Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to characterize endometrial secretion (in vitro) of prostaglandin F (PGF), 15-keto-13,14-dihydro-prostaglandin F2 alpha (PGFM), prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) on Day 5 following the first postpartum estrus of cows anticipated to have a short compared to a normal estrous cycle. Twenty-seven beef cows were randomly assigned into four groups. The Short Cycle (n = 6; control) and Short Cycle/Explant (n = 8; endometrial explants) groups had their calves weaned at 30-32 days postpartum. The Normal Cycle (n = 5, control) and Normal Cycle/Explant (n = 8; endometrial explants) groups received norgestomet (progestin) implants for 9 days beginning 21-23 days postpartum, and calves were weaned at implant insertion. Estrous cycle length (mean +/- SE; p less than 0.01) for the Short Cycle group was 11.5 +/- 1.9 days compared to 18.8 +/- 0.6 days for the Normal Cycle group. On Day 5 following the first postpartum estrus, cows in the Short Cycle/Explant and Normal Cycle/Explant groups were hysterectomized, and endometrial explants were incubated in Earle's Balanced Salt solution/Medium 199 for 90 min with or without arachidonic acid (AA) in the presence of three levels of oxytocin. Mean concentrations of PGF and PGFM were combined to obtain a value for total PGF. Concentrations of total PGF, PGE2 (from explants without AA treatment), and 6-keto-PGF1 alpha in medium of the Short Cycle/Explant group were higher (p less than 0.01) than in medium of the Normal Cycle/Explant group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro secretion of prostaglandins from endometrium of postpartum beef cows expected to have short or normal luteal phases. 201 68

The existing data on prostaglandins indicate that they are involved in human parturition and regulation of fetoplacental blood flow. The interference of endogenous and exogenous oxytocin and prostaglandins and, on the other hand, betamimetics, which are commonly used during pregnancy, in the regulation of these phenomena is poorly understood. The production of prostaglandins by fetal placental cotyledons was studied using an in vitro perfusion technique. Isolated cotyledons were perfused without (control) or with oxytocin (200 pg/ml, 2000 pg/ml) or the betasympathomimetic drug ritodrine (10 micrograms/ml, 50 micrograms/ml). The release of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2) was measured by radioimmunoassay. The release of prostaglandins was also studied during a recovery period after the drug infusion. Oxytocin at a concentration of 200 pg/ml significantly decreased the release of PGF2 alpha. A higher concentration of oxytocin did not cause any changes in prostaglandin production. During ritodrine infusion the perfusion pressure was decreased, but the addition of ritodrine to the perfusion medium had no effect on prostaglandin release. During the recovery period, after ritodrine infusion, the release of PGF2 alpha was significantly decreased. It is suggested that oxytocin at the physiological concentration may protect the fetus from adverse effects of PGF2 alpha before labor in decreasing the release of PGF2 alpha, yet this small decrease in formation of PGF2 alpha is obviously of minor clinical importance because the perfusion pressure remained constant. Ritodrine had no effect on prostaglandin release and so the decrease in the perfusion pressure is probably the result of beta 2-receptor stimulation.
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PMID:The effect of oxytocin and betamimetic stimulation on prostaglandin release in perfused human fetal placenta. 346 20

To study the role of the antiaggregatory and vasodilatory prostacyclin (PGI2) during human delivery, serial urine samples collected from 13 women delivered vaginally and from eight delivered abdominally were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, a breakdown product of PGI2) by high-performance-liquid-chromatography and radioimmunoassay. In women delivered vaginally the mean urinary 6-keto-PGF1 alpha concentration was 41.9 (SE 8.3) ng/mmol creatinine, before the onset of labour and increased progressively to a maximum of 186.5 (SE 47.6) ng/mmol creatinine 2 h after delivery irrespective of the use of oxytocin and epidural analgesia. In women delivered by caesarean section under epidural anaesthesia, the urinary 6-keto-PGF1 alpha rose from 33.4 (SE 4.2) ng/mmol creatinine to 2153 (SE 314) ng/mmol creatinine 2 h after section. In both groups the increased levels had fallen by 24 h postpartum to levels below those found before delivery. In neonatal urine 6-keto-PGF1 alpha concentrations were some 12-30 times higher than those in postpartum urine. Thus, vaginal and abdominal delivery is accompanied by significant increases in maternal PGI2 release, perhaps in the myometrium and/or intrauterine tissues. This may be of significance in the regulation of fetoplacental blood flow and in the prevention of intra- and postpartum thrombosis.
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PMID:Vaginal and abdominal delivery increases maternal urinary 6-keto-prostaglandin F1 alpha excretion. 376 89

Production of the antiaggregatory and vasodilatory prostacyclin (prostaglandin I2) and the proaggregatory and vasoconstrictory thromboxane A2 during human labor was studied by measuring serial concentrations of the stable metabolites of these prostanoids, 6-keto-prostaglandin F1 alpha and thromboxane B2, respectively, in the amniotic fluid of 43 parturients whose labor was induced by amniotomy. The concentration of 6-keto-prostaglandin F1 alpha at amniotomy in 28 healthy parturients (92.7 +/- 12.1 pg/ml, mean +/- SE) was higher (p less than 0.02) than that in 15 preeclamptic women (48.6 +/- 5.5 pg/ml). The concentration of thromboxane B2 at amniotomy was 292.4 +/- 56.1 pg/ml, with no difference between the healthy and preeclamptic parturients. Both prostanoid levels rose consistently during labor, reaching peak levels when the cervix was fully dilated, but this rise started only after the established uterine contractility. Epidural anesthesia and paracervical blockade had no effect on 6-keto-prostaglandin F1 alpha and thromboxane B2 in the amniotic fluid, whereas oxytocin infusion was accompanied by reduced levels of thromboxane B2. The rise in amniotic fluid 6-keto-prostaglandin F1 alpha was reduced at every stage of labor in the preeclamptic women (n = 15), and its maximal increase (112.4 +/- 28.3 pg/ml) was smaller (p less than 0.005) than in the healthy women (n = 28, 240.8 +/- 21.4 pg/ml). The ratio of 6-keto-prostaglandin F1 alpha to thromboxane B2 also shifted to thromboxane B2 dominance in the preeclamptic parturients. It is concluded that a relative prostacyclin deficiency deteriorates in preeclamptic women during labor.
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PMID:Amniotic fluid 6-keto-prostaglandin F1 alpha and thromboxane B2 during labor. 638 35

Normal human endometrium (classified by histology and date after last menstrual period) was cultured for 72h, and the output of prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha detected by radioimmunoassay. Hormones/stimuli were added to the culture during the second day of culture for 5h and 19h periods. The output of prostaglandin F2 alpha from cultured endometrium was significantly higher (p less than 0.05) at the beginning (d4-8) and end (d25-30) of the menstrual cycle, compared to mid-cycle (d13-24) endometrium. Significantly more prostaglandin F2 alpha was released from proliferative than from secretory phase endometrium (p less than 0.02). Prostaglandin F2 alpha release was rapidly stimulated by sodium arachidonate (20-300 micrograms/ml), and by calcium ionophore A23187 (5 micrograms/ml) at an extracellular calcium ion concentration of 1.8mM. The ionophore stimulation was greater in mid-cycle endometrium than in endometrium from the beginning or the end of the menstrual cycle. Estradiol-17 beta (10 ng/ml) gradually increased the output of prostaglandin F2 alpha from secretory phase endometrium, and this stimulation was observed in the post-incubation period after hormone had been removed from the incubation medium. Oxytocin (1 X 10(-5) U/ml caused a more rapid stimulation of prostaglandin F2 alpha output from secretory phase tissue (p less than 0.05 during the first 5h incubation period with hormone). Oxytocin (1 X 10(-5) U/ml) and estradiol (10ng/ml) together significantly stimulated prostaglandin F2 alpha production by proliferative as well as secretory phase endometria. A high dose of hydrocortisone (100 micrograms/ml) inhibited the output of prostaglandin F2 alpha from proliferative and secretory phase endometrium and also from ionophore-stimulated endometrium. However, this dose of hydrocortisone did not inhibit the synthesis of prostaglandin F2 alpha from exogenous arachidonic acid, or the estradiol-induced increase in prostaglandin F2 alpha production. Co-culture of endometrium with myometrium did not modify the output of prostaglandin F2 alpha or of 6-oxo-prostaglandin F1 alpha from cultured tissues. These experiments suggest that arachidonic acid supply to the cyclooxygenase enzyme may vary during the menstrual cycle; and indicate a gradual increase in prostaglandin synthesising capacity in response to estrogen, more rapid control via oxytocin, and an interaction between estrogen and oxytocin to modulate prostaglandin F2 alpha synthesis in human endometrium.
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PMID:The effect of oxytocin, estrogen, calcium ionophore A23187 and hydrocortisone on prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha production by cultured human endometrial and myometrial explants. 642 64

The metabolism of arachidonic acid (AA) by caruncular and allantochorionic tissues and its regulation was studied in normal cows (n = 13) and those with retained fetal membranes (RFM; n = 9). Tissues were taken via the vagina about 6 hours postpartum and incubated for 6 hours in minimum essential medium containing tritiated AA alone or in the presence of oxytocin, platelet activating factor (PAF), epidermal growth factor (EGF) or ionophore calcium (A23187). The metabolites of AA were separated by reverse phase-high pressure-liquid chromatography. Tissue concentrations of prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) and plasma 13,14-dihydro-15-keto-PGF2 alpha (PGFM) concentration were also measured by radioimmunoassay. For caruncular tissue, less thromboxane B2 (TXB2) and more 6-keto prostaglandin F1 alpha (PGIM) was synthesized in tissue from the animals with RFM than in the controls. Oxytocin, PAF, EGF and A23187 increased only PGIM production in the control animals; A23187 also decreased TBX2 synthesis. For the allantochorion, more PGE2, leukotriene B4 (LTB4) and PGIM and less TXB2, PGF2 alpha and hydroxyecosatetranoic acids (HETE) was synthesized in tissue from cows with RFM than from animals that delivered normally. All of the substances used in this study increased PGIM, PGF2 alpha and LTB4 and decreased TXB2 production by the allantochorionic tissue in control animals. The metabolism of AA by the allantochorionic tissue seems quantitatively under hormonal control. The metabolism of AA at the level of both maternal and fetal components of the placenta in cows with RFM differed from that seen in animals that expelled the membranes normally.
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PMID:Metabolism of arachidonic acid by caruncular and allantochorionic tissues in cows with retained fetal membranes (RFM). 838 Sep 36