Placental protein 21. Localization in human placenta and concentrations in the body fluids of men and nonpregnant and pregnant women

The immunohistochemical localization of placental protein 21 (PP21) was marked in the syncytial brush border and basal membrane during the 1st and 2nd trimesters of pregnancy and also in the chorionic epithelial brush border and basement membrane at term. A weaker stain was found in the cell membranes of amniotic epithelial and chorionic trophoblast cells. Neither heparin nor changes in temperature significantly influenced PP21 concentration. Relatively high serum PP21 concentrations were measured during the follicular and luteal phases in healthy nonpregnant women and in healthy men whose seminal plasma also showed a high PP21 concentration. Serum PP21 levels in normal pregnancy rose from a median of 29.1 ng/ml at 6-7 weeks of gestation to 82.0 ng/ml at 36-37 weeks of gestation. Although maternal urine showed low PP21 levels during pregnancy, amniotic fluid PP21 levels were higher at 7-21 weeks of gestation than at term. Cord blood sera showed almost the same PP21 concentration as maternal sera, but retroplacental blood showed much higher levels. Maternal serum PP21 levels in hydatidiform mole patients did not differ from the normal pregnancy range, although their molar vesicular fluids contained higher PP21 concentrations. These results suggest an extraplacental source for PP21.     

Increased maternal serum 3 alpha, 17 beta-androstanediol glucuronide concentrations during pregnancy

Maternal serum concentrations of 3 alpha, 17 beta-androstanediol glucuronide (3 alpha-diol-G), a substance that reflects peripheral androgen action and tissue 5 alpha-reductase activity, were measured in 33 normal men, 51 nonpregnant women, and 51 women with uncomplicated pregnancies. The 3 alpha-diol-G concentrations in men (median, 201 ng/ml) were significantly higher than in nonpregnant women (median, 42 ng/ml) or pregnant women (median, 124 ng/ml). The concentrations in pregnant women were significantly greater than those in nonpregnant women, and there were no significant differences between trimesters in maternal 3 alpha-diol-G concentrations. There were no fetal sex differences found in maternal serum or in third-trimester amniotic fluid. These results indicate that pregnancy is associated with increased androgen production by maternal tissues and that fetal 3 alpha-diol-G production is low.     

Concentration of placental protein 19 in body fluid and placental tissues

Summary Placental protein 19 (PP19) is one of the new placental tissue proteins identified in extracts from human term placenta by Bohn and Winkler [1]. We measured the PP19 concentration in body fluids and placental tissue by radioimmunoassay; the minimum detectable dose of standard was 1.5 ng/ml. Although ethylene diamine tetraacetic acid (EDTA-2K) inhibited the immunoreaction between PP19 (225/242) and anti-PP19 antibody (632 ZA), the PP19 concentration did not differ between serum and heparin and sodium citrate plasmas. The serum PP19 concentration was increased by hemolysis. In blood cell fractions separated by the Ficoll-Paque/Macrodex method, polymorphonuclear leukocyte fraction contained the highest PP19 concentration. The circulating serum PP19 concentration was 4.5±1.1 ng/ml (mean ± standard deviation) in the proliferative phase (n=8) and 5.1±1.6 ng/ml in the secretory phase (n=7) for nonpregnant women, and 4.6±2.2 ng/ml from men (n=12). Seminal plasma (n=8) contained 212.2±99.7 ng/ml. The maternal serum PP19 concentration in 291 normal pregnancies increased from 6.2 ng/ml (median) at 6–7 weeks of gestation to 34.1 ng/ml at 38–39 weeks. The mean PP19 concentration was higher in amniotic fluid and retroplacental blood, but lower in umbilical cord blood than that in circulating maternal serum. In hydatidiform mole, vesicular fluid contained high PP19 concentration (1154.6±659.5 ng/ml), although these maternal serum concentration was not statistically higher than normal range. The chorionic villous trophoblast contained more PP19 than decidua, chorion, and amnion. These results suggest that PP19 has an extraplacental source, even though the chorionic villous trophoblast may be the main source throughout pregnancy.     

Lead and cadmium concentrations in maternal and umbilical cord blood, amniotic fluid, placenta, and amniotic membranes

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.     

Labetalol pharmacokinetics in pregnancy-induced hypertension

Pharmacokinetic parameters of oral labetalol were studied in eight women with pregnancy-induced hypertension in the third trimester of pregnancy. Labetalol exhibited rapid absorption; peak serum concentrations of 881 +/- 219 ng/ml occurred at 20 minutes after labetalol ingestion. The terminal elimination half-life (mean, 1.7 +/- 0.27 hours) was found to be shorter than that reported for normotensive volunteers or nonpregnant hypertensive patients (mean, 6 to 8 hours). A mean apparent oral elimination clearance of 21.8 ml/min/kg compared favorably with that seen in other pregnant and nonpregnant populations. Food delayed the time to peak serum concentration to approximately 60 minutes. Labetalol was detected in fetal cord samples and amniotic fluid samples at concentrations approximately 50% and 16% that of simultaneous maternal vein samples, respectively.     

基质金属蛋白酶9及其组织抑制物1的水平变化与胎膜早破发病的关系

目的探讨母血、羊水、脐血中基质金属蛋白酶9(MMP-9)及金属蛋白酶组织抑制物1(TIMP-1)的水平变化与胎膜早破发病的关系。方法采用双抗体夹心酶联免疫吸附法,动态检测58例胎膜早破患者(胎膜早破组)及38例正常孕妇(对照组)的母血、羊水、脐血中MMP-9及TIMP-1的水平,同时进行胎膜组织的病理检查,对合并绒毛膜羊膜炎的患者也进行相应的MMP-9及TIMP-1的水平检测。结果(1)胎膜早破组母血、脐血及羊水中MMP-9水平分别为(141·9±84·6)、(138·2±81·4)及(85·6±27·5)ng/L,其水平均明显高于对照组,两组比较,差异有统计学意义(P<0·05、P<0·05及P<0·01);胎膜早破组母血、羊水、脐血中TIMP-1水平分别为(378·1±220·2)、(44·6±24·0)及(257·2±98·8)ng/L,其水平均明显低于对照组,两组比较,差异有统计学意义(P<0·05、P<0·05及P<0·01)。(2)母血、羊水、脐血中MMP-9的水平随破膜时间的延长而升高,尤其破膜时间超过24h时升高更为明显;而TIMP-1则随破膜时间的延长而下降,尤其破膜时间超过24h时降低更为明显。(3)两组共合并绒毛膜羊膜炎患者15例,其中胎膜早破组13例(13/58,22%),绒毛膜羊膜炎患者的母血、脐血、羊水中MMP-9水平分别为(183·8±84·7)、(171·2±92·9)及(95·5±21·1)ng/L,其水平均明显高于非绒毛膜羊膜炎患者(81例),两者比较,差异有统计学意义(P<0·05、P<0·05及P<0·01)。绒毛膜羊膜炎患者的母血、羊水、脐血中TIMP-1水平分别为(269·7±144·4)、(32·1±16·6)及(210·6±81·9)ng/L,其水平均明显低于非绒毛膜羊膜炎患者,两者比较,差异有统计学意义(P<0·05、P<0·05及P<0·01)。(4)胎膜早破组的新生儿Apgar评分≤7分者,其母血、脐血、羊水中MMP-9水平分别为(234·4±79·4)、(222·1±120·1)及(108·5±42·2)ng/L,其水平均明显高于Apgar评分≥8分者,两者比较,差异有统计学意义(P<0·05、P<0·05及P<0·01);与之相反,胎膜早破组的新生儿Apgar评分≤7分者,母血、羊水、脐血中TIMP-1的水平分别为(225·3±121·7)、(25·2±15·8)及(181·7±135·2)ng/L,其水平均明显低于Apgar评分≥8分者,两者比较,差异有统计学意义(P<0·05、P<0·05及P<0·01)。结论MMP-9水平的异常升高及TIMP-1水平的显著下降,是胎膜早破发病的重要机制。MMP-9及TIMP-1的水平检测可作为一种新的生物学标志物用于胎膜早破并绒毛膜羊膜炎感染的诊断,尤其适用于亚临床感染状态的早期诊断,并有助于评估新生儿预后。     

Distribution of placental protein 14 in tissues and body fluids during pregnancy

Placental protein 14 (PP14) levels were measured in serum samples from non-pregnant and pregnant women, amniotic fluid, cord blood, and extracts of placenta, decidua and fetal membranes. The levels were low (15-40 micrograms/l) in serum of non-pregnant women. In four pregnancies following in-vitro fertilization, the serum PP14 levels started to rise 2-12 days after embryo replacement. In normal pregnancy, the highest serum PP14 concentrations (up to 2200 micrograms/l) were detected between 6 and 12 weeks. After 16 weeks the level decreased and plateaued at 24 weeks to around 200 micrograms/l. In amniotic fluid, the highest PP14 levels (232 mg/l) were found between 12 and 20 weeks, being considerably higher than those in maternal serum throughout pregnancy. In cord blood, the levels were low (15-22 micrograms/l) or undetectable. In early pregnancy decidua, the PP14 content was higher (41-160 mg/g total protein) than in late pregnancy decidua (60-2700 micrograms/g total protein). In amnion and chorion laeve, the PP14 concentration varied from 50 to 750 and 50 to 1000 micrograms/g protein, respectively. Early pregnancy placenta contained 0.25-15 mg/g and late pregnancy placenta 3-430 micrograms/g protein of PP14. These results show that the levels of PP14 in pregnancy serum have a similar profile to hCG, but in contrast to other placental proteins, the amniotic fluid PP14 levels are remarkably high. This may be explained by suggesting that decidua is a source of PP14.     

Distribution of placental protein 14 in tissues and body fluids during pregnancy

Summary. Placental protein 14 (PP14) levels were measured in serum samples from non-pregnant and pregnant women. amniotic fluid, cord blood, and extracts of placenta, decidua and fetal membranes. The levels were low (15–40 μg/ l ) in serum of non-pregnant women. In four pregnancies following in-vitro fertilization, the serum PP14 levels started to rise 2–12 days after embryo replacement. In normal pregnancy, the highest serum PP14 concentrations (up to 2200 μg/l) were detected between 6 and 12 weeks. After 16 weeks the level decreased and plateaued at 24 weeks to around 200 μg/l. In amniotic fluid, the highest PP14 levels (232 mg/l) were found between 12 and 20 weeks, being considerably higher than those in maternal serum throughout pregnancy. In cord blood, the levels were low (15–22 μg/l) or undetectable. In early pregnancy decidua. the PP14 content was higher (41–160 mg/g total protein) than in late pregnancy decidua (60–2700 μg/g total protein). In amnion and chorion laeve, the PP14 concentration varied from 50 to 750 and 50 to 1000 μg/g protein, respectively. Early pregnancy placenta contained 0-25-15 mg/g and late pregnancy placenta 3–430 μg/g protein of PP14. These results show that the levels of PP14 in pregnancy serum have a similar profile to hCG, but in contrast to other placental proteins, the amniotic fluid PP14 levels are remarkably high. This may be explained by suggesting that decidua is a source of PP14.     

Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy

This study was performed to establish the dynamics of human chorionic gonadotropin, prolactin, and growth hormone throughout pregnancy in serum and amniotic fluid. Two hundred fifty healthy women at 8 to 42 weeks' gestation were studied. The highest serum human chorionic gonadotropin level was measured between weeks 8 to 12 (53,715 +/- 3574 mIU/ml, mean +/- SEM), with a decline to a mean plateau of 11,806 +/- 1250 mIU/ml from week 18. Amniotic fluid human chorionic gonadotropin had a similar pattern with a mean of 68,100 +/- 8422 mIU/ml at weeks 8 to 10, declining from week 18 to a plateau of 2005 +/- 260 mIU/ml. Human chorionic gonadotropin showed a significant correlation (r = 0.85, p less than 0.001) between levels of both compartments demonstrating an even distribution. Prolactin levels showed a dichotomy of patterns and levels. Serum prolactin showed a continuous rise from 45.3 +/- 14 ng/ml at week 8 to 224 +/- 20 ng/ml at week 36. In contrast, amniotic fluid prolactin remained low until week 14 (33.1 +/- 0.8 ng/ml), followed by a sharp and significant (p less than 0.001) increase to a plateau of 3750 +/- 200 ng/ml between weeks 18 to 26, declining to a second plateau of 500 +/- 50 ng/ml at week 36. Serum growth hormone increased from a mean of 3.5 +/- 1.4 ng/ml seen at weeks 8 to 10 to a mean of 14 +/- 2.0 ng/ml at weeks 28 to 30, followed by a plateau of similar levels. The pattern of growth hormone secretion in amniotic fluid demonstrated a sharp increase during the 14-16 interval with a maximum mean level of 15.5 +/- 1.5 ng/ml and a slow steady decline thereafter. In conclusion, the similar pattern and concentration of human chorionic gonadotropin throughout pregnancy in both maternal and amniotic fluid are probably the result of direct human chorionic gonadotropin diffusion from the placenta. The dissimilar pattern and concentration of prolactin are the result of two different sources of prolactin secretion during pregnancy. Serum prolactin originates from the pituitary and amniotic fluid prolactin from the decidua. Since the pattern of growth hormone secretion resembles that of prolactin, it is possible that growth hormone, like prolactin, is secreted by the same sources.     

Accumulation of colony-stimulating factor 1 in amniotic fluid during human pregnancy

Colony-stimulating factor 1 is a hematopoietic growth factor that increases 1000-fold in the uteri of pregnant mice, and its receptor is abundantly expressed in the human placenta. The concentration of colony-stimulating factor 1 in amniotic fluid at 33 to 40 weeks (9.0 +/- 1.1 ng/ml) was twofold higher than that at 16 to 18 weeks gestation (4.1 +/- 0.5 ng/ml), whereas maternal serum colony-stimulating factor 1 levels did not rise significantly. Colony-stimulating factor 1 was detected in endometrial extracts from pregnant women and levels were higher than those in extracts from nonpregnant women.     

Concentrations of growth hormone, prolactin and thyroid-stimulating hormone in the maternal, fetal and amniotic compartments

GH, PRL and TSH in the maternal, fetal and amniotic compartments were measured by radioimmunoassay in normal pregnant women (group I, n = 16) and patients with anencephalic fetuses (group II, n = 10). The concentrations of GH (20.6 +/- 8.5 ng/ml, mean +/- SD) in cord blood of normal fetuses were significantly higher (p less than 0.001) than those (5.1 +/- 3.5 ng/ml) in anencephalic fetuses. Both maternal PRL levels in group I and group II were lower than their respective cord bloods. The concentrations of PRL (283.1 +/- 127.5 ng/ml) in normal fetuses were higher, but not significantly, than those (199.4 +/- 111.8 ng/ml) in anencephalic fetuses. Also, compared with PRL levels in the maternal and cord blood, those in amniotic fluid were significantly higher (p less than 0.001) in both groups. On the contrary, GH and TSH levels in amniotic fluid were much lower than those in the maternal and fetal blood. The concentration of TSH (10.2 +/- 4.6 microU/ml) in normal fetuses was significantly higher (p less than 0.05) than those (7.1 +/- 3.1 microU/ml) in maternal blood, but not significantly different from those (11.3 +/- 3.6 microU/ml) in anencephalic fetuses. These results suggest that GH, PRL and TSH do not cross human placenta and biosyntheses of these hormones in the maternal and fetal pituitaries are independent.     

Prolactin in normal pregnancy: relationship of maternal, fetal, and amniotic fluid levels.

Serum prolactin was measured simultaneously by a homologous radioimmunoassay in 92 parturients and their offspring at term, and in maternal serum and amniotic fluid during various stages of normal pregnancy. Serum levels of 208 +/- 8 ng. per millilter were found in maternal blood; the corresponding levels in the cord serum were 354 +/- 14 ng. per milliliter. Prolactin levels in amniotic fluid were found to be 2- to 10-fold higher than the corresponding levels of the mothers. The possible source of the amniotic fluid prolactin molecule, which is identical with the human pituitary molecule, is discussed.     

Elevated amniotic fluid leptin levels in pregnant women who are destined to develop preeclampsia

OBJECTIVE: To analyze whether leptin levels of the amniotic fluid elevate during early pregnancy in women destined to develop preeclampsia and to evaluate the relationship between amniotic fluid leptin levels and gestational age, maternal body mass index, and fetal sex. STUDY DESIGN: Leptin levels of the amniotic fluid were compared in two groups of women, preeclamptic (n = 20) and normotensive pregnant (n = 40), matched for fetal sex, maternal body mass index at sampling, gravidity and fetal gestational age at sampling. Furthermore, amniotic leptin levels in 400 normotensive pregnant women were analyzed for their correlation with gestational age, maternal body mass index, and fetal sex. RESULTS: Median leptin concentrations were significantly higher (p < 0.001) in the women with preeclampsia (7.3+/-0.7 ng/ml) than in the normotensive pregnant women (4.1 +/- 0.3 ng/ml), independent of fetal sex. The leptin levels in the amniotic fluid decreased with advanced gestational age (r = 0.24, p < 0.001). Amniotic fluid leptin levels in the pregnant women carrying a female fetus (5.6+/-0.3ng/ml) were significantly higher than those carrying a male fetus (4.7+/-0.2 ng/ml) (p = 0.004). CONCLUSION: Higher amniotic fluid leptin levels were observed in the preeclamptic pregnant women, and they decreased as gestational age advanced. Furthermore, the women with a female fetus were noted to have higher amniotic fluid leptin levels.     

Alphafetoprotein by Radioimmunoassay in Maternal Serum and Amniotic Fluid

Summary: The use of a competitive inhibition radioimmunoassay allows the measurement of alphafetoprotein (AFP), a specific a-globulin produced by fetal and malignant liver cells, in serum and amniotic fluid at low concentrations of ng/ml. In normal pregnancy, mean AFP levels in maternal serum showed a slow rise, from undetectable levels (less than 20 ng/ml) before 12 weeks of gestation, to a maximum at 30 weeks. After that, there was a comparable decline in levels for the remainder of pregnancy, up to 42 weeks. From 14 weeks there was a wide variation in individual AFP values at all stages of gestation, but most of them fell within 2 standard deviations above the mean.
A correlation was found between AFP levels in samples of maternal serum and amniotic fluid taken simultaneously, with levels in amniotic fluid reading at least 50% higher. AFP levels in amniotic fluid in late pregnancy corresponded to the lecithin/sphingomyelin ratio in an inverse relationship.     

Creatinine, urea and uric acid in amniotic fluid, maternal and umbilical cord blood at delivery.

Amniotic fluid, maternal vein serum and umbilical cord serum were obtained almost simultaneously from 31 women after an uneventful course of pregnancy. Specimens of amniotic fluid contaminated by blood or meconium were excluded. Creatinine, urea and uric acid were measured by autoanalyser techniques. The concentrations of creatinine, urea and uric acid in amniotic fluid were significantly higher when compared with the levels in maternal vein serum or umbilical cord serum. Between maternal and umbilical cord serum there were only small or no differences. The linear correlations of creatinine, urea and uric acid between maternal and umbilical cord serum were greater than those between amniotic fluid and maternal serum of amniotic fluid and cord serum. It is suggested that the high levels of creatinine, urea and uric acid in amniotic fluid are primarily determined by fetal urine.     

Prolactin and amniotic fluid electrolytes.

Prolactin (PRL) levels and Na+, K+, Cl-, Ca++ concentrations in maternal serum and amniotic fluid from 64 women in normal term pregnancy were measured by immunoenzymetric assay and flame photometry. The mean amniotic fluid PRL concentration was 597.7 (SE 31.5) ng/ml and the mean amniotic fluid Na+, K+, Cl- and Ca++ levels were 125.6 (SE 0.9) mmol/l, 4.5 (SE 0.1) mmol/l, 109.3 (SE 1.3) mmol/l and 2.0 (SE 7.5 E-02) mmol/l, respectively. There was no correlation between PRL levels in maternal serum and amniotic fluid, and the electrolyte concentrations in amniotic fluid. A close correlation was found between the concentrations of Na+ and Cl- in maternal serum and amniotic fluid. Thus, even though PRL may participate in the regulation of electrolytes in the amniotic fluid compartments, our findings provide indirect evidence for the existence of other regulatory mechanisms.     

Concentration of placental protein 10 (PP10) in maternal serum and amniotic fluid throughout normal gestation and in pregnancy complicated by fetal growth retardation

PP10, a new placental glycoprotein, was studied by a specific and sensitive double-antibody radioimmunoassay in maternal serum and other body fluids throughout pregnancy. The mean value of serum PP10 in healthy nonpregnant individuals was approximately 10 microU/l. During normal pregnancy it rose to 3,500 microU/l. The rate of rise was obtained from 78 normal pregnancies with 279 single assay values from weeks 6-40. The shape of the curve resembled that for other placental proteins (HPL, SP1). PP10 levels in amniotic fluid were measured in 145 samples from weeks 13-55 of normal pregnancies and at term. The mean concentration was 500 microU/l until week 18 and then rose slowly. Cord blood contained only trace amounts. PP10 was not found in maternal urine. The concentration in maternal serum and amniotic fluid was higher in twin pregnancies than in singleton pregnancies. In 46 cases with low birth weights the PP10 levels in maternal serum were significantly lower than normal. Simultaneous measurements of PP10 and E3, HPL and SP1 were made in 17 individual follow-up's. PP10 was comparable with E3 and appeared to be better than HPL and SP1 in predicting intrauterine fetal growth retardation.     

HLA-G antigen and parturition: maternal serum, fetal serum and amniotic fluid levels during pregnancy

OBJECTIVE: To determine whether soluble HLA-G1 (sHLA-G1) concentrations in maternal serum and in amniotic fluid are lower at term than in the second trimester. METHODS: In this prospective study amniotic fluid and maternal serum samples were aspirated from 21 pregnant women during genetic amniocentesis at 16-20 weeks' gestation, and from 19 women undergoing a cesarean section at term. In the latter group arterial umbilical cord blood was aspirated as well. sHLA-G1 levels were determined using ELISA assay. This assay included the anti-HLA-G monoclonal antibodies 87G and 16G1, both as capture antibodies and horseradish-peroxidase-labeled rabbit anti-human beta(2)-microglobulin antibodies, as the detection antibody. The relative concentrations of sHLA-G1 were measured from the absorbancy of the blue product at 650 nm. Student's t test was used for statistical analysis. RESULTS: sHLA-G1 levels in amniotic fluid were significantly lower at term than in the second trimester (0.160 +/- 0.05 vs. 0.272 +/- 0.150 OD units; p < 0.05). Levels of sHLA-G1 in maternal serum declined toward term, but the difference from the second trimester was not statistically significant (0.266 +/- 0.157 vs. 0.205 +/- 0.120 OD units; p = 0.193). There was a strong correlation of sHLA-G1 concentrations between cord serum and maternal serum (R(2) = 0.79; p < 0.001), but not between cord serum and amniotic fluid (R(2) = 0.00004) or amniotic fluid and maternal serum (R(2) = 0.02). CONCLUSIONS: sHLA-G1 antigen expression is higher in amniotic fluid than in maternal-fetal compartments and significantly decreases toward term. We speculate that the declining amniotic fluid sHLA-G1 levels may stimulate a maternal immunological response against the fetus and contribute to the initiation of parturition.     

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.     

Distribution of the concentrations of angiotensin II (A II), A II receptors, hPL, prolactin, and steroids in human fetal membranes]

By analyzing human trophoblastic tissues at the full term of pregnancy, this study shows the highest levels of angiotensin-II (729 +/- 111 and 602 +/- 105 pg/g of tissue), angiotensin-II receptors (295 +/- 30 and 250 +/- 32 fmol/mg proteins), human placental lactogen (973 +/- 154 and 680 +/- 28 micrograms/g) and progesterone (1,501 +/- 193 and 1,070 +/- 151 ng/g) in chorionic villi and in placental basal plate respectively. Tissue values of angiotensin-II, hPL and Progesterone were 4 times superior to those obtained in amniotic fluid and in umbilical and maternal blood. Estradiol values in chorionic villi were similar to those in placental basal plate, in chorionic plate and in chorion, but significantly higher (p less than 0,001) than in amnion, amniotic fluid and in umbilical and maternal blood. The concentrations of prolactin in chorion were 3 times superior than those found in amnion, in placental tissue, in amniotic fluid and in umbilical and maternal blood. A positive correlation was observed between Angiotensin-II and its receptors and also with hPL, P4/hPL ratio and E2/P4 ratio. Thus, angiotensin-II could play an important role in the physiology of pregnancy, due to its vasopressive action and due to its interactions with other peptides and chorio-placental steroids.