Phospholipid composition of fetal lung fluid and amniotic fluid during late gestation in sheep.
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The lead and cadmium concentrations in maternal and umbilical cord blood and amniotic fluid were determined in 19 parturient women at delivery. Six placental and amniotic membrane tissue specimens were also investigated. The mean lead concentrations (mean +/- SD) in maternal (40.4 +/- 18.2 ng/ml) and umbilical cord (37.1 +/- 13.5 ng/ml) blood were similar and correlated significantly with each other (r = 0.77, p less than 0.001). The lead concentration in amniotic fluid (59.6 +/- 8.3 ng/ml) was significantly higher than in maternal or umbilical cord blood. Cadmium concentrations in maternal blood (1.1 +/- 0.9 ng/ml) and amniotic fluid (1.0 +/- 0.2 ng/ml) were significantly higher (p less than 0.001) than in umbilical cord blood (0.4 +/- 0.2 ng/ml) and there was no significant correlation among these values. The highest concentrations of cadmium (35.1 +/- 24.2 ng/gm of wet weight) and lead (87.3 +/- 154.2 ng/gm of wet weight) were found in the amniotic membranes. Our results show that lead and cadmium accumulate in amniotic fluid and amniotic membranes and that the distribution of lead and cadmium is different in the human maternal-fetoplacental unit. The fetal exposure to lead is similar and that to cadmium, lower, compared with maternal exposure. The inability of the placenta to totally prevent the fetus from exposure to lead and cadmium suggests that pregnant women should avoid occupations where exposure to these toxic elements is possible.
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Qualitative amniotic fluid volume determination is a routine part of fetal biophysical profile score testing. The relationship between polyhydramnios and poor perinatal outcome has been previously documented. We have undertaken a retrospective chart review which relates qualitative amniotic fluid volume as determined at the time of last biophysical profile score assessment to perinatal outcome in 7562 referred high-risk obstetric patients. Gross and corrected perinatal mortality in association with normal qualitative amniotic fluid volume ranged from 4.65/1000 and 1.97/1000, respectively, to 32.9/1000 and 4.12/1000 in association with increased qualitative amniotic fluid volume, respectively. The incidences of major congenital anomaly and fetal macrosomia were significantly related to qualitative amniotic fluid volume.
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Human amniotic fluid contains an inhibitor of prostaglandin synthesis. The activity of the inhibitor was measured in amniotic fluid obtained in early pregnancy, and at term both before and after the onset of labor. The inhibitory activity was greater in amniotic fluid taken in early pregnancy than in fluid taken at term before the onset of labor (P less than 0.05). There was a further significant reduction in inhibitory activity (P less than 0.01) in amniotic fluid collected during labor. These results are suggestive that the onset of labor is associated with a local withdrawal of inhibition of prostaglandin biosynthesis.
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INTRODUCTION: In spite of confirming an association between type I diabetes of pregnancy with hydramnios, in the most recent studies there is still no clarity about which of the maternal or foetal metabolic parameters linked with amniotic fluid volume play the most important role. AIM: To determine which of the maternal or foetal metabolic parameters has the closest association with amniotic fluid volume. MATERIAL AND METHODS: The research was performed in two groups: normal healthy pregnant women (n=43) and group of pregnant women with insulin-dependent diabetes mellitus (n=17) and their newborns. We measured: amniotic fluid index, glucose level in serum and in amniotic fluid, in newborn serum, HbA1c level in serum of women and newborns. RESULTS: We found statistically significant higher values of amniotic fluid index 16.3 +/- 5.2 cm (p<0.01), glucose level in amniotic fluid 2.7 +/- 0.3 mmol/l (p<0.01), serum glucose level before delivery 8.4 +/- 1.6 mmol/l (p<0.001), glycosylated haemoglobin in serum levels 7.9 +/- 0.4% (p<0.05), levels of glucose and glycosylated haemoglobin in serum newborns 3.4 +/- 0.3 mmol/l (p<0.05), 7.7 +/- 0.4% (p<0.001) in patients with insulin-dependent diabetes mellitus as compared with these values in the group of healthy parturient women and their newborn infants. Performed correlation study shows statistical correlation between amniotic fluid index and glycosylated hemoglobin serum levels in the group of women with insulin-dependent diabetes mellitus (p<0.05), t=0.56. CONCLUSION: We conclude that long hyperglycemia or increased HbA1c level have an important role in amniotic fluid index increase in patients with insulin-dependent diabetes mellitus.
Fetuses are surrounded by amniotic fluid rich in nutrients and other factors essential to fetal development and possibly to its scarless wound healing. The purpose of this study was to determine whether amniotic fluid contains factors that regulate activities of major proteases involved in the process of wound healing (e.g., collagenase, hyaluronidase, elastase, and cathepsin B). Human amniotic fluid was assayed in vitro for inhibition or stimulation of the activity of these enzymes. Our results showed that amniotic fluid enhanced collagenase activity at a concentration of 66 micrograms protein (p < 0.01), but inhibited activities of hyaluronidase (132 micrograms protein; p < 0.05), elastase (170 micrograms protein; p < 0.05), and cathepsin B (19 micrograms protein; p < 0.01). This finding suggests that amniotic fluid could have an important role in flawless fetal wound healing by regulating these matrix-degrading enzymes.
Amniotic fluid was once considered to be a stagnant pool, approximately circulating with a turnover time of one day. Adequate amniotic fluid volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Even though different hypotheses have been advanced on the mechanisms regulating this turnover, the inflow and outflow mechanism that keeps amniotic fluid volume within the normal range is not entirely clear. Regulatory mechanisms act at three levels: placental control of water and solute transfer; regulation of inflows and outflows from the fetus; and, maternal effect on fetal fluid balance. Amniotic fluid is 98-99% water. The chemical composition of its substances varies with gestational age. When fetal urine begins to enter the amniotic sac, amniotic osmolarity decreases slightly compared with fetal blood. After keratinization of the fetal skin, amniotic fluid osmolarity decreases further with advancing gestational age. The low amniotic fluid osmolarity, which is produced by the inflow of markedly hypotonic fetal urine, provides a large potential osmotic force for the outward flow of water across the intramembranous and transmembranous pathways. Within certain limits, amniotic fluid mirrors the metabolic status of the fetoplacental unit; for that reason, a study of its components and their respective variations in the different weeks of pregnancy provides useful indications, both for a correct assessment of fetal maturation and for an evaluation of kidney function parameters and placental insufficiency.
Amniotic fluid assessment is a tool for the evaluation of fetal well-being. Because of the uterine cavity being irregular direct evaluation is difficult and subsequently, indirect techniques have been utilized. The three ultrasound techniques currently used for the evaluation of amniotic fluid include 1) maximum vertical pocket, 2) subjective assessment, and 3) amniotic fluid index. A review of these techniques show that the amniotic fluid index technique is valid, and the subjective technique and the amniotic fluid index technique appear to have a good inter- and intraobserver variability. All three techniques have been shown to predict peripartum morbidity and mortality when they define decreased amniotic fluid. Amniotic fluid volume is a weak predictor of morbidity and should be used in conjunction with other fetal biophysical variables to predict perinatal outcome.
Amniotic fluid creatinine has been used to evaluate fetal maturity, but there is evidence that maternal diseases may affect amniotic fluid creatinine levels. We report a case of a pregnant woman with renal insufficiency who had markedly elevated amniotic fluid creatinine. Review of data from 9 patients with elevated serum and amniotic fluid creatinine levels showed a statistically significant relationship between maternal serum creatinine and amniotic fluid creatinine. Review of data from 19 patients with amniotic fluid creatinine levels higher than 3 mg/dl showed no relationship between the amniotic fluid creatinine and fetal weight. We conclude that amniotic fluid creatinine in women with elevated serum creatinine is an unreliable predictor of fetal maturity.
OBJECTIVE: To assess the association between cytokines in the amniotic fluid (AF) and preterm delivery, the isolation of bacteria from the AF or chorioamnion, and histologic chorioamnionitis. METHODS: Fifty afebrile women with intact membranes in preterm labor at or before 34 weeks' gestation underwent amniocentesis. Cytokine levels were measured in AF, and cultures were performed. Placentas were cultured and examined histologically. RESULTS: Thirty-two (64%) of the 50 patients delivered at or before 34 weeks' gestation. Delivery at or before 34 weeks, compared with delivery after 34 weeks, was related to increased levels of interleukin-6 (IL-6) (88 versus 12%; P < .001), interleukin-1 (IL-1) alpha (50 versus 6%; P = .004), IL-1 beta (42 versus 0%; P = .002), and prostaglandin (PG) E2 (66 versus 22%; P = .008). Bacteria were recovered from the AF of nine (18%) of the 50 patients. All of the cytokines with increased levels, plus tumor necrosis factor (TNF)-alpha, were related to bacteria in the AF. Increased IL-6, IL-1 alpha, IL-1 beta, TNF-alpha, and PGE2 were also associated with histologic chorioamnionitis among women who delivered within 1 week of amniocentesis. Elevated cytokine levels were not related to chorioamnion infection. CONCLUSIONS: Elevated AF cytokines and PGE2 predicted delivery before 34 weeks' gestation and delivery within 7 days of the amniocentesis, as well as AF infection and histologic chorioamnionitis. These findings support the hypothesis that infection is one cause of preterm delivery, operating via a mechanism involving induction of cytokine production.
Clara cell protein (CC16) is an endogenous anti-inflammatory agent. It is produced mainly in the respiratory and urogenital tracts. CC16 has been quantified in serum, but not in cerebrospinal fluid (CSF). The aim of this study was to examine CSF CC16 in relation to age, gender and serum CC16, and to examine CC16 levels in parturients. If CC16 levels are increased with age and during pregnancy, it may be responsible for the attenuation of inflammatory diseases such as multiple sclerosis during these conditions. CC16 was measured in CSF and serum taken just before Caesarean section (n=33) or just before an elective surgical procedure in females (n=52) or males (n=31). Fetal serum, amniotic fluid, and maternal urine were also sampled during Caesarean section. CC16 levels in CSF did not differ between parturients and an age and gender matched non-pregnant group, but was higher in male than in female patients. There was a significant and positive relationship between age and CSF CC16 levels and between serum and CSF CC16 levels. Fetal CC16 was significantly and positively correlated with amniotic fluid CC16. The present study suggests that CC16 found in CSF originates from passive diffusion from blood, and that CC16 found in amniotic fluid is derived from the fetal lung. During pregnancy, CC16 does not appear to contribute to alterations which occur in the progression of inflammatory disorders.
Amniotic fluid embolism is an important complication of pregnancy with high mortality. The diagnosis of amniotic fluid embolism is generally made postmortem and rests upon the histological demonstration of amniotic fluid debris, including foetal epithelial squames and hair, in the pulmonary vasculature. We have made the diagnosis of amniotic fluid embolism in two patients by detection of the amniotic fluid debris in the blood vessels of the cervix in their hysterectomy specimens. These two patients presented with profuse primary postpartum haemorrhage and evidence of disseminated intravascular coagulation after uneventful deliveries. Amniotic fluid debris were only demonstrated in the blood vessels of the cervix but not in the corpus. This observation emphasizes the importance of a thorough histological examination of the cervix in cases of suspected amniotic fluid embolism.
Human amniotic fluid inhibits the contraction of fibroblast-populated collagen lattices. Amniotic fluid of 21 weeks' gestation was previously reported to have peak inhibiting activity. An attempt to isolate the inhibitory factor(s) from human amniotic fluid employing a molecular sieving column demonstrated an inhibitory factor near 70,000 molecular weight (repeated three times with triplicate samples). Since albumin has a molecular weight of 68,000 and is in high concentration in amniotic fluid, the removal of albumin by an Affi-Gel Blue (an albumin binding affinity column) was the first step in the purification scheme. The bound human amniotic fluid albumin fraction was eluted from the Affi-Gel Blue column, and the unexpected finding was that this fraction inhibited fibroblast-populated collagen lattice contraction (three repetitions in duplicate). We previously showed that prostaglandins and saturated and unsaturated fatty acids affect fibroblast-populated collagen lattice contraction, and albumin is a carrier for lipids. The eluted albumin fraction was separated into its protein and lipid components. The lipid-free albumin fraction had no fibroblast-populated collagen lattice contraction inhibiting activity (run four times in duplicate). The isolated lipid fraction inhibited fibroblast-populated collagen lattice contraction in a dose-responsive manner (repeated twice in triplicate). It was demonstrated that lipid bound to albumin isolated from human amniotic fluid inhibited fibroblast-populated collagen lattice contraction.