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At least 19 recordsLinked to original sources
PubMed1991

Plasma estradiol-17 beta, progesterone, prostaglandin F, and prostaglandin E2 concentrations during natural oviposition in the loggerhead turtle (Caretta caretta).

Changes in plasma concentrations of steroids and prostaglandins (PGs) during natural nesting and oviposition in the loggerhead turtle were studied. Blood samples were obtained during nine distinct behavioral stages of oviposition. Emerging females had no detectable prostaglandin F (PGF) or prostaglandin E2 (PGE2) whereas plasma estradiol-17 beta averaged 255 pg/ml and mean plasma progesterone was 395 pg/ml. Plasma steroid concentrations did not vary significantly during nesting. In contrast, plasma PGF and PGE2 exhibited significant elevations during nest digging about 15 min after emergence. A further significant increase in plasma PGs was observed 10 min later during early oviposition. Plasma PGE2 peaked during mid oviposition whereas maximal plasma PGF levels occurred during nest covering although mean values were not significantly different than those observed during oviposition. Both PGs showed an abrupt decline (within 10 min) during body pit covering to concentrations similar to those observed during nest construction. Our data suggest that PGs have an active role during oviposition and nesting in the loggerhead turtle and are consistent with hypotheses that PGF2 alpha stimulates uterine contractions promoting egg expulsion while PGE2 may be more important in promoting cervical relaxation.

Animals↗
PubMed2004

Synthesis of prostaglandin F ethanolamide by prostaglandin F synthase and identification of Bimatoprost as a potent inhibitor of the enzyme: new enzyme assay method using LC/ESI/MS.

Prostaglandin (PG) D(2) ethanolamide (prostamide D(2)) was reduced to 9alpha,11beta-PGF(2) ethanolamide (9alpha,11beta-prostamide F(2)) by PGF synthase, which also catalyzes the reduction of PGH(2) and PGD(2) to PGF(2alpha) and 9alpha,11beta-PGF(2), respectively. These enzyme activities were measured by a new method, the liquid chromatographic-electrospray ionization-mass spectrometry (LC/ESI/MS) technique, which could simultaneously detect the substrate and all products. PGF(2alpha), 9alpha,11beta-PGF(2), PGD(2), PGH(2), 9alpha,11beta-prostamide F(2), and prostamide D(2) were separated on a TSKgel ODS 80Ts column, ionized by electrospray, and detected in the negative mode. Selected ion monitoring (SIM) of m/z 353 ([M-H](-)), 353 ([M-H](-)), 351 ([M-H](-)), 333 ([M-H-H(2)O](-)), 456 ([M+59](-)), and m/z 358 ([M-37](-)) was used for quantifying PGF(2alpha), 9alpha,11beta-PGF(2), PGD(2), PGH(2), 9alpha,11beta-prostamide F(2), and prostamide D(2), respectively. The detection limit for PGF(2alpha) and 9alpha,11beta-PGF(2) was 0.01pmol; that for PGH(2) and PGD(2), 0.1pmol; and that for prostamide D(2) and 9alpha,11beta-prostamide F(2), 0.5 and 0.03pmol, respectively. The LC/ESI/MS technique for measuring PGF synthase activity showed higher sensitivity than other methods. Using this method, we found that Bimatoprost, the ethyl amide analog of 17-phenyl-trinor PGF(2alpha) and an anti-glaucoma agent, inhibited all three reductase activities of PGF synthase when used at a low concentration. These results suggest that Bimatoprost also behaves as a potent PGF synthase inhibitor in addition to having prostamide-like activity.

Amides↗
PubMed1980

Evaluation of the role of the F prostaglandins in canine bile flow.

Prostaglandin F2 alpha (PGF2 alpha) has been shown to be an effective stimulant of hepatic bile flow producing a specific chloride rich bile. Subsequent evaluation by radioimmunoassay has shown that prostaglandin F compounds are present in relatively large amounts in canine hepatic bile. This study evaluates the effect of PGF2 alpha administration and of prostaglandin synthetase inhibition by aspirin and indomethacin on bile flow and radioimmunoassayable prostaglandin F (iPGF) secretion. Chronic, canine bile fistula preparations were utilized and the enterohepatic circulation was maintained by intravenous bile salts. Bile volume and composition were evaluated by standard techniques as well as bile PGF concentration by radioimmunoassay during bile salt infusion and during bile salt and PGF2 alpha, aspirin and indomethacin infusion in varying doses. Both aspirin and PGF2 alpha were potent stimulants of hepatic bile flow with aspirin producing a chloride rich bile similar to that produced by PGF2 alpha. PGF2 alpha produced dose related increases in bile iPGF concentration and output indicating that as the systemic concentration increases during infusion of PGF2 alpha the lipid appears in bile. Aspirin in the highest dose administered, decreased iPGF concentration in bile while output was unchanged. Indomethacin was ineffectual in consistently altering bile flow or iPGF secretion. This study demonstrates that iPGF is present in canine bile, that its concentration can be altered by prostaglandin infusion while prostaglandin synthetase inhibition has minimal effects on bile iPGF secretion.

Animals↗
PubMed1983

Prostaglandin F and 13,14-dihydro-15-keto prostaglandin F in the endometrium and uterine flushings of sheep before implantation.

The concentrations of prostaglandin F (PGF) and its major metabolite, 13,14-dihydro-15-keto prostaglandin F-2 alpha (PGFM), were measured in caruncular and intercaruncular endometrium of pregnant and non-pregnant ewes on Days 9, 11, 13 and 15 after mating (Day 0) and related to the content of PGF and PGFM in the uterine flushings. The tissue concentrations of PGF and PGFM increased with time after mating particularly on Days 13 and 15 and to a greater extent in pregnancy. However, the ratio of PGF to PGFM remained constant at 0.7, except on Day 15 in non-pregnant endometrium when it fell to 0.3 (P less than 0.05), suggesting that synthesis rather than metabolism was limiting tissue concentrations of PGs. The changes in tissue concentrations of PGF and PGFM were reflected in the contents of PGF and PGFM in the uterine flushings of non-pregnant, but not pregnant ewes. Pregnant ewes had relatively more PGF and less PGFM than did non-pregnant ewes on Day 15. Moreover, there was always 5-10-fold less PGFM than PGF in the uterine flushings. It is concluded that the increase in PG in the uterine lumen in pregnancy has its origin in the blastocyst, and that pregnancy may be associated with an increase in the synthesis and retention of PGs in the endometrium, rather than a redistribution towards the uterine lumen away from the uterine venous drainage.

Animals↗
PubMed1986

GnRH effects on placental hormones during gestation. III. Prostaglandin E, prostaglandin F, and 13,14-dihydro-15-keto-prostaglandin F.

We studied the release of prostaglandin E (PGE), prostaglandin F (PGF) and 13,14-dihydro-15-keto-prostaglandin F (MPF) from explants of human placentas of different gestational ages and the effect of gonadotropin-releasing hormone (GnRH) on this release. The greatest basal release of PGE, PGF and MPF was in the cultures from 9- to 13-wk placentas, with the release on the second and third days of culture increasing 4- to 10-fold from that of the first day. In cultures from 15-wk to term placentas, the initial basal release (Day 1) of these prostaglandins was only slightly higher than in cultures from 6-wk placentas. In cultures from term placentas, the later increase with extended culture was absent or very small. Addition of synthetic GnRH to the cultures from 6- to 9-wk placentas effected no significant change in release of PGE, PGF or MPF. However, GnRH added to the cultures from 13-wk placentas effected a dose-related inhibition of these prostaglandins. After 15 wk, we observed a stimulation of these prostaglandins by GnRH that was as much as 50-fold; stimulation was highly significant in the cultures from 16- and 17-wk, as well as in those from the term placentas. These data demonstrate an action of GnRH on prostaglandin release and indicate that both the basal release of PGE, PGF and MPF and the response to GnRH are related to the gestational age of the placenta.

Dinoprost↗
PubMed2002

Nitric oxide induced cervical ripening in the human: Involvement of cyclic guanosine monophosphate, prostaglandin F(2 alpha), and prostaglandin E(2).

OBJECTIVE: The purpose of the study was to investigate possible mechanisms and morphologic changes involved in nitric oxide-induced cervical ripening. STUDY DESIGN: Women scheduled for surgical termination of first trimester pregnancy were randomized to 1 of 3 groups: isosorbide 5-mononitrate 40 mg 4 hours or 10 hours before the operation or no preoperative treatment. Cervical specimens were obtained for the analysis of tissue levels of cyclic guanosine monophosphate, cyclic adenosine monophosphate, cyclo-oxygenase 1, cyclo-oxygenase 2, prostaglandin F(2 alpha), and prostaglandin E(2) or were fixed in glutaraldehyde for microscopy. RESULTS: Increased levels of cyclic guanosine monophosphate, cyclo-oxygenase 2, prostaglandin F(2 alpha), and prostaglandin E(2) were found in samples that were exposed to isosorbide 5-mononitrate compared with control samples. Electron microscopy revealed stromal edema and collagen disorganization after isosorbide 5-mononitrate treatment. CONCLUSION: Cyclic guanosine monophosphate, prostaglandin F(2 alpha), and prostaglandin E(2) are involved in nitric oxide-induced cervical ripening. Nitric oxide causes morphologic changes similar to those changes seen during spontaneous cervical ripening.

Cervical Ripening↗
PubMedDate not supplied

Interaction of prostaglandin F(2alpha) and prostaglandin E(2) on progesterone production in human granulosa-luteal cells.

This study examined the effects of prostaglandin-F(2alpha) (PGF(2alpha)), prostaglandin-E(2) (PGE(2)) and their interactions on progesterone production in human granulosa-luteal cells (GLCs). Human GLCs collected from in vitro fertilization patients were cultured for 1 (D(1)) or 8 days (D(8)), followed by a 24-hour treatment period, after which media were collected and radioimmunoassayed for progesterone. Seven-point PGF(2alpha) and PGE(2) concentration-response curves were crossed into a matrix of 49 separate treatments. Responses were plotted in three dimensions and as two-dimensional "slices". In D(1) cultured human GLCs neither PGF(2alpha) nor PGE(2) alone had any effect on progesterone production, however two different combinations of these hormones led to at least a 3-fold increase in progesterone production. This stimulation was seen when cells were treated with 10(-6) M PGF(2alpha) plus 10(-9) M PGE(2), and when they were treated with 10(-10) M PGF(2alpha) plus 10(-9) M PGE(2). In D(8) GLCs, PGF(2alpha) stimulated progesterone production maximally at 10(-9) M, while the lowest (10(-11) M) and highest concentrations (10(-6) M) tested were ineffectual. On the contrary, in the presence of high concentrations of PGE(2) (10(-6) to 10(-7) M), PGF(2alpha)-mediated stimulation of progesterone production was attenuated. In a similar fashion to PGF(2alpha), PGE(2) also acted in a luteotrophic manner, although the maximal stimulation of progesterone production was seen at a higher concentration (10(-8) to 10(-7) M). Likewise, PGE(2)-mediated progesterone production was attenuated by the presence of high concentrations of PGF(2alpha) (10(-6) to 10(-7) M). In conclusion, in D(1) human GLCs neither PGF(2alpha) nor PGE(2) alone were luteotrophic, although specific combinations of these hormones were. Conversely, in D(8) GLCs both PGF(2alpha) and PGE(2) stimulated progesterone production in a biphasic manner, while the presence of a high concentration of either of these prostaglandins attenuated the luteotrophic effects of the other. Therefore, PGF(2alpha) and PGE(2) interacted in a concentration-dependent manner, resulting in a multimodal progesterone response, which was easily visualized using three-dimensional plots.

Cells, Cultured↗
PubMed1977

F prostaglandin levels in amniotic fluid in premature labour.

The concentration of prostaglandin F (PGF) in amniotic fluid was measured by radioimmunoassay in 27 patients admitted in premature labour. There was a strong correlation between PGF levels in amniotic fluid and both cervical dilatation (r = 0.81; P less than 0.001) and duration of labour (r = 0.79; P less than 0.001). Cervical dilatation greater than 7 cm was associated with levels exceeding 2000 pg/ml. When contractions were present for less than one hour, levels of PGF were below 50 pg/ml. Low levels of PGF were found in amniotic fluid from a separate group of three patients, of whom two had cervical incompetence. It is concluded that the onset of premature labour is not associated with elevated levels of PGF in amniotic fluid. During premature labour, concentrations rise to an extent comparable to that observed in labour at term.

Amniotic Fluid↗
PubMed1977

Changes in prostaglandin F and 13,14-dihydro-15-keto-prostaglandin F concentrations in amniotic fluid at the onset of and during labour.

Concentrations of prostaglandin F (PGF) and its major circulating metabolite 13,14-dihydro-15-keto-PGF (PGFM) have been measured in amniotic fluid during spontaneous labour at term. Levels of both PGF and PGFM were significantly higher during early spontaneous labour, at a cervical dilatation of less than 4 cm, than before the onset of labour. Patients who started labour spontaneously but later required oxytocin therapy for failure to progress in first stage had lower levels of PGF and PGFM than patients who progressed adequately without oxytocin therapy. During spontaneous labour, concentrations of both PGF and PGFM increased significantly with advancing cervical dilatation. These indicate that the accumulation of prostaglandins in amniotic fluid during labour is not due to decreased metabolism. They furthermore provide the strongest evidence available so far for an increase in intrauterine prostaglandin synthesis during human parturition.

Amniotic Fluid↗
PubMed1975

[Intra-amniotic administration of prostaglandin F 2 alpha, 12-methyl-prostaglandin F 2 alpha and hypertonic sodium chloride solution for induction of abortion in second-trimester pregnancy].

The authors had performed comperative studies of the effect of the induction of abortion in late pregnancy according to the medical indications by intra-amniotic injection of 20% hypertonic NaCl saline in 26 pregnant patients, of 25 mg prostaglandin F2alpha with 6 hours' intervals in 25 patients, a single dose injection of 40 mg PGF2alpha in 27 cases and single dose injection of 2,5 mg 15-me-PGF2alpha given to 25 patients. The highest success rate was obtained with the single dose injection of 2,5 mg 15-me-PGF2alpha and the lowest success rate was obtained with 25 mg prostaglandin F2alpha with 6 hours' intervals. Despite of rather high procentage of success rate in using the hypertonic NaCl saline, this method is more dangerous in the moment of the injection of saline and complications during the abortion (water intoxication, necrosis of tissue, coagulation defects and other). The most frequently incountered side-effects in using PGs were vomiting and diarhea. Histologic examinations of the placenta revealed massive bleedings, at frequency rate being the same for prostaglandins and the hypertonic saline. The degree of isoimmunisation was lower with prostaglandins than with hypertonic NaCl saline, despite of the late dates of pregnancy termination. The intro-amniotic injection of the small volume solution of 15-me-PGF2alpha or PGF2alpha is more simpler and easier from the technical point of view than any methodic recommended for using saline and at the same time it is more effective.

Abortion, Induced↗
PubMed2003

Quantification of 8-iso-prostaglandin-F(2alpha) and 2,3-dinor-8-iso-prostaglandin-F(2alpha) in human urine using liquid chromatography-tandem mass spectrometry.

Quantification of 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) has been suggested to be a reliable indicator of lipid peroxidation that may be related to in vivo free radical generation, oxidative damage, and antioxidant deficiency. We have developed a LC-MS/MS method to quantify 8-iso- PGF(2alpha) and its dinor metabolite, 2,3-dinor-8-iso-prostaglandin F(2alpha) (2,3-dinor-8-iso-PGF(2alpha)), in human urine samples. After an initial purification step using an automated C18 solid phase extraction procedure, the urine sample was injected directly into a liquid chromatography (LC) system and detected with tandem mass spectrometry. The detection limit of the assay was 9 pg for 8-iso-PGF(2alpha) and 3 pg for 2,3-dinor-8-iso-PGF(2alpha) with both inter- and intraday variations of less than 12%. The inaccuracies were less than 3% for both analytes at three different levels. The urinary excretion rate of 2,3-dinor-8-iso-PGF(2alpha) was higher than that of 8-iso-PGF(2alpha), and changed in proportion to the parent compound (R = 0.70, n = 60). Values obtained with this method showed good linear correlation to duplicate 8-iso-PGF(2alpha) measurements performed with GCMS (R = 0.97, n = 15). The mean excretion rates of 8-iso-PGF(2alpha) and 2,3-dinor-8-iso-PGF(2alpha) were significantly higher in smokers than in nonsmokers (0.53 +/- 0.37 vs. 0.25 +/- 0.15 microg/g creatinine, p = 0.002 for 8-iso-PGF(2alpha) and 8.9 +/- 3.8 vs. 4.6 +/- 2.6 microg/g creatinine, p = 0.003 for 2,3-dinor-8-iso-PGF(2alpha), respectively). The excellent accuracy, reproducibility, and high throughput of this method should permit it to be used in large clinical studies and standard clinical laboratories.

Chromatography, High Pressure Liquid↗
PubMed2000

Synthetic modification of prostaglandin f(2alpha) indicates different structural determinants for binding to the prostaglandin F receptor versus the prostaglandin transporter.

Several principles governing the binding of E series prostaglandins to EP receptors have emerged in recent years. The C-1 carboxyl group binds electrostatically to a conserved arginine residue in the seventh transmembrane segment of the receptor. Prostaglandin E analogs involving bioisosteric replacements of the carboxyl group, such as acylsulfonamide, are also active. In addition, structurally similar esters may also exhibit similar affinity, presumably by virtue of hydrogen bonding. Other regions of the substrate molecule appear to bind to other domains of EP receptors, either via hydrophobic interactions or by hydrogen bonding. Less information is available about the structural requirements for substrate binding to FP receptors. Prostanoids also bind to the prostaglandin transporter PGT. In this case, a conserved C-1 carboxyl group is critically important, since C-1 esters exhibit little affinity. Here we examined the binding of chemically diverse PGF(2alpha) structural analogs to the FP receptor and compared these with binding by the PG transporter. PGT recognized a wide range of anionic substituents. In contrast, the carboxylic acid group was essential for optimal binding to the FP receptor, since replacement by larger moieties with a similar pK(a), such as acylsulfonamide and tetrazole, substantially decreased binding affinity. Interestingly, insertion of cyclic substituents in the omega chain increased binding to the FP receptor but reduced affinity for PGT, and substitution for the 15-hydroxyl group produced only a modest reduction in FP receptor binding, but eliminated binding by PGT. Because extracellular PGF(2alpha) may compete for binding between FP receptors and PGT, these findings have implications for designing PGF(2alpha) analogs for treating disease states.

Animals↗