Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMNIOTIC FLUID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2006

Antidepressants in amniotic fluid: another route of fetal exposure.

OBJECTIVE: The authors' goal was to determine the concentration of antidepressants in amniotic fluid during maternal treatment of depression. METHOD: Women treated with antidepressants undergoing amniocentesis for obstetrical reasons were enrolled. Antidepressant concentrations in amniotic fluid and maternal serum were determined with high-performance liquid chromatography. RESULTS: Amniotic fluid was obtained from 27 women, and the amniotic fluid's antidepressant concentrations were highly variable. For the parent compounds, the amniotic fluid concentrations of selective serotonin uptake inhibitors averaged 11.6% (SD=9.9%) of maternal serum concentrations (N=22). Amniotic fluid to maternal serum ratios were higher for venlafaxine: 172% (SD=91%) (N=3). Of interest, the amniotic fluid to maternal serum ratios for the metabolites (N=19) did not demonstrate a consistent pattern compared to the parent compound ratios. In 10 subjects, the amniotic fluid to maternal serum ratio for the metabolites was higher than the parent compound and lower in the remaining nine subjects. CONCLUSIONS: The pattern of antidepressant concentrations in amniotic fluid is similar to recent data for placental passage. Although the significance of amniotic fluid exposure remains to be determined, these results demonstrate that maternally administered antidepressants are accessible to the fetus in a manner not previously appreciated.

Amniocentesis↗
PubMed1992

Cholinesterases exhibiting aryl acylamidase activity in human amniotic fluid.

Acetylcholinesterase (EC 3.1.1.7) and butyrylcholinesterase (EC 3.1.1.8) in human amniotic fluid were estimated in the presence of selective inhibitors. Amniotic fluid cholinesterases (mixture of acetylcholinesterase and butyrylcholinesterase) purified by procainamide-Sepharose affinity chromatography exhibited aryl acylamidase activity which was sensitive to serotonin inhibition (a property of aryl acylamidases associated with both acetyl- and butyrylcholinesterases) and tyramine activation (shown exclusively by aryl acylamidase associated with butyrylcholinesterase). Tyramine activation was unaffected in the presence of the selective acetylcholinesterase inhibitor BW284C51 whereas it was abolished in the presence of the selective butyrylcholinesterase inhibitor ethopropazine, suggesting the presence of both types of aryl acylamidases in amniotic fluid, one associated with acetylcholinesterase and the other associated with butyrylcholinesterase. Butyrylcholinesterase and the associated aryl acylamidase activity in the affinity purified enzyme was selectively immunoprecipitated by a polyclonal antibody raised against human serum butyrylcholinesterase. Estimation of the activity ratio of acetylcholinesterase to butyrylcholinesterase in a few samples of amniotic fluid showed that this could vary depending on the butyrylcholinesterase arising from contaminating blood in the samples. Gel electrophoresis under non-denaturing conditions and enzyme staining showed that butyrylcholinesterase band was detectable on the gel in all the samples whereas acetylcholinesterase band was below detectable levels in normal samples but visible in samples from pregnancies of neural tube defect fetuses. It is suggested that the use of selective cholinesterase inhibitors along with gel electrophoresis and immunoprecipitation studies may be useful in the assessment of cholinesterase activities in human amniotic fluid.

Acetylcholinesterase↗
PubMed2003

Influence on fetal blood pH when adding amniotic fluid: an in vitro model.

OBJECTIVE: To assess the effect of contamination with amniotic fluid in different quantities on fetal capillary blood pH. DESIGN: In vitro model. SETTING: Department of Obstetrics, St Pölten Hospital. SAMPLE: Venous umbilical blood and amniotic fluid from 35 women who underwent amniotomy during labour. METHODS: Venous umbilical blood was mixed in vitro with amniotic fluid in diluted series (venous umbilical blood/amniotic fluid, 10:1 to 1:1). In every case two parallel runs of the dilution series in an inverted fashion were performed to rule out a possible time-dependent bias of the pH measurements. MAIN OUTCOME MEASURES: pH change in dilutions of umbilical venous blood with amniotic fluid: 10:1, +0.07 (0.02); 8:1, +0.08 (0.02); 6:1, +0.08 (0.03); 4:1, +0.07 (0.02); 2:1, +0.09 (0.03); 1:1, +0.12 (0.05); all P < 0.001. RESULTS: Amniotic fluid pH increases, whereas umbilical blood pH decreases slightly over time since collection. Dilutions of umbilical venous blood with amniotic fluid resulted in a significant pH rise. There was no significant difference between the two inversely performed dilution series. CONCLUSION: Amniotic fluid influences in vitro fetal venous blood pH immediately after contact. This observation indicates the possible masking of a fetus in distress by fetal scalp blood pH determination when amniotic fluid contaminates the sample.

Adult↗
PubMed1992

Distribution of relaxin between human maternal and fetal circulations and amniotic fluid.

Relaxin was measured in maternal blood and amniotic fluid samples at 9-40 weeks and in fetal blood samples at 19-41 weeks of pregnancy. In amniotic fluid, concentrations of relaxin rose from 58 ng/l (geometric mean) at 10 weeks to 142 ng/l at 14 weeks and declined subsequently to 55 ng/l at 22 weeks. In maternal blood, mean relaxin concentrations were ten times greater than in amniotic fluid, and concentrations decreased with gestation. Since there was no significant association between the relaxin concentrations in the two compartments, relaxin in the amniotic fluid may be derived from the decidualized endometrium rather than the maternal circulation, alternatively its metabolism may be different in the two compartments. The absence of detectable concentrations of relaxin in any of the fetal blood samples demonstrates that there is no significant placental transfer or fetal synthesis of this peptide.

Amniotic Fluid↗
PubMed1994

Cocaine and metabolites in amniotic fluid may prolong fetal drug exposure.

OBJECTIVE: Cocaine and metabolites can be found in the amniotic fluid after maternal use, presumably as a result of fetal urination. The fetus may be repeatedly exposed to the effects of these drugs through contact with amniotic fluid that contains these substances. The purpose of this study was to determine whether the naive fetal lamb generates detectable fetal blood levels of cocaine and metabolites when cocaine is placed directly into the amniotic fluid and, if so, whether fetal swallowing accounts for these findings. STUDY DESIGN: Six pregnant ewes with singleton fetuses of 120 to 125 days' gestation were chronically catheterized for daily sampling of cocaine and metabolite levels in maternal venous plasma, fetal venous plasma, and amniotic fluid over a 7-day period. Esophageal ligation was performed in three additional animals similarly instrumented to evaluate the role of fetal swallowing in the distribution of amniotic fluid cocaine and its metabolites. In each case, at the time of surgery, an Alzet osmotic pump delivering cocaine at 0.5 mg/kg estimated fetal weight per hour into the amniotic fluid was secured to the fetal back. Cocaine and metabolites (benzoylecgonine, ecgonine methyl ester, and norcocaine) were measured daily in material and fetal plasma, amniotic fluid, and meconium by solid-phase extraction and derivatization and quantified by high-performance gas chromatographic techniques. RESULTS: The concentrations of ecgonine methyl ester were highest in the amniotic fluid followed by cocaine and benzoylecgonine. In the normal and esophagus-ligated groups, cocaine, benzoylecgonine, and norcocaine were found in fetal plasma in concentrations of approximately 3% that of amniotic fluid. Ecgonine methyl ester was not detected in fetal plasma from either group. Meconium samples from sheep with and without esophageal ligation demonstrated high levels of norcocaine. CONCLUSION: We conclude that cocaine and metabolites in amniotic fluid enter the fetal circulation to produce detectable plasma levels through routes other than swallowing. Moreover, the results of meconium analyses in the two groups of fetuses suggest that fetal swallowing is not the primary mechanism by which cocaine and metabolites enter the intestine.

Absorption↗
PubMed1990

[Purification and characterization of insulin-like growth factor binding proteins (IGF-BP) in amniotic fluid--existence of a 160K IGF-BP].

Human amniotic fluid has been reported to contain 28-34K insulin-like growth factor (IGF) binding protein (32K-AFBP). The existence of 160K IGF-binding protein (160K-AFBP) in amniotic fluid was also demonstrated by affinity labeling studies. In this paper we describe procedures for purification of 160K-AFBP as well as 32K-AFBP from pre-term amniotic fluid and characterize these two binding proteins. IGF binding proteins were purified from batches of 500ml of pre-term amniotic fluid using ammonium sulphate precipitation, anion-exchange chromatography (Q-Sepharose) and Sephacryl S-200 HR chromatography. IGF binding activity during purification was quantitated by incubation with 125I-IGF-I and dextran-coated charcoal separation. The total recovery and purification of binding protein were 38% and 81.5-fold, respectively. The three major binding activities were eluted in fractions corresponding to a relative molecular mass of 160K, 60K and 30K when Q-Sepharose purified AFBPs were chromatographed on Sephacryl S-200 HR at neutral pH. HPLC of purified 160K binding activity on size exclusion column yielded a single peak of absorbance at 280nm, corresponding to an apparent molecular weight of 160K with three predominant peaks of binding to 125I-IGF-I, corresponding to molecular weights of 160K, 79K and 32K, respectively. On the other hand, purified 30K binding activity on HPLC yielded a single peak of absorbance at 280nm, corresponding to an apparent molecular weight of 32K coincident with a peak of binding to 125I-IGF-I. SDS-PAGE of HPLC purified 160K-AFBP in the presence of mercaptoethanol revealed eight bands by Coomassie Blue staining, five major bands corresponding to 160K, 78K, 69K, 54K, and 51K and three weaker bands corresponding to 45K, 36K, and 28K. The HPLC purified 32K-AFBP showed a single band of a molecular mass estimate of 32K on SDS-PAGE. These results indicate that human amniotic fluid contains at least two distinct IGF-binding proteins, and the structure of 160K-AFBP is similar to those of 150K binding protein in the circulation.

Amniotic Fluid↗
PubMed1983

Amniotic fluid beta-endorphin and beta-lipotropin concentrations during the second and third trimesters.

Amniotic fluid beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) were measured by radioimmunoassay after silicic acid extraction and gel chromatographic separation of the two peptides in uncomplicated second-trimester and term pregnancies, in diabetic patients at term, and in pregnancies complicated by Rh-isoimmunization, premature labor, and intrauterine growth retardation. Furthermore, the lecithin/sphingomyelin (L/S) ratios as well as the dehydroepiandrosterone sulfate (DHEA-S) and cortisol levels were determined in most of the amniotic fluid specimens. Both the mean (+/- SE) beta-EP (65.3 +/- 9.1 fmol/ml) and beta-LPH (150 +/- 15.8 fmol/ml) concentrations were significantly higher in the 20 patients with normal pregnancies of 16 to 21 weeks' duration than those found in 21 patients with uncomplicated term pregnancies of 38 weeks' gestation, averaging 42.6 +/- 6.0 and 80.1 +/- 10.7 fmol/ml, respectively. The mean amniotic fluid beta-EP and beta-LPH concentrations measured in the latter subjects were similar to those observed in 23 diabetic patients with otherwise uncomplicated term pregnancies. The mean amniotic fluid beta-EP and beta-LPH levels found in the limited number of patients with Rh-isoimmunization (N = 9), premature labor (n = 8), and intrauterine growth retardation (n = 5) with pregnancies of 24 to 36, 24 to 36, and 34 to 38 weeks' gestation, respectively, were not significantly different from the mean amniotic fluid beta-EP and beta-LPH concentrations of uncomplicated term pregnancies. In all patients but those with Rh-isoimmunization, beta-EP concentrations exhibited a positive correlation with beta-LPH levels. However, the molar beta-LPH:beta-EP ratio was significantly lower at term than during the early second trimester. Neither beta-EP nor beta-LPH correlated with the amniotic fluid L/S ratio and only beta-LPH exhibited a significant inverse correlation with amniotic fluid DHEA-S. The latter was significantly higher in uncomplicated term than second-trimester pregnancies. These results confirm that immunoassayable beta-EP is present in amniotic fluid and declines toward term. These data demonstrate that immunoassayable beta-LPH is present in amniotic fluid and show a more pronounced decrease toward the end of pregnancy than beta-EP. Neither peptide, at least on account of the amniotic fluid levels, appears to be associated with fetal maturation. The physiologic significance of amniotic fluid beta-EP and beta-LPH and their possible role as markers of fetal response to stress remain to be elucidated.

Amniotic Fluid↗
PubMed1984

Enhancement of the antibacterial property of amniotic fluid by hyperthermia.

The intrinsic ability of human amniotic fluid to prevent growth of Escherichia coli varies with the test strain employed, but is enhanced by increasing the temperature of incubation, as demonstrated by viable counts of test organisms in amniotic fluid compared with growth media at various temperatures. The antibacterial activity of amniotic fluid is reversed at all temperatures by the addition of potassium phosphate, but residual inhibition is seen at temperatures above 37C. When purified inhibitor preparations are tested, complete reversal by phosphate at the highest temperatures is seen. Thus, the augmented inhibition in whole amniotic fluid depends on the combined effects of phosphate-sensitive and -insensitive inhibitors. Test organisms in the presence of partially purified inhibitor were not adversely affected at 4C, indicating that bacteria must be metabolically active to be inhibited. It is concluded that temperatures above 37C enhance the antibacterial effect. This may enhance protection during pyrexia.

Amniotic Fluid↗
PubMed1998

Clinical significance of echogenic amniotic fluid.

PURPOSE: This study aimed to determine the clinical significance of echogenic amniotic fluid. METHODS: We prospectively studied 19 twin pregnancies in which the amniotic fluid in 1 sac was anechoic and that in the other sac was echogenic. Morphologic characteristics of amniotic fluid were assessed from samples taken at amniocentesis or upon delivery within 48 hours after sonographic examination. RESULTS: In twins with echogenic amniotic fluid, assessment revealed clear fluid in 6 cases (32%), vernix caseosa in 12 (63%), and meconium in 1 (5%). In co-twins with anechoic amniotic fluid, assessment revealed clear fluid in 9 cases (47%), vernix caseosa in 6 (32%), and meconium in 4 (21%). CONCLUSIONS: Echogenic amniotic fluid on prenatal sonography is not predictive of meconium.

Adult↗
PubMed1987

Immunocytochemical characterization of amniotic fluid macrophages in cases of fetal neural tube defects.

Amniotic fluid cells from 31 pregnancies with fetuses having open neural tube defects (NTDs) and from 43 pregnancies with fetuses free of NTDs were studied with the use of the immunoperoxidase method for alpha-fetoprotein (AFP) and glial fibrillary acidic protein (GFAP). The authors also used cytochemical stains for endogenous peroxidase and nonspecific esterase activity. In cases of NTDs, macrophages were present in the amniotic fluid, and in the authors' system they showed intense immunoreactivity for both AFP and GFAP and showed very strong activity for peroxidase and nonspecific esterase, whereas the epithelial cells and red blood cells showed no activity. In six cases of anencephaly, sections from the margin of the cranial end of defective spinal cords at the aperture of the open lesion were also studied for AFP and GFAP. In these cases, AFP- and GFAP-positive cells were found, indicating the possible neural (glial) origin of a part of amniotic fluid macrophages. Although the determination of AFP levels in maternal blood and amniotic fluid is widely used in the prenatal diagnosis of NTDs, demonstration of AFP in amniotic fluid cells by means of immunocytochemistry has not been described.

Amniotic Fluid↗
PubMed1985

Amniotic fluid thyrotropin (TSH) following maternal administration of thyrotropin releasing hormone.

Cord blood and amniotic fluid thyrotropin (TSH), T4, T3, and rT3 concentrations were measured in 49 women who received 400 micrograms thyrotropin releasing hormone (TRH) iv during labor and in 16 control women who received saline. Cord blood serum TSH concentrations were elevated for as long as 4 hours after TRH administration and peak values (38.0 +/- 4.2 microU/ml) were observed from 61-120 minutes after TSH as compared to control values of 5.0 +/- 0.3 microU/ml. The elevations in fetal TSH concentration stimulated the fetal thyroid, resulting in a progressive increase in cord blood T4 and T3 but not rT3 concentrations. These TRH induced elevations in fetal cord blood TSH concentrations were not accompanied by increases in unconcentrated and 4 fold concentrated amniotic fluid TSH concentrations which were almost always below 0.6 microU/ml, the limit of assay sensitivity. Unconcentrated amniotic fluid T4 concentrations were barely detectable and no variation was observed between the TRH treated and saline treated mothers; amniotic fluid T3 was not detectable in any of the groups; and amniotic fluid rT3 concentrations ranged between 46.4 and 55.6 ng/dl and did not differ between groups. These findings suggest that term amniotic fluid TSH values do not reflect transient but marked elevations in fetal serum TSH concentrations and that amniotic fluid TSH determination is probably not useful in the detection of primary fetal hypothyroidism. It is possible, but unlikely, that long-term and even greater elevations in fetal serum TSH concentrations would result in increased amniotic fluid TSH concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1985

Amniotic fluid prolactin and fetal lung maturation.

Concentrations of prolactin in amniotic fluid, fetal plasma, and maternal plasma were determined in 34 rhesus monkeys delivered by hysterotomy under general anesthesia at gestational ages of 110 to 160 days (term, 165 days). Included were 15 cases (gestational ages 110 to 143 days) in which the mothers received 2 mg of betamethasone intramuscularly daily for 3 days prior to delivery. Fetal lung maximum volumes were determined in addition to the following indices of fetal lung surfactant: lung alveolar stability, lung phosphatidylcholine concentrations, lung extract surface tensions, and amniotic fluid lecithin to sphingomyelin ratios. Amniotic fluid prolactin was found to correlate significantly with lung alveolar stability (r = 0.51; p less than 0.01), lung phosphatidylcholine (r = 0.51; p less than 0.01), lung extract surface tension (r = -0.39, p less than 0.05) and amniotic fluid lecithin/sphingomyelin ratio (r = 0.50; p less than 0.01). These correlations remained statistically significant even when the effects of gestational age were taken into account. These findings suggest that amniotic fluid may modulate fetal production of surfactant via its prolactin content.

Amniotic Fluid↗
PubMed1977

Effect of amniotic fluid on bacterial growth.

The bacteriostatic effect of amniotic fluid was studied using four pathogenic organisms which are encountered in the perinatal period, E. coli, S. aureus, L. monocytogenes, and Group B beta hemolytic streptococci. Amniotic fluid inhibited the growth of all four organisms, with a wide degree of individual variation among specimens. The greatest degree of inhibition was noted for L. monocytogenes and the least for E. coli. The time in gestation in which the amniotic fluid sample was obtained did not appear to be related to its bacteriostatic capacity. The ability of amniotic fluid to inhibit the growth of certain pathogenic organisms may be significant in prevention of perinatal infection.

Amniotic Fluid↗
PubMed1984

Methods for extracting phospholipids from human amniotic fluid compared.

Phospholipids were extracted from human amniotic fluid by various procedures, including the two most commonly applied to amniotic fluid for evaluation of fetal lung maturity. We find that the yield of phospholipid is greatly procedure dependent. This should be taken into account when one is considering the various reported methods of evaluating fetal lung maturity, because in some of them phospholipid data are expressed in terms of absolute concentration in the amniotic fluid. There were also significant differences in phospholipid composition in extracts prepared by the various procedures, but in general these were not large enough to influence evaluation of fetal lung maturity by methods in which phospholipid data are expressed in relative terms, as ratios or percentages--e.g., in the lecithin/sphingomyelin ratio and "lung profile" procedures. In the extraction method originally recommended for determination of the lecithin/sphingomyelin ratio, both the yield and composition of phospholipid depend on the extent of mixing.

Amniotic Fluid↗
PubMed1996

Effect of indomethacin on individual amniotic fluid indices in multiple gestations.

To determine the effect of indomethacin on the amniotic fluid index of individual fetuses in multiple gestations, we evaluated seven sets of twins and two sets of triplets in preterm labor (eight cases) or with polyhydramnios (one case). The dose of oral indomethacin was either 25 mg every 12 hours or 25 mg every 6 hours. The amniotic fluid volume of individual amniotic sacs was estimated serially by the amniotic fluid index. When an oral dose of indomethacin of 25 mg every 6 hours was used, oligohydramnios eventually occurred in five of eight amniotic sacs and a subjective decrease in amniotic fluid occurred in one sac. Oligohydramnios was detected in only one of 13 amniotic sacs when the dose of indomethacin was 25 mg every 12 hours. The amniotic fluid volume returned to normal in these seven amniotic sacs within 4 days of discontinuing indomethacin. We conclude that maternal indomethacin therapy has a variable effect on the individual amniotic fluid volumes in multiple gestations.

Amniotic Fluid↗
PubMed1991

Maternal hydration increases amniotic fluid index.

Although adequate amniotic fluid (AF) volume is considered an important aspect of fetal well-being, the etiology of decreased AF volume is not well understood. A randomized blinded trial was designed to examine our hypothesis that maternal hydration would increase the AF index in women with low AF indexes. Women seen in our testing centers were randomized into control or hydration groups. The control group was instructed to drink their normal amount of fluid; the hydration group was instructed to drink 2 L of water, in addition to their usual amount of fluid, 2-4 hours before the post-treatment AF index. The women returned for the post-treatment AF index the same or following day. The mean post-treatment AF index was significantly greater in the hydration group (6.3 versus 5.1; P less than .01), as was the mean change in AF index (post-treatment AF index--pre-treatment AF index: 1.5 versus 0.31; P less than .01). These findings suggest that maternal oral hydration increases AF volume in women with decreased fluid levels.

Amniotic Fluid↗
PubMed2002

Fatal amniotic fluid embolism diagnosed histologically.

Although the mortality of amniotic fluid embolism remains very high, there are more and more reports of patients surviving after prompt and aggressive therapy. However its pathogenesis is controversial, and, in some cases, an anaphylactic reaction to the amniotic fluid rather than the hemodynamic changes following mechanical obstruction by an embolus has been proposed as the underlying pathophysiological mechanism. In this paper we describe a case of amniotic fluid embolism with florid clinical features and a difficult and delayed diagnosis. On autopsy, clear-cut histological changes of amniotic fluid embolism were found.

Adult↗