 weeks. A second amniocentesis performed 48 hours later indicated an increase in the number of neutrophils in the amniotic fluid. Treatment with erythromycin, ampicillin, gentamicin, and clindamycin was instituted for a period of 6 days. Amniotic fluid analysis from a third amniocentesis performed 24 hours after discontinuation of antibiotic treatment revealed only a few white blood cells and was negative for microorganisms. The pregnancy continued for 22 days after admission, at which time spontaneous labor began. The neonate survived with no sequelae and had negative blood cultures. Antibiotic treatment was associated with eradication of Ureaplasma urealyticum from the amniotic cavity, pregnancy prolongation, and neonatal survival.

Adult↗
PubMed1976

Individual free fatty acids in amniotic fluid and in plasma of pregnant women.

Individual free fatty acids (FFA) were measured in 77 amniotic fluid samples and in 57 maternal plasma samples. Gestational age ranged from 16 to 40 weeks. Amniotic fluid FFA decreased from 20-4 +/- 6-0 mumol/l in the second trimester to 17-0 +/- 6-0 mumol/l in the last six weeks of pregnancy. This was almost entirely accounted for by a decrease in the concentration of free stearic acid, while oleic acid increased slightly. No correlation between amniotic fluid FFA and maternal plasma FFA was found in samples obtained on the same day. It is suggested that amniotic fluid FFA may partly derive from renal excretion by the fetus.

Amniotic Fluid↗
PubMed1991

Heterogeneity of serum and amniotic fluid prolactin in humans.

The molecular heterogeneity of PRL was studied in serum and amniotic fluid using immunoperoxidase electrophoresis. In the amniotic fluid, larger molecular variants (greater than 117 kD), small PRL (20 and 23 kD) and cleaved PRL were present in the nonreduced condition. Newly, three mercaptoethanol (MCE)-resistant forms (76, 64 and 53 kD), and 25- and 23-kD forms appeared after treatment with MCE. Two variants, 64 and 23 kD, did not bind to concanavalin A (Con A), indicating a simple peptide without sugars. Other glycosylated forms, 76, 53 and 25 kD, bound to Con A. In maternal serum, the same components as those in the amniotic fluid were seen, except for a scanty amount of 23 kD and a newly appearing glycosylated variant of 28 kD in the reduced condition. This 23-kD form also appeared with the administration of TRH in women.

Amniotic Fluid↗
PubMed1983

A rapid and specific enzymatic method for the quantification of phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylglycerol in amniotic fluid.

An enzymatic procedure for the quantification of phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylglycerol in amniotic fluid is described. By use of this method, choline and glycerol are released enzymatically from phosphatidylcholine and phosphatidylglycerol, respectively, in reactions catalyzed by phospholipase D. The hydrogen peroxide generated from choline (by the action of choline oxidase) and from glycerol (by the combined action of glycerokinase and glycerol-3-phosphate oxidase) is quantified spectrophotometrically after the addition of horseradish peroxidase, aminoantipyrine, and phenol. The phosphatidylcholine concentration in amniotic fluid was found to be approximately 10 to 30 nmol/ml between the twenty-third and thirty-sixth week of gestation and increased sevenfold to eightfold between the thirty-seventh week and term. The procedure can be modified for the quantification of disaturated phosphatidylcholine. The concentration of phosphatidylglycerol was approximately 2 nmol/ml between the twenty-third and thirty-sixth week and increased to 10 to 20 nmol/ml between the thirty-seventh and forty-first week of pregnancy. Since contamination of amniotic fluid with bile pigments does not interfere with either assay, the phosphatidylcholine and phosphatidylglycerol concentrations in amniotic fluid can be determined in samples that are contaminated with meconium.

Amniotic Fluid↗
PubMed2000

Role of amniotic fluid homocysteine level and of fetal 5, 10-methylenetetrahydrafolate reductase genotype in the etiology of neural tube defects.

A mutation in the gene 5,10-methylenetetrahydrofolate reductase (MTHFR), leading to altered homocysteine metabolism, has been identified in parents and fetuses with fetal neural tube defects. We sought to determine which is of greater importance in fetal neural tube defect formation: the fetal MTHFR mutation or elevated amniotic fluid homocysteine level. We retrieved stored amniotic fluid from cases of isolated fetal neural tube defect diagnosed from 1988 to 1998 (n = 80), and from normal controls matched for race, month and year of amniocentesis, and maternal age. The presence or absence of the 677C-->T mutation of MTHFR was determined and homocysteine levels were measured; cases and controls were compared. Significantly more cases than controls were heterozygous or homozygous for the 677C-->T MTHFR mutation (44% vs 17%, P < or = 0.001). Cases were also significantly more likely than controls to have an amniotic fluid homocysteine level above the 90th centile (>1.85 micromol per liter); 27% vs 10%, P = 0.02. Thirty one cases and 12 controls had an abnormal genotype; however, amniotic fluid homocysteine levels were not significantly different between these two groups (6/31, or 19% of cases had an elevated homocysteine compared to 1/12, or 8% of controls; P = 0.65). In contrast, 40 cases and 60 controls had a normal genotype; the neural tube defect cases had significantly higher homocysteine levels (13/40, or 32% of cases had an elevated homocysteine level compared to only 6/60, or 10% of controls; P = 0.008). Although both abnormal fetal MTHFR genotype and abnormal amniotic fluid homocysteine concentration are significantly associated with neural tube defects, the association with amniotic fluid homocysteine concentration is significant regardless of the fetal MTHFR genotype. The relationship between maternal and fetal homocysteine metabolism is complex.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed1990

Amniotic fluid ingestion enhances opioid-mediated but not nonopioid-mediated analgesia.

Ingestion of amniotic fluid or placenta by rats has been shown to enhance several types of opioid-mediated analgesia: that induced by morphine, footshock, vaginal/cervical stimulation, and late pregnancy. This enhancement has also been blocked by administration of opioid antagonists. The present study was designed to examine further the specificity of the enhancement effect for opioid-mediated analgesia by testing for enhancement following administration of aspirin, a nonopioid analgesic. The formalin test was used as the pain threshold assay. Amniotic fluid or beef bouillon was administered by orogastric tube to rats that were treated either with morphine sulfate or saline, or pretreated with naltrexone, then treated with aspirin or vehicle. Both morphine and aspirin treatments produced analgesia. Amniotic fluid significantly enhanced the analgesia produced by morphine, but did not enhance the analgesia produced by aspirin, further suggesting that the enhancing effect of amniotic fluid ingestion is specific for opioid-mediated analgesia, such as that existing at the start of parturition.

Amniotic Fluid↗
PubMed1982

Detection, isolation and characterization of cell free HLA A and B antigens from human amniotic fluid.

Cell-free HLA A and B antigens, paternal and maternal, have been detected in human amniotic fluids obtained from women at 16-18 weeks' gestation. Fractionation of amniotic fluid samples on sephadex showed that HLA A and B antigen activity was mainly in the 40,000 to 70,000 mol. wt. fractions. Lentil lectin sepharose 4B affinity chromatography of 30,000 to 70,000 sephadex molecular weight fraction of amniotic fluids isolated proteins which gave 2 bands, M and N, on discontinuous polyacrylamide gel electrophoresis (disc PAGE without SDS). SDS disc PAGE of the LcH bound glycoproteins recovered from amniotic fluids indicated 4 main protein bands approximately 12,900, 32,000, 52,600 and 78,500 mol. wt. Schiff's stain of the SDS gels showed that all the proteins except the 12,900 mol. wt. polypeptide contained carbohydrate. It was suggested that the 12,900 and 32,000 mol. wt. proteins obtained on disc PAGE gels represented the 2 subunits of the HLA A and B antigen molecule, i.e., beta 2-microglobulin and the allospecific heavy chains, similar to the papain-solubilized moiety of membrane antigens. In the absence of SDS the 2 polypeptides migrate in polyacrylamide gels as 1 protein band M, representing the intact (undissociated) antigen molecules. Enzyme linked immunosorbent assays were proposed for the estimation of cell-free HLA antigens.

Amniotic Fluid↗
PubMedDate not supplied

Eosinophil cationic protein and eosinophil protein X: human amniotic fluid concentrations and gestational tissue content at term.

The aim of this study was to determine the presence and concentration of immunoreactive eosinophil cationic protein (ECP) and eosinophil protein X (EPX) in human amniotic fluid at term and assess labour-associated changes in their mean concentrations. In addition, ECP and EPX content in term amnion, choriodecidua and placenta obtained before and after labour and delivery was established. Immunoreactive ECP and EPX were identified in all samples of amniotic fluid (n=47) and gestational tissue (n=60) assayed. EPX was quantitatively more abundant than ECP in both amniotic fluid and gestational tissues. In amniotic fluid, ECP and EPX concentrations increased 8-fold (P<0.02) and 1.5-fold (P<0.02), respectively, with labour onset. In gestational tissues, a labour-associated change in tissue content was only identified for ECP in choriodecidua, which increased 1.9-fold with labour and delivery (P<0.01). The labour-associated increase in amniotic fluid concentrations of ECP and EPX demonstrated in this study is consistent with the well-characterized role of these proteins in inflammatory reactions. It remains to be established whether the observed increase in ECP and EPX amniotic fluid concentrations is an epiphenomenon of labour onset or is involved causally in this process.

Adult↗
PubMed1998

Study of interleukin-6 and tumor necrosis factor-alpha levels in maternal serum and amniotic fluid of patients with premature rupture of membranes.

To study the change and clinical significance of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels in the maternal serum and amniotic fluid of pregnant women with chorioamnionitis and with premature rupture of membranes. Twenty-six normal-term pregnant women formed the control group, and forty-six pregnant women with premature rupture of membranes were enrolled for the study. Maternal serum and amniotic fluid IL-6 and TNF-alpha levels were measured using a sensitive radioimmunoassay and enzyme-linked immunosorbent assay (ELISA); chorioamnionitis was diagnosed by fetal membrane pathology. The maternal serum IL-6 levels and amniotic fluid IL-6 and TNF-alpha levels were higher than those of the control (P < 0.01). There was a significant relationship between maternal serum IL-6 and maternal serum and amniotic fluid IL-6 and TNF-alpha with the time of the premature rupture of membranes, i.e. the longer the time, the higher the maternal serum and amniotic fluid IL-6 and TNF-alpha. There were 12 patients with chorioamnionitis in premature rupture of membranes and their maternal serum and amniotic fluid IL-6 and TNF-alpha levels were higher than that of non-chorioamnionitis patients (P < 0.01-0.05). IL-6 and TNF-alpha levels in maternal and amniotic fluids are a valuable index in identification of the chorioamnionitis in patients with premature rupture of membranes.

Adult↗
PubMed1997

Effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume in sheep.

OBJECTIVE: Our purpose was to determine the effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume and composition. STUDY DESIGN: Twelve pregnant ewes underwent surgery at 115 +/- 2 days after mating (term approximately 147 days) for the implantation of fetal vascular, bladder, and amniotic sac catheters. At 125 +/- 1 days seven fetuses were studied during 6 days of hypoxemia and five control fetuses were studied over six days of normoxemia. Index values of fetal renal function and amniotic fluid volume were measured. RESULTS: During hypoxemia fetal SaO2 and PaO2 were reduced from 60.9% +/- 1.6% and 21.9 +/- 0.6 mm Hg to 29.6% +/- 3.8% and 14.9 +/- 0.8 mm Hg, respectively. Fetal hypoxemia was associated with a transient acidemia (arterial pH 7.29 +/- 0.02) at 4 hours. There were no sustained alterations in fetal urine production (9.5 +/- 0.8 ml/hr/kg) or glomerular filtration rate (1.3 +/- 0.1 ml/min/kg) during hypoxemia. In control fetuses the amniotic fluid volume increased over 7 days, from 717 +/- 169 ml to 1031 +/- 147 ml, whereas in the hypoxemic fetuses it did not change (741 +/- 68 ml) over the same period. CONCLUSION: During prolonged fetal hypoxemia in the absence of acidemia, fetal urine production is maintained, whereas the normal gestational increase in amniotic fluid volume is prevented, raising the possibility that intramembranous reabsorption of amniotic fluid is increased by hypoxemia.

Amniotic Fluid↗
PubMed1982

Vitamin A concentration in amniotic fluid and maternal serum related to neural-tube defects.

The vitamin A concentration of amniotic fluid and maternal serum was measured during the second trimester of pregnancy in 106 women, 12 of whom had a baby with a neural-tube defect. In these 12 pregnancies the amniotic fluid vitamin A concentration was significantly higher than in 94 normal pregnancies. There was a highly significant correlation between amniotic fluid vitamin A and both zinc and alpha-fetoprotein (AFP) levels. The maternal serum vitamin A levels were also significantly related to serum zinc levels. Women with a raised serum AFP level, but a normal baby, had significantly higher amniotic fluid vitamin A levels and significantly lower serum vitamin A levels compared with those in women with normal serum AFP levels.

Adult↗
PubMed2006

N-acetyl-cysteine suppresses amniotic fluid and placenta inflammatory cytokine responses to lipopolysaccharide in rats.

OBJECTIVE: Maternal infections may induce placental, amniotic and, potentially, fetal inflammatory responses. As cytokine responses may be mediated by oxidative stress, we determined whether the antioxidant N-acetyl-cysteine (NAC), can attenuate maternally induced amniotic and placental cytokine responses to maternal infection (modeled by lipopolysaccharide [LPS]). STUDY DESIGN: Gestation day 18 pregnant rats were (1) treated with LPS (100 microg/kg, body weight; intraperitoneally) alone; (2) pretreated with NAC (300 mg/kg body weight; intraperitoneally) 30 minutes before LPS; (3) posttreated with NAC 120 minutes after LPS; or (4) treated with NAC 30 minutes before and 120 minutes after LPS. Six hours after LPS administration, maternal serum and amniotic fluid interleukin-6 (IL-6) and IL-10 levels, and placental IL-6 messenger RNA levels were determined. RESULTS: LPS increased maternal serum IL-6 (50 +/- 25 to 3444 +/- 584 pg/mL) and IL-10 (40 +/- 20 to 958 +/- 339 pg/mL) and amniotic fluid IL-6 (59 +/- 25 to 891 +/- 128 pg/mL). Pretreatment and/or posttreatment with NAC attenuated IL-6 in the maternal serum and amniotic fluid and IL-10 in the amniotic fluid. LPS also induced placental IL-6 messenger RNA that was inhibited by treatment with NAC before and after LPS. CONCLUSION: NAC inhibition of inflammatory responses may protect the fetus from potential long-term sequelae.

Acetylcysteine↗
PubMed1999

Fetal unilateral cleft lip and palate: detection of enzymic anomalies in the amniotic fluid.

Aims of this study were to evaluate whether it is possible to determine, by means of isoelectric focusing, an enzymic differentiation in human amniotic fluid, and whether the onset of fetal cleft lip and palate is accompanied by a pathologic enzymatic differentiation pattern in amniotic fluid. From January of 1993 to June of 1996, amniotic fluid samples from 315 healthy pregnant women (ages 22 to 43 years, mean 37 years; gestational age 14 to 22 weeks, mean 17 weeks) were examined. The normality of all pregnancies was confirmed at birth. Moreover, amniotic fluid samples were examined from three pregnancies (ages 36, 35, and 30 years; gestational ages 16, 18, 24 weeks) with fetal unilateral cleft lip and palate (confirmed at birth), diagnosed by ultrasound. The authors have tested as "metabolic" markers the enzymes lactate dehydrogenase and creatine phosphokinase. For the concentration rates of both the tested enzymes, a statistically significant difference (p = 0.003) was found between amniotic fluid samples obtained from normal and affected pregnancies. These data, in the authors' opinion, corroborate the hypothesis that a local metabolic impairment is somehow involved in the pathogenesis of cleft lip and palate.

Adult↗
PubMed1986

Pancreatic secretory trypsin inhibitor from human amniotic fluid and fetal and neonatal urine: concentrations and physicochemical characterization.

The levels and physicochemical properties of the pancreatic secretory trypsin inhibitor, also known as Kazal type trypsin inhibitor, were studied in human amniotic fluid. In the second trimester, the median concentration was 160 ng/ml, which exceeds the maternal serum levels 20-fold. Towards term, the amniotic fluid levels declined about 5-fold, whereas the maternal serum values remained constant. In fetal urine, the concentration of the trypsin inhibitor was similar to that in amniotic fluid in early gestation, whereas in newborn urine, the median level was 4-to 5-fold higher than in term amniotic fluid. The physiochemical characteristics of the trypsin inhibitor in amniotic fluid, neonatal urine and cancer urine from an ovarian cancer patient were similar, as studied by gel filtration, high performance reverse phase liquid chromatography, and complete immunological identity in immunodiffusion. The physicochemical similarity and levels in various compartments suggest fetal contribution to amniotic fluid levels of the trypsin inhibitor.

Amniotic Fluid↗
PubMed1990

Increased maternal plasma concentration of endothelin-1 during labor pain or on delivery and the existence of a large amount of endothelin-1 in amniotic fluid.

The concentration of endothelin-1 (ET-1) in plasma and amniotic fluid from normal pregnant women was determined by a sensitive sandwich-enzyme immunoassay system, established recently. The plasma ET-1 level increased gradually during normal pregnancy as the pregnancy advanced, the levels (0.40 +/- 0.02 pmol/l, n = 45) being significantly (p less than 0.05) higher after 29 weeks of gestation than those (0.32 +/- 0.01 pmol/l, n = 30) before 28 weeks of gestation. The plasma ET-1 level during labor pain was significantly higher (0.59 +/- 0.06 pmol/l, n = 10) than that (0.40 +/- 0.02 pmol/l, n = 45) in the 3rd trimester of pregnancy without labor pain (p less than 0.02). Moreover, a high level of ET-1 (17.38 +/- 0.25 pmol/l, n = 18) was detected in amniotic fluid on term delivery. The ET-1 level in amniotic fluid was significantly higher than the levels in maternal and umbilical cord plasma (p less than 0.001 and p less than 0.001, respectively). After delivery the maternal ET-1 level decreased gradually and 2 day postpartum ET-1 levels reached the normal non-pregnant level.

Adult↗
PubMed1986

Kinetic comparisons of amniotic fluid inactive renin and renal renin using synthetic and human renin substrates.

Inactive renin has been isolated from pooled amniotic fluid and purified approximately 642-fold. Prior to activation the isolates had approximately 4% of the activity found after activation. The observation is similar to that reported for inactive renin from chorionic cell culture and suggests a placental origin of amniotic fluid inactive renin. Using plasma from an estrogen-treated woman, renin substrate was recovered free of renin and inactive renin and a portion was separated into NMW and HMW components. The NMW form constituted approximately 93% and the HMW form approximately 7% of the renin substrate. Amniotic fluid inactive renin was used for determinations of enzyme-substrate kinetics with the pooled, NMW, and HMW plasma substrate and tetradecapeptide synthetic substrate, and the results were compared to similar determinations using standard renal renin. Using synthetic substrate, the kinetics of renal renin and amniotic fluid inactive renin before and after activation were similar. The kinetics of renal renin with pooled, NMW, and HMW plasma substrate were also similar. Amniotic fluid inactive renin had a lower Km with pooled than with NMW substrate, however, which resulted from a significantly smaller Km with HMW component. Although the affinity constants with pooled substrate were not different for renin and inactive renin, the Km of inactive renin was significantly less with the HMW component of plasma renin substrate. The observations are compatible with a role for placental inactive renin in normal pregnancy and suggest the possibility of a further role in hypertensive pregnancy.

Amniotic Fluid↗
PubMed1992

Microvillar enzyme activity in amniotic fluid, extraembryonic coelomic fluid and maternal serum in the first trimester of pregnancy.

The activities of two microvillar enzymes, gamma-glutamyl transpeptidase and total alkaline phosphatase, have been measured in samples of amniotic fluid and extraembryonic coelomic fluid obtained by high-resolution transvaginal ultrasound-guided amniocentesis from 40 women between 7 and 12 weeks of gestation. There was a highly significant difference between gamma-glutamyl transpeptidase activity in amniotic fluid (median level 31 U/l; range 2-409 U/l) and extraembryonic coelomic fluid (median level 2 U/l; range less than 2-16 U/l) (P less than 0.001; Mann-Whitney U-test). Alkaline phosphatase activity was not detected in 84% of amniotic fluid samples and 97% of extraembryonic coelomic fluid samples. No difference was found between total alkaline phosphatase activity in these fluids (P = 0.14; Mann-Whitney U-test). Enzyme activities in amniotic fluid increased with gestational age. A significant linear correlation was found between amniotic fluid gamma-glutamyl transpeptidase activity and stage of gestation (r = 0.86; P less than 0.001) and total alkaline phosphatase activity in amniotic fluid and stage of gestation (r = 0.66; P less than 0.001).

Alkaline Phosphatase↗