Dinoprostone
Oxytocics
Labor, Induced
Administration, Intravaginal
Misoprostol
Term Birth
Suppositories
Expression of both P1 and P2 purine receptor genes by human articular chondrocytes and profile of ligand-mediated prostaglandin E2 release. (1/6240)
OBJECTIVE: To assess the expression and function of purine receptors in articular chondrocytes. METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to screen human chondrocyte RNA for expression of P1 and P2 purine receptor subtypes. Purine-stimulated prostaglandin E2 (PGE2) release from chondrocytes, untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radioimmunoassay. RESULTS: RT-PCR demonstrated that human articular chondrocytes transcribe messenger RNA for the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor subtypes A1 and A3. The P1 receptor agonists adenosine and 5'-N-ethylcarboxamidoadenosine did not change PGE2 release from chondrocytes. The P2Y2 agonists ATP and UTP stimulated a small release of PGE2 that was potentiated after pretreatment with rHuIL-1alpha. PGE2 release in response to ATP and UTP cotreatment was not additive, but release in response to coaddition of ATP and bradykinin (BK) or UTP and BK was additive, consistent with ATP and UTP competition for the same receptor site. The potentiation of PGE2 release in response to ATP and UTP after rHuIL-1alpha pretreatment was mimicked by phorbol myristate acetate. CONCLUSION: Human chondrocytes express both P1 and P2 purine receptor subtypes. The function of the P1 receptor subtype is not yet known, but stimulation of the P2Y2 receptor increases IL-1-mediated PGE2 release. (+info)Cortisol in fetal fluids and the fetal adrenal at parturition in the tammar wallaby (Macropus eugenii). (2/6240)
Glucocorticoid hormones may play a critical role in initiating parturition in tammar wallabies. In this study, we investigated the concentration of cortisol in fetal fluids and cortisol production by fetal adrenals over the last 3 days of the 26-day pregnancy and within 24 h postpartum. The fetal adrenals almost doubled in size between Days 24 and 26 of pregnancy, and their cortisol content increased over 10-fold during this period, from 10 pg to over 100 pg per adrenal pair. After birth, neonatal adrenals continued to grow, but cortisol content fell dramatically to 20 pg. The prepartum increase in adrenal cortisol was reflected by a substantial rise in cortisol concentrations in yolk sac fluid, allantoic fluid, and fetal blood, which were below 10 ng/ml on Day 24 and rose to over 40 ng/ml by Day 26. Cortisol concentrations in neonatal blood decreased postpartum, mirroring decreased cortisol content in neonatal adrenals. Cortisol production by the fetal adrenal was stimulated in vitro by ACTH and prostaglandin E2, suggesting that the in vivo increase may be stimulated by release of ACTH from the fetal hypothalamic-pituitary axis and prostaglandin E2 from the placenta. These results indicate that increasing cortisol production by the fetal adrenal is a characteristic of late pregnancy in the tammar wallaby and support the suggestion that fetal cortisol may trigger the initiation of parturition in this marsupial species. (+info)Down-regulation of oxytocin-induced cyclooxygenase-2 and prostaglandin F synthase expression by interferon-tau in bovine endometrial cells. (3/6240)
Oxytocin (OT) is responsible for the episodic release of luteolytic prostaglandin (PG) F2alpha from the uterus in ruminants. The attenuation of OT-stimulated uterine PGF2alpha secretion by interferon-tau (IFN-tau) is essential for prevention of luteolysis during pregnancy in cows. To better understand the mechanisms involved, the effect of recombinant bovine IFN-tau (rbIFN-tau) on OT-induced PG production and cyclooxygenase-2 (COX-2) and PGF synthase (PGFS) expression in cultured endometrial epithelial cells was investigated. Cells were obtained from cows at Days 1-3 of the estrous cycle and cultured to confluence in RPMI medium supplemented with 5% steroid-free fetal calf serum. The cells were then incubated in the presence or absence of either 100 ng/ml OT or OT+100 ng/ml rbIFN-tau for 3, 6, 12, and 24 h. OT significantly increased PGF2alpha and PGE2 secretion at all time points (p < 0.01), while rbIFN-tau inhibited the OT-induced PG production and reduced OT receptor binding in a time-dependent manner. OT increased the steady-state level of COX-2 mRNA, measured by Northern blot, which was maximal at 3 h (9-fold increase) and then decreased with time (p < 0.01). OT also caused an increase in COX-2 protein, which peaked at 12 h (11-fold increase), as measured by Western blot. Addition of rbIFN-tau suppressed the induction of COX-2 mRNA (89%, p < 0.01) and COX-2 protein (50%, p < 0.01) by OT. OT also increased PGFS mRNA, and this stimulation was attenuated by rbIFN-tau (p < 0.01). To ensure that the decrease in COX-2 was not solely due to down-regulation of the OT receptor, cells were stimulated with a phorbol ester (phorbol 12-myristate 13-acetate; PMA) in the presence and absence of rbIFN-tau. The results showed that rbIFN-tau also decreased PMA-stimulated PG production and COX-2 protein. It can be concluded that rbIFN-tau inhibition of OT-stimulated PG production is due to down-regulation of OT receptor, COX-2, and PGFS. (+info)Delay of preterm delivery in sheep by omega-3 long-chain polyunsaturates. (4/6240)
A positive correlation has been shown between dietary intake of long-chain omega-3 fatty acids in late pregnancy and gestation length in pregnant women and experimental animals. To determine whether omega-3 fatty acids have an effect on preterm labor in sheep, a fish oil concentrate emulsion was continuously infused to six pregnant ewes from 124 days gestational age. At 125 days, betamethasone was administered to the fetus to produce preterm labor. Both the onset of labor and the time of delivery were delayed by the fish oil emulsion. Two of the omega-3-infused ewes reverted from contractions to nonlabor, an effect never previously observed for experimental glucocorticoid-induced preterm labor in sheep. Maternal plasma estradiol and maternal and fetal prostaglandin E2 rose in control ewes but not in those infused with omega-3 fatty acid. The ability of omega-3 fatty acids to delay premature delivery in sheep indicates their possible use as tocolytics in humans. Premature labor is the major cause of neonatal death and long-term disability, and these studies present information that may lead to a novel therapeutic regimen for the prevention of preterm delivery in human pregnancy. (+info)Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (5/6240)
Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin. (+info)The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (6/6240)
1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2. (+info)Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4. (7/6240)
1. The effect of IL-4 on responses to intraplantar (i.pl.) carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8 and PGE2 was investigated in a model of mechanical hyperalgesia in rats. Also, the cellular source of the IL-4 was investigated. 2. IL-4, 30 min before the stimulus, inhibited responses to carrageenin, bradykinin, and TNFalpha, but not responses to IL-1beta, IL-8 and PGE2. 3. IL-4, 2 h before the injection of IL-1beta, did not affect the response to IL-1beta, whereas IL-4, 12 or 12+2 h before the IL-1beta, inhibited the hyperalgesia (-30%, -74%, respectively). 4. In murine peritoneal macrophages, murine IL-4 for 2 h before stimulation with LPS, inhibited (-40%) the production of IL-1beta but not PGE2. Murine IL-4 (for 16 h before stimulation with LPS) inhibited LPS-stimulated PGE2 but not IL-1beta. 5. Anti-murine IL-4 antibodies potentiated responses to carrageenin, bradykinin and TNFalpha, but not IL-1beta and IL-8, as well as responses to bradykinin in athymic rats but not in rats depleted of mast cells with compound 40/80. 6. These data suggest that IL-4 released by mast cells limits inflammatory hyperalgesia. During the early phase of the inflammatory response the mode of action of the IL-4 appears to be inhibition of the production TNFalpha, IL-1beta and IL-8. In the later phase of the response, in addition to inhibiting the production of pro-inflammatory cytokines, IL-4 also may inhibit the release of PGs. (+info)The effects of inflammation and inflammatory mediators on nociceptive behaviour induced by ATP analogues in the rat. (8/6240)
1. We have studied the behavioural effects of intraplantar injections of adenosine 5'-triphosphate (ATP) and related compounds in freely moving rats and investigated whether these nociceptive effects are augmented in the presence of inflammatory mediators. 2. We find that in normal animals ATP and analogues produce dose-dependent nocifensive behaviour (seen as bursts of elevation of the treated hindpaw), and localized thermal hyperalgesia. The rank order of potency was: alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-methylene ATP) > 2-methylthioadenosine triphosphate (2-methylthio ATP) > ATP. After neonatal treatment with capsaicin, to destroy small calibre primary sensory neurones, nocifensive behaviour was largely absent. 3. The effects of ATP analogues were assessed in three models of peripheral sensitization: 2 h after dilute intraplantar carrageenan (0.25% w v(-1)); 24 h after irradiation of the hindpaw with ultraviolet (U.V.) B; immediately following prostaglandin E2 (PGE2) treatment. In all models the effect of alpha,beta-methylene ATP was greatly augmented. After carrageenan, significant hindpaw-lifting behaviour activity was induced by injection of only 0.05 nmol of alpha,beta-methylene ATP, some 100 times less than necessary in normal skin. 4. Our data suggest that it is much more likely that endogenous levels of ATP will reach levels capable of exciting nociceptors in inflamed versus normal skin. Our data also suggest the involvement of P2X3 receptor subunits in ATP-induced nociception. (+info)Dinoprostone is a prostaglandin E2 analog used in medical practice for the induction of labor and ripening of the cervix in pregnant women. It is available in various forms, including vaginal suppositories, gel, and tablets. Dinoprostone works by stimulating the contraction of uterine muscles and promoting cervical dilation, which helps in facilitating a successful delivery.
It's important to note that dinoprostone should only be administered under the supervision of a healthcare professional, as its use is associated with certain risks and side effects, including uterine hyperstimulation, fetal distress, and maternal infection. The dosage and duration of treatment are carefully monitored to minimize these risks and ensure the safety of both the mother and the baby.
Oxytocics are a class of medications that stimulate the contraction of uterine smooth muscle. They are primarily used in obstetrics to induce or augment labor, and to control bleeding after childbirth. Oxytocin is the most commonly used oxytocic and is naturally produced by the posterior pituitary gland. Synthetic forms of oxytocin, such as Pitocin, are often used in medical settings to induce labor or reduce postpartum bleeding. Other medications with oxytocic properties include ergometrine and methylergometrine. It's important to note that the use of oxytocics should be monitored carefully as overuse can lead to excessive uterine contractions, which may compromise fetal oxygenation and increase the risk of uterine rupture.
Induced labor refers to the initiation of labor before it begins spontaneously, which is usually achieved through medical intervention. This process is initiated when there is a medically indicated reason to deliver the baby, such as maternal or fetal compromise, prolonged pregnancy, or reduced fetal movement. The most common methods used to induce labor include membrane stripping, prostaglandin administration, and oxytocin infusion. It's important to note that induced labor carries certain risks, including a higher chance of uterine hyperstimulation, infection, and the need for assisted vaginal delivery or cesarean section. Therefore, it should only be performed under the close supervision of a healthcare provider in a clinical setting.
Intravaginal administration refers to the delivery of medications or other substances directly into the vagina. This route of administration can be used for local treatment of vaginal infections or inflammation, or to deliver systemic medication that is absorbed through the vaginal mucosa.
Medications can be administered intravaginally using a variety of dosage forms, including creams, gels, foams, suppositories, and films. The choice of dosage form depends on several factors, such as the drug's physicochemical properties, the desired duration of action, and patient preference.
Intravaginal administration offers several advantages over other routes of administration. It allows for direct delivery of medication to the site of action, which can result in higher local concentrations and fewer systemic side effects. Additionally, some medications may be more effective when administered intravaginally due to their ability to bypass first-pass metabolism in the liver.
However, there are also potential disadvantages to intravaginal administration. Some women may find it uncomfortable or inconvenient to use this route of administration, and there is a risk of leakage or expulsion of the medication. Additionally, certain medications may cause local irritation or allergic reactions when administered intravaginally.
Overall, intravaginal administration can be a useful route of administration for certain medications and conditions, but it is important to consider the potential benefits and risks when choosing this method.
Misoprostol is a synthetic prostaglandin E1 analog used in obstetrics and gynecology to prevent and treat ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs), reduce the risk of gastric ulcers in patients taking NSAIDs long term, induce labor, manage postpartum hemorrhage, and cause abortion. It is also used off-label for cervical ripening before gynecologic surgery and to treat miscarriage.
In addition, Misoprostol has been found to be effective in reducing the risk of gastric ulcers and NSAID-induced dyspepsia (upper abdominal pain or discomfort) in patients with rheumatoid arthritis and other inflammatory conditions who require long-term NSAID therapy.
It is important to note that Misoprostol should not be used during pregnancy unless under the supervision of a healthcare provider for specific medical indications, such as preventing or treating stomach ulcers in pregnant women taking NSAIDs or inducing labor. It can cause miscarriage and birth defects if taken during early pregnancy.
A "term birth" is a medical term that refers to a delivery or pregnancy that has reached 37 weeks or more. It is the normal length of a full-term pregnancy and is considered a healthy and low-risk period for childbirth. Babies born at term have the best chance of being healthy and not experiencing any significant medical issues, compared to those born preterm (before 37 weeks) or postterm (after 42 weeks). The different types of term births are:
* Early Term: Between 37 weeks and 38 weeks, 6 days.
* Full Term: Between 39 weeks and 40 weeks, 6 days.
* Late Term: Between 41 weeks and 41 weeks, 6 days.
* Postterm: 42 weeks or later.
It is important to note that while a term birth is generally considered low-risk, there can still be variations in the health of babies born at different points within this range. For example, research has shown that babies born at 39 weeks have better outcomes than those born at 37 or 38 weeks. Therefore, it is always best to consult with a healthcare provider for individualized guidance and recommendations regarding pregnancy and childbirth.
A suppository is a solid medicinal formulation, often medicated, that is intended to be introduced into the rectum (rectal suppository), vagina (vaginal suppository), or urethra (urethral suppository) for absorption or for localized effect. Suppositories are designed to melt or dissolve at body temperature and release the active ingredients. They come in various shapes, such as cones, cylinders, or torpedo-shaped, and are typically made from a base of cocoa butter, polyethylene glycol, or other biocompatible materials that allow for controlled drug release. Common uses for suppositories include the treatment of constipation, hemorrhoids, local infections, menstrual cramps, and as an alternative method of administering medication for individuals who have difficulty swallowing pills or prefer not to use oral medications.
Pregnancy is a physiological state or condition where a fertilized egg (zygote) successfully implants and grows in the uterus of a woman, leading to the development of an embryo and finally a fetus. This process typically spans approximately 40 weeks, divided into three trimesters, and culminates in childbirth. Throughout this period, numerous hormonal and physical changes occur to support the growing offspring, including uterine enlargement, breast development, and various maternal adaptations to ensure the fetus's optimal growth and well-being.
Prostaglandin E
Prostaglandin E2
Abortifacient
Uterine atony
Enprostil
Cervical effacement
Prostamide
Labor induction
Misoprostol
Carbetocin
Uterotonic
Carboprost
Fred Mecklenburg
Off-label use
Forest Laboratories
Uterine myomectomy
List of drugs: Df-Di
List of MeSH codes (D10)
ATC code G02
List of MeSH codes (D23)
Dinoprostone: MedlinePlus Drug Information
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Vaginal4
- Dinoprostone comes as a vaginal insert and as a gel that is inserted high into the vagina. (medlineplus.gov)
- Vaginal Insert: 10 mg of dinoprostone contained within a knitted polyester pouch retrieval system. (nih.gov)
- For an unriped cervix, Foley catheter balloon and controlled release dinoprostone vaginal inserts are two methods of inducing labour, and a 2018 systematic review found no differences in safety or effectiveness for patients without a prior C-section. (physiciansweekly.com)
- dinoprostone vaginal gel 2 mg). (bvsalud.org)
Misoprostol3
- Ces différences mécaniques peuvent affecter les résultats chez les femmes traitées au dinoprostone, une formule identique au PGE2 endogène, comparé au misoprostol, un PGE1 analogue. (afar.info)
- Résultats : Bien que le dinoprostone et le misoprostol soient tous deux efficaces pour la maturation du col et le déclenchement du travail, ils se différencient par leurs profils cliniques et pharmacologiques. (afar.info)
- Le misoprostol a démontré qu'il provoquait un effet dose dépendant sur la contractilité du myomètre, ce qui peut affecter les taux d'hypercinésie utérine en pratique clinique. (afar.info)
Prostaglandin E22
- Dinoprostone is a molecule that is structurally similar to prostaglandin E2, and is used as a medication to induce labor, or to abort a pregnancy. (inchikey.info)
- Types include: Prostaglandin E1 also known as alprostadil Prostaglandin E2 also known as dinoprostone Both types are on the World Health Organization's List of Essential Medicines. (wikipedia.org)
Prostin E21
- Prostin E2 - dinoprostone - E2 (Prostin) is supplied for Tenders/ Emergency imports/ Un - licensed, Specials, Orphan drug/ Name patient line/ RLD supplies/ Reference listed drugs/ Comparator Drug/ Bio-Similar/ Innovator samples For Clinical trials. (gnhindia.com)
CERVIDIL1
- Administer one CERVIDIL insert (10 mg) intravaginally for use up to 12 hours (approximately 0.3 mg of dinoprostone is released per hour) [see Dosage and Administration (2.2) ]. (nih.gov)
Labour induction1
- Overall, this study showed that for patients with one prior C-section, time to delivery following controlled release dinoprostone labour induction was significantly quicker compared to the use of a Foley catheter balloon, although no differences in satisfaction were found. (physiciansweekly.com)
Oxytocin1
- dinoprostone increases effects of oxytocin by pharmacodynamic synergism. (medscape.com)
Cervix1
- Dinoprostone is used to prepare the cervix for the induction of labor in pregnant women who are at or near term. (medlineplus.gov)
Adverse effects1
- It has a higher incidence of adverse effects than dinoprostone and is therefore not recommended for labor induction. (e-lactancia.org)
Cervical1
- Objectif : Les Prostaglandines jouent un rôle critique dans la maturation cervicale en augmentant les médiateurs inflammatoires du col et induisant un remodelage cervical. (afar.info)
Medication1
- Prostaglandin E₂, also known as dinoprostone, is a naturally occurring prostaglandin with oxytocic properties that is used as a medication. (trustpharmacie.com)
Drugs1
- tell your doctor and pharmacist if you are allergic to dinoprostone or any other drugs. (medlineplus.gov)
Common2
- Side effects from dinoprostone are not common, but they can occur. (medlineplus.gov)
- A summary of the most common chemical descriptors (InChI Key and SMILES codes) for Dinoprostone are summarized together with 3D and 2D structures and relevant physico-chemical properties. (inchikey.info)
Labor1
- Dinoprostone is used in labor induction, bleeding after delivery, termination of pregnancy, and in newborn babies to keep the ductus arteriosus open. (trustpharmacie.com)
General1
- In general, it affects about 1 in 7,000 pharmacie en ligne france births. (terminally-incoherent.com)
Medicine1
- Medicine Central , im.unboundmedicine.com/medicine/view/Davis-Drug-Guide/51224/all/dinoprostone. (unboundmedicine.com)