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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While levels of maternal immunoglobulin G (IgG) increase in the fetal circulation during the third trimester, actual trophoblastic concentrations have not been extensively studied. To investigate this process, placentas from 71 patients with gestational ages between 26 and 42 weeks were examined by means of a peroxidase-antiperoxidase immunostaining technique specific for IgG. Linear regression revealed a significant increase in antibody with advancing gestational age (r = 0.36, p less than 0.01). In addition, placentas from patients in spontaneous term labor revealed a significantly higher antibody level when compared with those of patients at term delivered electively before the onset of labor (mean +/- SEM 2.6 +/- 0.2 vs 1.7 +/- 0.3, p less than 0.02). Patients in premature labor failed to demonstrate this increase in antibody staining. One possible explanation for these findings is an enhanced recognition of the fetal trophoblastic tissue by the maternal immune system at term. It also suggests immunologic factors may play an important role in the initiation of normal labor.
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PMID:Increasing quantity of maternal immunoglobulin G in trophoblastic tissue before the onset of normal labor. 218 45

An improved sensitive assay for collagenase, which uses [3H]telopeptide-free collagen as a substrate, was used to measure changes in serum collagenase levels in 96 women and ten men (18-35 years old). Both latent and active forms of collagenase were detected in serum by molecular sieve chromatography; these forms had a relative molecular weight (Mr) of 65,000 and 45,000, respectively. Only latent collagenase was detected in crude serum after destroying inhibitors by treatment with 3 M potassium thiocyanate. Collagenase levels in males were lower than in nongravid females (34 +/- 5 versus 53 +/- 5 U/dL; mean +/- SEM; 1 unit = 1 microgram collagen digested per minute at 30C). During pregnancy there was no significant change in serum collagenase levels until the onset of spontaneous labor in full-term pregnancies (37-42 weeks), at which point there was a 66% increase over the nongravid level to a value of 88 +/- 5 U/dL. There was a further rise at one day postpartum, and high levels continued for at least four days. Women in premature labor (24-36 weeks) exhibited an eightfold increase in the level of serum collagenase to 405 +/- 110 U/dL; 16 of 17 patients in this group had collagenase levels above the 95th percentile for women at 16-40 weeks but not in labor. This evaluation of serum collagenase may provide a key for detecting premature labor. It is suggested that the increase in serum collagenase arises from the lower uterine segment and cervix.
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PMID:High levels of serum collagenase in premature labor--a potential biochemical marker. 243 51

Because of the potential of dihydropyridine calcium channel blockers in the management of premature labor, we have studied the direct effects of nitrendipine on actomyosin in the pregnant and nonpregnant uterus and in the term human placenta. Actomyosin adenosinetriphosphatase in the three tissues and another model of actin-myosin interaction, superprecipitation of placental actomyosin, were inhibited by nitrendipine. The inhibition was not diminished by high concentrations of calcium. To identify the mechanism, placental myosin was phosphorylated in the absence and presence of 0.8 X 10(-4) mol/L of nitrendipine. The myosin phosphorylated in the presence of nitrendipine had lower actin-activated adenosinetriphosphatase, which is consistent with the inhibition of myosin light chain phosphorylation. However, nitrendipine did not affect the adenosinetriphosphatase activity of myosin nor did further reduce the adenosinetriphosphatase of the already phosphorylated placental actomyosin. Thus nitrendipine inhibition is directed to the phosphorylation reaction but not to the adenosinetriphosphatase site of myosin. Myometrial relaxation in vivo or in vitro occurs at the pharmacologic nitrendipine levels of 10(-9) to 10(-8) mol/L, which is at least 10,000 times lower than that of the concentration of 50% inhibition of myosin light chain phosphorylation (0.0026 +/- 0.00015 mol/L of nitrendipine, mean +/- SEM) demonstrated in the present work. Because of this difference, the direct intracellular actions of dihydropyridine calcium channel blockers are not expected to cause adverse effects in the uteroplacental system when these drugs are used in the prevention or treatment of premature labor.
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PMID:Pharmacologic levels of nitrendipine do not affect actin-myosin interaction in the human uterus and placenta. 293 50

Indomethacin is a potent agent in the treatment of premature labor, but its use has been limited because of concern about its constrictive effects on the fetal ductus arteriosus. To study these effects we used serial fetal echocardiography in 13 pregnant women in premature labor who received indomethacin according to three different dose schedules, ranging from 100 to 175 mg per day, for a maximum of 72 hours. The gestational ages of the fetuses ranged from 26.5 to 31.0 weeks. The detection of ductal constriction in 7 of the 14 fetuses by echocardiography led to the discontinuation of indomethacin. Three fetuses also had tricuspid regurgitation. There was no statistically significant difference between the mean (+/- SEM) gestational age of the fetuses with ductal constriction and that of those without constriction (29.3 +/- 0.59 and 28.4 +/- 0.52, respectively). There was no relation between serum indomethacin levels in the mothers and ductal constriction. In all seven fetuses affected, ductal constriction had resolved by the time they were restudied 24 hours after the discontinuation of indomethacin. Persistent fetal circulation was not detected in any of the 11 neonates studied after delivery. Indomethacin used to treat premature labor appears to cause transient constriction of the ductus arteriosus in some fetuses, even after short-term use.
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PMID:Indomethacin in the treatment of premature labor. Effects on the fetal ductus arteriosus. 339 94

Plasma CRH was measured in maternal plasma throughout the third trimester of pregnancy, during labor, and postpartum. CRH levels were also measured in arterial and venous umbilical cord plasma samples. In normal pregnant women, plasma CRH increased from 50 +/- 15 (+/- SEM) pg/mL at 28 weeks gestation (n = 41) to 1462 +/- 182 pg/mL at 40 weeks (n = 55) and 1680 +/- 101 pg/mL (n = 65) in labor. Women with pregnancy-induced hypertension (n = 49) had plasma CRH levels significantly elevated above this normal range. Similarly, women who subsequently went into premature labor had raised levels several weeks before the onset of labor. After delivery, plasma CRH returned to normal within 15 h. Total plasma cortisol levels varied little throughout the third trimester, but increased during labor and remained elevated 2-3 days postpartum. There was, therefore, no correlation between plasma cortisol and CRH, implying that this placental CRH is not primarily involved in the control of the maternal hypothalamo-pituitary adrenal axis during pregnancy. The concentrations of CRH in umbilical cord plasma samples were considerably lower than those in the maternal circulation and were close to those in normal nonpregnant adults.
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PMID:Plasma corticotropin-releasing hormone concentrations during pregnancy and parturition. 349 36

The pharmacokinetics in the human of 1-deamino-2-D-Tyr(OEt)-4-Thr-8-Orn-vasotocin (dE-TVT), was studied after iv and intranasal administration in 11 subjects at 12 experiments each route. The plasma concentration of the analogue was analysed by means of an arginine vasopressin antibody, which cross-reacted with dE-TVT to 4.7%. When given intravenously as bolus injection (10 nmol/kg/body weight), the total body clearance amounted to 0.623 +/- 0.099 (SEM) l/h kg and the half-life to 16.2 +/- 2.4 min. After intranasal administration (100 nmol/kg/body weight), the bioavailability was 10.5 +/- 2.9%. Peak concentrations in plasma appeared 2-8 min after iv and 10-45 min after intranasal administration. At the end of an observation period of 2 h measurable amounts in plasma were still found in one of the iv and seven of the intranasal experiments. It is concluded that the moderately long half-life is suitable for the treatment of hospitalized patients in premature labour where promising results with intravenous infusion (50 micrograms/min) of dE-TVT have been obtained. It is still uncertain whether or not the absorption of dE-TVT is sufficient for intranasal administration to out-patients with uterine hyperactivity in late pregnancy and to patients with primary dysmenorrhoea, where significant relief of symptoms were seen after iv administration (10 micrograms/kg body weight).
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PMID:Pharmacokinetics in the human of a new synthetic vasopressin and oxytocin uterine antagonist. 375 61

The mean platelet cyclic AMP (cAMP) value in normal pregnant women between 20 and 37 weeks of gestation was 8.2 +/- 0.4 (SEM) pmol cAMP/10(9) platelets (n = 100). From 35 patients with premature labor, 81 blood samples were obtained from measurement of the platelet cAMP before, during and after treatment with fenoterol/verapamil. During the first 4 days of therapy there was an increase of cAMP (p < 0.005); with long-term therapy the blood platelet cAMP was decreased (p < 0.005). Because platelet aggregation has a negative correlation with platelet cAMP, fenoterol should be used cautiously in patients with defective platelet function, in severe bleeding, and before surgery. With long-term treatment platelet aggregation may be increased and thus contribute to the formation of thrombi. Placental perfusion is not likely to be improved by increased platelet aggregation during long-term treatment with fenoterol.
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PMID:Blood platelet cyclic AMP during long-term treatment of premature labor. 625 51

Plasma cAMP was determined using the method of Tovey et al. in normal pregnant women with a mean concentration of 18.9 +/- 0.8 pmol/ml (x- +/- SEM). Between weeks 9-12 and 33-36 of gestation, there were two peaks, with a mean cAMP of 22.5 +/- 2.4 which were significantly increased in comparison to the other weeks of pregnancy. Significantly decreased values were found in patients with threatened abortion (weeks 12-28) which terminated in abortion (11.6 +/- 2.4; p < 0.01). In premature labor no differences were found. During therapy with fenoterol there were highly significantly increased plasma cAMP levels (48.2 +/- 2.8; p < 0.0005). During thyroid hormone therapy in euthyroid goiter, cAMP was significantly decreased (14.0 +/- 1.4; p < 0.05). 1 week after cessation of therapy a highly significant increase of cAMP was observed (38.2 +/- 6.9; p < 0.0005). There was a negative linear regression between T3 and cAMP (2p < 0.01). In pregnancy with hypertension cAMP was significantly elevated (30.5 +/- 3.8 p < 0.0005), but nearly normal under antihypertensive therapy. In pregnancy with edema only, no difference was found. Induction of labor with PGE2 alpha was followed by a decrease of plasma cAMP.
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PMID:Plasma cAMP in normal and abnormal human pregnancy. 625 65

We determined whether ACTH1-24, infused into fetal lambs at a rate that is known to cause premature labor, elicits changes in the responsiveness of the fetal adrenal glands, and alters the pattern of corticosteroid output. Plasma cortisol (F), corticosterone (B) and progesterone (P4) were measured during 72 h of infusion of saline or ACTH (10 micrograms/h) beginning on Day 127 of pregnancy. Adrenals were then dispersed into isolated cells, and the output of F, B and P4 after exogenous ACTH determined in vitro. Plasma concentrations of F and B were higher in ACTH-treated fetuses. The increment in F (5-to 7-fold) was greater than that in B (2-fold) such that the F:B ratio in plasma of ACTH-treated fetuses on Days 2 and 3 of infusion was 2.5 times higher than in controls. After 72 h of infusion, the adrenal weights in ACTH-treated fetuses (741 +/- 38 mg, +/- SEM; n = 4) were greater than in the control animals (349 +/- 11 mg). There was a significant effect of ACTH pretreatment in vivo on F output by isolated adrenal cells in vitro. Mean increments in F output after addition of ACTH1-24 (5000 pg/ml) in vitro rose from 368 +/- 235 pg/50,000 cells in controls, to 64,639 +/- 19,875 pg/50,000 cells after ACTH in vivo. There was no significant effect of ACTH in vivo on B output in vitro; the ratio of F:B output, either in the absence or presence of ACTH in vitro, was significantly higher in cells from ACTH-pretreated fetuses. There was a significant effect of in vivo ACTH on in vitro P4 output. After ACTH treatment in vivo there was an increase in the vitro output ratio of F:P4, but no change in the output ratio of B:P4. We conclude that ACTH treatment of the fetal lamb in vivo results in activation of fetal adrenal function, increased fetal adrenal responsiveness to ACTH, and directed corticosteroid biosynthesis towards cortisol. Our results are consistent with an increase in fetal adrenal 17 alpha-hydroxylase activity after ACTH treatment.
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PMID:Activation of adrenal function in fetal sheep by the infusion of adrenocorticotropin to the fetus in utero. 629 26

The use of beta-mimetic tocolytics has been associated with various metabolic derangements which have been the topic of investigational reports. Lactic acidosis has been reported to follow concomitant steroid administration. The purpose of this investigation was to delineate more clearly hyperlactacidemia in patients receiving various tocolytics with and without concomitant use of steroids in a prospective manner. Twenty patients in premature labor who received ritodrine had markedly increased blood levels of lactate (baseline, 1.0 +/- 0.1 mmol/L [SEM] versus 3.5 +/- 0.3 mmol/L [SEM] after 6 hours' intravenous infusion). In the other treatment groups, ritodrine plus hydrocortisone, hydrocortisone alone, and magnesium sulfate alone, lactate levels failed to change significantly. Clinical relevance and implications for metabolic alterations associated with beta-mimetic tocolysis are discussed.
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PMID:Hyperlactacidemia associated with acute ritodrine infusion. 684 9


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