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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chief obstetrical problems encountered today in the prenatal evaluation of the high-risk fetus are presented. Advantages and pitfalls or recent techniques utilized in the management of the high-risk pregnancy are discussed. They include: a prenatal scoring system for identifying the high-risk population; examination of the karyotype of cells in amniotic fluid, and quantitation of alpha-fetoprotein levels in maternal plasma and amniotic fluid for the early prenatal detection of birth defects; ultrasonography for the intrauterine diagnosis of fetal growth retardation and assessment of fetal maturity; the use of maternal urinary estriol excretion, maternal plasma human placental lactogen levels and the oxytocin stress test for the early detection of fetal distress; estimation of fetal maturity by amniotic fluid analysis of lecithin or lecithin-sphingomyelin ratios, creatinine and Blue Nile fetal cell staining. Newer, still experimental, techniques (e.g., fatal breathing movements, fetoscopy, and dehydroepiandrosterone plasma clearance) are viewed in light of further possible decreases in maternal and perinatal mortality.
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PMID:Antepartum evaluation of the high-risk fetus: problems and prospects. 7 Dec 31

Placental steroid sulfatase deficiency is an unusual cause of low estriol production during pregnancy. Its importance lies in the differentiation of this disorder from the more ominous fetal defects that result in low estriol levels. Serum free estriol levels were found to be low or absent in a 25-year-old gravida 3, para 2 woman, while placental lactogen and chorionic gonadotropin levels were normal. An abdominal x-ray revealed no apparent congenital abnormalities and an oxytocin challenge test was negative. The dehydroepiandrosterone sulfate (DHEA-S) level in the patient's amniotic fluid was 6.8 to 18.4 times greater than those found in control amniotic fluids. The patient's amniotic fluid cortisol level was normal. Twenty-four hours following a normal, spontaneous labor and delivery at 39 weeks, the male infant underwent a synthetic ACTH1-24 stimulation test, with serum cortisols rising from 3.7 to 46 mug/dl at 1 hour. The placenta was morphologically normal on gross, light, and electron microscopic examinations. Steroid 3-alcohol sulfatase and arylsulfatase activities in the patient's placenta were virtually absent. These data indicate that this benign cause of low serum estriol levels may be diagnosed prenatally by elevated amniotic fluid DHEA-S levels.
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PMID:Prenatal diagnosis of placental steroid sulfatase deficiency. 13

Lactation is controlled by hormones from several endocrine glands. An undisturbed function of the anterior pituitary, of the adrenals, and of the ovaries is a prerequisite for a normal morphogenesis of the mammary gland. The epithelial ducts proliferative under the combined influence of estrogens, glucocorticoids and growth hormone, whereas the lobuloalveolar development depends on progesterone and prolactin in addition to the fore-mentioned hormones. During pregnancy pituitary prolactin may be substituted by placental lactogen. Milk synthesis begins in the second half of pregnancy. It is supported by prolactin and cortisol, which directly act on enzyme activities and processes of differentiation of the alveolar cells. The sudden surge in the secretion of milk after parturition is most likely due to the rapid decline of the serum levels of progesterone. The ejection of milk from the lactating mammary gland is controlled by a neuroendocrine reflex mechanism. Suckling is the appropriate stimulus for the release of oxytocin from the posterior pituitary. Oxytocin increases intramammary pressure by inducing contraction of the myoepithelial cells and thus aids in expelling the milk from the mammary glands. Maintenance of normal postpartum lactation depends on frequent and intensive suckling. Suckling does not only stimulate the release of oxytocin, but also provokes secretion of prolactin and ACTH. This increase in prolactin caused by suckling guarantees galactopoesis. Influencing secretion of prolactin has been proven to be a useful tool for regulating lactation. The experimental ergot derivative 2-Brom-alpha-ergocryptine is a potent suppressor of prolactin secretion from the anterior pituitary. In contrast to estrogens, alone or in combination with progestagens or androgens, this drug is not only effective in suppressing the onset of lactation, but also in inhibiting lactation once milk secretion had started. As to stimulating lactation in the human there is no effective drug available up to now.
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PMID:[Hormonal regulation of lactation (author's transl)]. 18 42

Serial blood samples were collected from ten patients at between 40 and 42 weeks gestation, who were having labour induced by amniotomy and intravenous oxytocin. The plasma levels of human placental lactogen and pregnancy-specific beta 1 glycoprotein showed no more than their normal late pregnancy variability during labour; oestradiol-17 beta showed a small rise in early labour followed by a fall in the second stage of labour; unconjugated oestriol and 11-hydroxycorticosteroids showed a progressive rise throughout labour and progesterone a progressive fall. The ratio of progesterone to oestradiol-17 beta fell throughout labour. The significance of these changes in our understanding of the control of placental hormone secretion and of the hormone profile of spontaneous labour is discussed.
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PMID:Maternal hormone profile in oxytocin induced labour. 31 90

By using a specific heterologous double-antibody RIA, changes in the blood levels of PRL during pregnancy, pseudopregnancy, and lactation have been investigated for the first time in the rabbit. Blood levels fluctuate during early and midpregnancy in a manner similar to that in pseudopregnancy. Levels decline in the third trimester of pregnancy and increase dramatically (3- to 25-fold) at or 1--2 days before delivery. Pituitary levels of PRL showed no significant alteration, and fetal serum and amniotic fluid levels of PRL remain low (less than 10 ng/ml) throughout pregnancy. No significant PRL-like, GH-like, or placental lactogen-like activity could be demonstrated either in serum or in extracts of placenta (n = 262) taken between days 10 and 31 of pregnancy. Postpartum blood levels of PRL were similar in lactating and postpartum nonlactating females. In lactating females, suckling evoked an immediate increase (15- to 25-fold) in circulating PRL levels. Handling the female or the iv injection of oxytocin during lactation did not cause PRL release. In contrast, manual test stimulation caused an immediate increase in blood levels of PRL and a response pattern very similar to that of natural suckling. These results suggest that PRL release during suckling occurs solely in response to the tactile stimulation of the teats.
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PMID:Prolactin during pregnancy and lactation in the rabbit. 57 Apr 85

In order to estimate the human placental lactogen (HPL) level and its value as an indicator of fetoplacental function during labor, we determined HPL levels (N equals 225) before, during, and after labor in normal (N equals 16) and preeclamptic (N equals 14) subjects or in patients with benign intrahepatic cholestasis of pregnancy (N equals 5). During labor, greater decreases in this value were found in preeclamptic than in normal subjects and similarly in mothers with fetoplacental dysfunction than with normal fetoplacental function. The rupture of the membranes had no effect on the level of HPL, which was not related to parity, oxytocin infusion, time interval from rupture of the membranes to delivery, nor to relative placental weight. The half-life of HPL varied in the range of 20-23 minutes immediately after delivery and in the range of 30-39 minutes some time later. During labor, greater decreases in HPL level in cases of preeclampsia or fetoplacental dysfunction may be caused by relative uteroplacental ischemia during uterine contractions, but from this finding it is hard to expect any advantage of HPL as a monitor of fetoplacental function during labor.
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PMID:Human placental lactogen levels during and after labor. 115 51

This article reviews the current state of our knowledge about the hormonal basis of maternal behavior in the rat. Considered are the ovarian hormones estrogen and progesterone, the pituitary hormones beta-endorphin and prolactin, and the hormone oxytocin, secreted by several hypothalamic nuclei and associated brain regions. The hormones of pregnancy, estrogen and progesterone, prime the female to respond to a terminal rise in estrogen that stimulates a high level of maternal responsiveness even before parturition begins. Studies on the role of prolactin, using hypophysectomy, prolactin release blockers and anterior pituitary and prolactin replacement, indicate that prolactin is required for the ovarian hormones to be effective in stimulating maternal behavior. During the latter half of pregnancy, placental lactogen may displace prolactin in this role. Although prolactin serves as a chronic stimulus for maternal behavior, it also may act over a short period. Oxytocin stimulates maternal behavior in a specific strain of rat, but not in other strains, and only when administered introcerebroventricularly (ICV) in estrogen-primed females. The decline in the high brain levels of beta-endorphin around parturition has been proposed as a requirement for the onset of maternal behavior; morphine blocks the onset of maternal behavior and disrupts ongoing maternal behavior and maternal aggression in lactating females. However, blocking beta-endorphin action at parturition interferes with pup cleaning and eating of the placenta as well.
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PMID:Hormonal basis during pregnancy for the onset of maternal behavior in the rat. 296 17

To detect antigens in the plasma of pregnant women that were not found in nonpregnant untreated normal women or males, highly sensitive immunodiffusion techniques with hyperimmune rabbit antiserum were used. The number of pregnancy-associated plasma constituents increased as pregnancy progressed in the 165 patients studied, with all 4 constituents usually seen in the third trimester. The 60 males and 111 nonpregnant women studied did not show any of these antigens. There were significant differences between second and third trimester reactions. (p less than .001). None of the antigens represented human chorionic gonadotropin, human placental lactogen, oxytocin, C-reactive protein, oxytocinase, alkaline phosphatase, or esterase. One of these constituents is present during combined estrogen-progesterone therapy.
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PMID:Antigenic constituents in pregnancy plasma which are undetectable in normal non-pregnant female or male plasma. 462 19

We recently suggested that the 11 beta-hydroxysteroid dehydrogenase (11-HSD) activity in midgestational human fetal lung (HFL) cultures comprised at least two enzymes, one oxidative--associated with epithelial cells, the other reductive--related to fibroblast-like cells. In this study, the effects of various hormones on 11-HSD activity were studied by measuring the interconversion of [3H]cortisol and [14C]cortisone. Human chorionic gonadotrophin, placental medium, and low oxygen concentration increased the conversion of cortisone to cortisol while activity in the reverse direction remained unchanged. No effects were seen when adrenocorticotrophin, prolactin, placental lactogen, estrogens, triiodothyronine or oxytocin were added in physiological amounts.
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PMID:Investigation of factors influencing 11 beta-hydroxysteroid dehydrogenase (EC 1.1.1.146) activity in midgestational human fetal lung monolayer and explant cultures. 659 17

Literature on the etiology, diagnosis, and treatment of missed abortion is reviewed. Missed abortion during the 1st 28 weeks of gestation is defined as retention in the uterus of an abortus. The incidence of missed abortion among spontaneous miscarriages is 2.6-9.4%. Etiology of missed abortion is associated with intrauterine infections, severe abnormalities, inhibition of uterine contraction, or impairment of the hormonal balance. Prolonged retention of an abortus can result in fetal maceration or mummification. Clinical manifestations of missed abortion include absence of fetal heart tone, discharge from the breasts and diminution of their size, general fatigue, fever, and sometimes skin itch. Diagnosis of missed abortion is based upon the results of general and gynecologic examinations. Missed abortion is characterized by cessation of growth of the uterus, decrease in cyanosis of the cervix uteri, decrease in urinary excretion of estriol (up to 0-5 mg/day), drastic decrease in excretion of chorionic gonadotropin, decrease in blood level of placental lactogen, and decrease in pregnadiol excretion. Echographic signs of missed abortion during the 1st trimester include absence of heart activity, absence of fetal movements, and changes in the size of the uterus, amniotic cavity, and embryo. The most frequent complications of missed abortion are uterine hemorrhage, infection, and malignant transformation. Treatment of women with missed abortion consists of administration of abortifacient agents and curettage. The most frequently used abortifacient agents are oxytocin in large dosages, intravenous infusions of prostaglandin e2 (PGE2) or single intraamniotic injection of 15-methyl-PGF2alpha. The women with threatening uterine hemmorrage can be subjected to hysterectomy.
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PMID:[Diagnosis and treatment of missed abortion]. 661 58


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