Stimulation of uterine activity by administration of prostaglandin F-2alpha during parturition in sheep.
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Animals↗
Biomedical subjects
M D Mitchell
Publications and source records attributed to M D Mitchell.
Prostaglandins in the plasma and amniotic fluid of rhesus monkeys during pregnancy and after intra-uterine foetal death.
Prostaglandin F (PGF) was measured in amniotic fluid, and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) was measured in maternal peripheral venous plasma and amniotic fluid of rhesus monkeys during late pregnancy. 13,14-Dihydro-15-keto-PGF2 alpha was determined in the maternal peripheral venous plasma of two animals following intra-uterine foetal death. The mean concentration of PGF and PGFM in amniotic fluid increased fourfold during the last 5 days of pregnancy. This increase was associated with an increase in the oestrone concentration in amniotic fluid and in maternal plasma. In normal pregnancy there was no increase in PGFM levels in the maternal peripheral vein, up to 1-2 days pre partum. After intra-uterine death, progesterone concentration in the maternal peripheral vein was unaltered, but oestrone and oestradiol declined. In plasma samples taken within 12 h of delivery, the concentration of PGFM was raised. It is concluded that an increase in prostaglandin production accompanies delivery at normal term, and at delivery past term following intra-uterine foetal death.
Amniotic Fluid↗
Swine tuberculosis in South Dakota.
Mycobacteria were isolated from 195 of 200 lesions in lymph nodes identified as granulomatous by meat inspectors at 4 abattoirs in South Dakota. Mycobacterium avium serotypes 1 and 2 accounted for 89% of the isolants. Mycobacteria were isolated more frequently from lesions than acid-fast bacilli were observed on microscopic examination (P less than 0.001). The frequency with which mycobacteria was isolated was similar to the occurrence of granulomatous lesions. The numbers of the various kinds of mycobacteria isolated at each of the 4 abattoirs and for the 3 meat inspection disposition classes were not significantly different.
Abattoirs↗
Stimulation by oxytocin of prostaglandin f levels in uterine venous effluent in pregnant and puerperal sheep.
The purpose of this work was to investigate the effect of oxytocin on prostaglandin F (PGF) concentrations in uterine venous effluent. PGF was measured in utero-ovarian venous plasma from three pregnant ewes and in posterior vena caval plasma from two puerperal ewes, during oxytocin administration. Oxytocin caused 4.9 - 5.3-fold increases in PGF concentrations in the pregnant animals, the response increasing towards term. In the puerperal animals oxytocin caused 3.7 - 17.2-fold increases in PGF concentrations with a marked latency in the response. Measurement of uterine activity and progesterone and total unconjugated oestrogen concentrations indicated that neither uterine contractions nor a decreased uterine blood flow accounted for the elevated PGF levels stimulated by oxytocin.
Animals↗
Temporal relationship between changes in oxytocin and prostaglandin F levels in response to vaginal distension in the pregnant and puerperal ewe.
To investigate the rôle of oxytocin in the increase in utero-ovarian venous prostaglandin F (PGF) level caused by vaginal distension, jugular venous oxytocin and utero-ovarian venous PGF were measured simultaneously in one sheep in late pregnancy and in one sheep shortly before parturition. Vaginal distension raised oxytocin and PGF levels in both animals and oxytocin levels increased before those of PGF. These findings support the suggestion that the elevated PGF levels resulting from vaginal distension are caused by the reflex secretion of oxytocin.
Animals↗
Proceedings: Effect of oxytocin on plasma prostaglandin F levels in the pregnant and post-partum ewe.
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Animals↗
Effects of gestational age on prostaglandin production and its regulation in human myometrial cells.
The objective of this study was to evaluate the effects of known stimulants of prostaglandin production on cultured myometrial cells from women who are at various gestational ages. To evaluate this, myometrial segments were obtained from 12 patients at 27-40 weeks gestation at cesarean delivery. Myometrial cells were then isolated and grown to confluence in culture. Incubations were conducted in quadruplicate for 16 hours with interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA), or ionomycin. Prostaglandins E2, F2 alpha, and 6-keto F1 alpha (the stable metabolite of prostacyclin) were measured by radioimmunoassay and cellular protein determined. The results revealed that cultured myometrial cells produced prostaglandins in response to IL-1 beta, TNF-alpha, EGF, PMA, and ionomycin at all gestational ages tested at a significantly increased rate (P < 0.05 vs controls at and above 10 ng/ml of IL-1 beta, TNF alpha, and EGF; 1 microM for PMA, and 5 microM for ionomycin). The major prostaglandin produced in response to each stimulant was 6-keto-PGF1 alpha. Cultured human myometrial cells respond to known stimulants of prostaglandin production throughout the third trimester of pregnancy in the absence of labor. The myometrium may therefore be a source of prostaglandins that influences uterine activity.
6-Ketoprostaglandin F1 alpha↗
Prostaglandin production by human chorion laeve cells in response to inflammatory mediators.
Cytokines produced during an intrauterine infection may cause increased prostaglandin production and thus preterm labor. Previously, we have shown that cytokines increase prostaglandin production by human amnion and decidual cells. In the present study we examined the effect of interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF), and endotoxin on prostaglandin production by chorion laeve cells. Upon reaching confluence at day 3 and after 10 days in culture, human chorion laeve cells in primary culture were incubated with each substance. On day 3 of culture the chorion cells demonstrated limited responsiveness to the test agents with a maximum response of less than two times basal production. However, after 10 days the cultures were highly responsive to the test agents with maximum responses of greater than ten times basal production. We conclude that early in culture chorion cells may express fewer functional receptors for the test agents. Alternatively, a subpopulation of chorion cells responsive to cytokines and endotoxin may predominate by day 10 of culture. Chorion laeve, therefore, could contribute to the increased intrauterine prostaglandin production associated with infection-driven preterm labor.
6-Ketoprostaglandin F1 alpha↗
Current topic: the regulation of placental eicosanoid biosynthesis.
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Amnion↗
Regulation of chorion laeve prostaglandin E2 production by epidermal growth factor, protein kinase C activation and calcium.
The effects of epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA), A23187, and ionomycin on prostaglandin production by chorion laeve cells in culture for 3 days and 10 days were tested. Experiments were conducted at day 3 because at this time the cultures became confluent and again at day 10 because changes have been observed in the biochemical properties of these cells with time in culture. At 3 days of culture the cells did not respond to EGF but at 10 days EGF (10 ng/ml) induced a significant increase in prostaglandin E2 production. PMA (10(-9) to 10(-6) M) induced a significant increase in PGE2 production at both times in culture. The calcium ionophores, A23187 and ionomycin, were less effective in eliciting a response at either time in culture. Only A23187 (1 microM) induced a significant increase in PGE2 production at day 10 of culture. These data suggest that the presence of functional EGF receptors may increase with time in culture. Furthermore, activation of the protein kinase C pathway in the chorion laeve stimulates prostaglandin biosynthesis. On the other hand, chorion laeve cell prostaglandin biosynthesis is not responsive to increases in intracellular calcium induced by mobile ion carriers such as the ionophores used in this study.
Calcimycin↗
Macrophage inflammatory protein-I alpha regulates prostaglandin E2 and interleukin-6 production by human gestational tissues in vitro.
OBJECTIVE: To determine if the inflammatory cytokine macrophage inflammatory protein-1 alpha (MLP-1 alpha) stimulates the production of prostaglandin E2 (PGE2) and interleukin-6 (IL-6) by human gestational tissues. METHODS: Human decidual cells, chorion cells, and amnion cells were isolated from term placentas of women with normal pregnancies, and primary cultures of each cell line were established. In various concentrations, MIP-1 alpha was then applied to each cell culture for 16 hours at 37C, and culture supernatants were assayed for PGE2 and IL-6. RESULTS: After incubation with MIP-1 alpha, decidual cells produced increased amounts of both IL-6 (P < .05) but not PGE2. When subjected to similar conditions, chorion cells produced increased amounts of both IL-6 and PGE2 (P < .05). Conversely, amnion cells produced increased amounts of only PGE2 in response to increasing concentrations of MIP-1 alpha (P < .05). CONCLUSION: Maternal and fetal gestational tissues differentially respond to MIP-1 alpha with regard to PGE2 and IL-6 production; MIP-1 alpha may play a role in both the initiation and propagation of the inflammatory response associated with intrauterine infection.
Amnion↗
Amniotic fluid epidermal growth factor levels in normal and abnormal pregnancies.
OBJECTIVE: To determine the concentrations of epidermal growth factor (EGF) in amniotic fluid (AF) from women during late pregnancy, with and without pathophysiologic complications. METHODS: All AFs were collected by amniocentesis from the following groups: gestational age at least 38 weeks (n = 15); gestational age 36-37 weeks (n = 10); gestational age 35 weeks (n = 5); labor 34 weeks or less, delivered within 7 days (n = 10); labor 34 weeks or less, undelivered (n = 10); chorioamnionitis (n = 7); gestational age-matched controls (n = 7); term, in labor (n = 8); term, not in labor (n = 8); intrauterine growth restriction (IUGR) 38 weeks or more (n = 8); macrosomia at 38 weeks or more (n = 10). Epidermal growth factor was assayed using a specific radioimmunoassay. RESULTS: Amniotic fluid EGF levels increase rapidly in late pregnancy but are not altered by chorioamnionitis or by term or preterm labor. Intrauterine growth restriction is associated with lower EGF levels in AF, but macrosomia is without effect. CONCLUSIONS: Epidermal growth factor levels in AF are increased near term and decreased in pregnancies complicated by IUGR; they may be an indicator of specific maturational events.
Amniotic Fluid↗
Regulation of fetal fibronectin production in human amnion cells.
OBJECTIVE: We evaluated the role of human amnion in the production of fetal fibronectin and assessed the regulation of fetal fibronectin production by inflammatory products and cytokines. METHODS: Human amnion cells were grown in culture. At confluence, the cell were incubated with and without lipopolysaccharide, interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6. Fetal fibronectin production was measured in the supernatant fluid using an enzyme-linked immunosorbent assay technique. RESULTS: Unstimulated amnion cells produced fetal fibronectin, and production was increased by lipopolysaccharide, interleukin-1 beta, tumor necrosis factor-alpha, and interleukin-6. CONCLUSION: Human amnion cells in vitro produce fetal fibronectin in substantial quantities. This production is stimulated by inflammatory products and mediators that are considered to be important in the initiation of some cases of preterm labor.
Amnion↗
Prostanoids in blood for neonatal transfusion.
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Blood Transfusion↗
Mechanism of interleukin-1 beta stimulation of human amnion prostaglandin biosynthesis: mediation via a novel inducible cyclooxygenase.
We have evaluated the mechanism by which interleukin-1 beta (IL-1 beta) increases amnion cell PGE2 production in a concentration-dependent manner. IL-1 beta-stimulated amnion cell PGE2 biosynthesis was time-dependent, and significant stimulation occurred within 2 h of incubation. IL-1 beta stimulation occurred in the presence of added arachidonic acid but was abrogated by treatment with cycloheximide and actinomycin D. Amnion cells treated with IL-1 beta recovered rapidly from aspirin pretreatment suggesting an action on fatty acid cyclooxygenase (COX). Increased amounts of COX protein were demonstrated by Western blot analysis within 2 h of IL-1 beta treatment of amnion cells. Northern blot analysis using a probe specific for a novel form of COX (COX-II) showed an increase in mRNA for this COX within 30 min. This finding using a homologous detection system and human cells of fetal origin in primary culture provides strong support for a physiological role for COX-II in man.
Amnion↗
Cytokine networking in the placenta.
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Amniotic Fluid↗
Renin stimulates decidual prostaglandin production via a novel mechanism that is independent of angiotensin II formation.
Renin is a proteolytic enzyme that has been considered to have only one function which is to cleave angiotensinogen between the 10th and 11th amino acids to form angiotensin-1. This is then converted to angiotensin-II, a potent vasoconstrictor, antinatriuretic and antidiuretic by angiotensin-converting enzyme. We have investigated the action of renin to stimulate prostaglandin production by decidual cells and in so doing have generated data that challenge the prevailing dogma. Renin stimulates decidual prostaglandin production in a concentration-related fashion that is unaffected by saralasin treatment. This stimulatory action of renin is enhanced rather than reduced by arachidonic acid treatment but abolished by treatment with cycloheximide or actinomycin D. Renin caused a more rapid recovery of decidual prostaglandin biosynthesis from acetylsalicylic acid treatment than did control media. Moreover, renin treatment of both decidual and amnion cells induced increased levels of PGHS-2 within 2 h. Collectively, these results indicate that renin can act directly, separately from the generation of angiotensin-I and II. In this case renin can induce PGHS expression.
Amnion↗
Regulation of activin-A production by human amnion, decidua and placenta in vitro by pro-inflammatory cytokines.
Activin-betaA subunits are expressed by the human placenta and extraplacental membranes at term and preterm. The regulation of activin-A production by these tissues has not been characterized to date, however. To determine the effects on activin-A production of pro-inflammatory cytokines, amnion, decidual and placental cells were isolated by enzyme dispersion and treated in primary culture with interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha). Activin-A production (determined by ELISA) by amnion, decidual and placental cultures was 1.2 +/-0.27, 31.1+/-9.9, and 50.7+/-28.5 pg/microg protein/16 h, respectively (mean+/-SEM; n=5-7 experiments). Both IL-1beta and TNF-alpha stimulated activin-A production in a concentration-dependent fashion in all cultures; maximal stimulation was achieved at 0.25-1.0 ng/ml IL-1beta and 25-50 ng/ml TNF-alpha, respectively. In amnion, decidual and placental cultures IL-1beta stimulated activin-A production to 747+/-274, 190+/-11, and 254+/-60.2 per cent of controls, while TNF-alpha stimulated production to 312+/-81.5, 194+/-22.5, and 193+/-12.5 per cent, respectively (mean+/-SEM; n=5; P<0.05 by ANOVA). These studies show for the first time that pro-inflammatory cytokines are potent stimulators of activin-A production by intrauterine tissues. This may provide an explanation for the elevated concentrations of activin-A measured in the sera of some women in preterm labour.
Activins↗