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1.
In a group of 20 matched primigravid patients labour was induced by forewater amniotomy followed by intravenous oxytocin (Syntocinon) administered in escalating doses. Ten of these patients, in a double-blind trial, also received prostaglandin E2 infused simultaneously with the oxytocin. In the combined prostaglandin-oxytocin group there was a noticeable reduction in the dosage of oxytocin required to produce effective uterine action, and the duration of labour was also reduced. No side effects were observed.  相似文献   

2.
We have previously demonstrated that decreased cortical prostaglandin metabolism can contribute significantly to an increase in renal tissue levels and activity of prostaglandin E2 in bilateral ureteral obstruction, a model of acute renal failure. In the present study, we have further investigated whether alterations in prostaglandin metabolism can occur in a nephrotoxic model of acute renal failure. Prostaglandin synthesis, prostaglandin E2 metabolism (measured as both prostaglandin E2-9-ketoreductase and prostaglandin E2-15-hydroxydehydrogenase activity), and tissue concentration of prostaglandin E2 were determined in rabbit kidneys following an intravenous administration of uranyl nitrate (5 mg/kg). No changes in the rates of cortical microsomal prostaglandin E2 and prostaglandin F synthesis were noted at the end of 1 and 3 days, while medullary synthesis of prostaglandin E2 fell by 47% after 1 day and 43% after 3 days. Cortical cytosolic prostaglandin E2-9-ketoreductase activity was found to be decreased by 36% and 76% after 1 and 3 days respectively. No significant changes were noted in cortical cytosolic prostaglandin E2-15-hydroxydehydrogenase activity after 3 days. Cortical tissue levels of prostaglandin E2 increased by 500% at the end of 3 days. These data demonstrate that in nephrotoxic acute renal failure, decreased prostaglandin metabolism (i.e., prostaglandin E2-9-ketoreductase activity) can result in increased tissue levels of prostaglandin E2 in the absence of increased prostaglandin synthesis and suggest that alterations in prostaglandin metabolism may be an important regulator of prostaglandin activity in acute renal failure.  相似文献   

3.
15-Methyl prostaglandin E2, a compound which is not a substrate for 15-hydroxy prostaglandin dehydrogenase, is a more potent pyretic agent than prostaglandin E2 when injected into the third ventricle of conscious cats. This finding raises the possibility that 15-hydroxy prostaglandin dehydrogenase contributes to prostaglandin inactivation in brain, notwithstanding its low activity.  相似文献   

4.
We studied the uterine venous plasma concentrations of prostaglandins E2, F, 15 keto 13,14 dihydro E2 and 15 keto 13,14 dihydro F in late pregnant dogs in order to evaluate the rates of production and metabolism of prostaglandin E2 and F in pregnancy in vivo. We used a very specific and sensitive gas chromatography-mass spectrometry assay to measure these prostaglandins. The uterine venous concentrations of prostaglandin E2 and 15 keto 13,14 dihydro E2 were 1.35±.27 ng/ml and 1.89±.37 ng/ml, respectively; however, we could not find any prostaglandin F and very little of its plasma metabolite in uterine venous plasma. Since uterine microsomes can generate prostaglandin F and E2 from endoperoxides, prostaglandin F production in vivo must be regulated through an enzymatic step after endoperoxide formation. Prostaglandin E2 is produced by pregnant canine uterus in quantities high enough to have a biological effect in late pregnancy; however, prostaglandin F does not appear to play a role at this stage of pregnancy.  相似文献   

5.
Changes in arterial blood pressure and heart rate were observed in the spontaneous hypertensive (SH) rat following the intravenous administration of arachidonic acid, the precursor of prostaglandin E2 (PGE2). The pronounced fall in blood pressure and the increase in heart rate induced by arachidonic acid were also observed in SH rats receiving either prostaglandin E1 (PGE1) or PGE2. In SH rats receiving various anti-inflammatory agents the cardiovascular responses to arachidonic acid were inhibited, but the blood pressure responses to the E-type prostaglandins were not altered. The data are interpreted to suggest that cardiovascular changes induced by arachidonic acid are mediated via its conversion to PGE2.  相似文献   

6.
Rat adipocyte plasma membranes sacs have been shown to be a sensitive and specific system for studying prostaglandin binding. The binding of prostaglandin E1 and prostaglandin A1 increases linearly with increasing protein concentration, and is a temperature-sensitive process. Prostaglandin E1 binding is not ion dependent, but is enhanced by GTP. Prostaglandin A1 binding is stimulated by ions, but is not affected by GTP.Discrete binding sites for prostaglandin E1 and A1 were found. Scatchard plot analysis showed that the binding of both prostaglandins was biphasic, indicating two types of binding sites. Prostaglandin E1 had association constants of 4.9 · 109 1/mole and 4 · 108 1/mole, while the prostaglandin A1 association constants and binding capacities varied according to the ionic composition of the buffer. In Tris-HCl buffer, the prostaglandin A1 association constants were 8.3 · 108 1/mole and 5.7 · 107 1/mole, while in the Krebs—Ringer Tris buffer, the results were 1.2 · 109 1/mole and 8.6 · 106 1/mole.Some cross-reactivity between prostaglandin E1 and A1 was found for their respective binding sites. Using Scatchard plot analysis, it was found that a 10-fold excess of prostaglandin E1 inhibited prostaglandin A1 binding by 1–20% depending upon the concentration of prostaglandin A1 used. Prostaglandin E1 competes primarily for the A prostaglandin high-affinity binding site. Similar Scatchard analysis using a 20-fold excess of prostaglandin A1 inhibited prostaglandin E1 binding by 10–40%. Prostaglandin A1 was found to compete primarily for the E prostaglandin low-affinity receptor.All of the bound [3H]prostaglandin E1, but only 64% of the bound [3H]-prostaglandin A1 can be recovered unmetabolized from the fat cell membrane. There is no non-specific binding of prostaglandin E1, but 10–15% of prostaglandin A1 binding to adipocyte membranes is non-specific. Using a parallel line assay to measure relative affinities for the E binding site, prostaglandin E1 > prostaglandin A2 > prostaglandin F. Prostaglandin E2 and 16,16-dimethyl prostaglandin E2 were equipotent with prostaglandin E1, while other prostaglandins had lower relative affinities. 7-Oxa-13-prostynoic acid does not appear to antagonize prostaglandin activity in adipocytes at the level of the receptor.  相似文献   

7.
We determined the effect of 2 mg/kg intravenous furosemide on the production and metabolism of prostaglandin E2 in the utero-placental unit of pregnant dogs. Uterine venous prostaglandins E2 and 15-keto-13,14-dihydro E2 were measured by gas chromatography-mass spectrometry. Even though the dose of furosemide was adequate to effect a good diuresis, neither the production nor the metabolism of prostaglandin E2 by the uterus was altered by that dose of the drug. Using radioactive microspheres to measure hemodynamic parameters, we observed no change in uterine vascular resistance while renal vascular resistance decreased. Although the renal concentration of furosemide may be higher than the uteroplacental concentration, there is so far no evidence that usual doses of furosemide enhance the production or inhibit the metabolism of prostaglandin E2.  相似文献   

8.
C3b or lipopolysaccharide treatment of human peripheral blood monocytes in culture stimulates an early release of thromboxane B2 and a delayed release of prostaglandin E into culture supernatants. Immunoreactive thromboxane B2 release is maximal from 2–8 h, whereas prostaglandin E release is maximal from 16–24 h after stimulation of monocytes in culture. We further examined this process by comparing the time course of labelled prostaglandin E2, prostaglandin E1 and thromboxane B2 release from human monocytes which were pulse or continuously labelled with [3H]arachidonic acid and [14C]eicosatrienoic acid. The release of labelled eicosanoids was compared with the release of immunoreactive prostaglandin E and thromboxane B2. The time course of prostaglandin E2 release was virtually identical to the release of prostaglandin E1 in all culture supernatants regardless of labelling conditions. However, release of immunoreactive prostaglandin E paralleled the release of labelled prostaglandin E1 and E2 only for continuously labelled cultures. The release of labelled prostaglandin E1 and E2 from pulse labelled cultures paralleled the release of thromboxane B2 and not immunoreactive prostaglandin. In contrast, labelled and immunoreactive thromboxane B2, quantitated in the same culture supernatants, demonstrated similar release patterns regardless of labelling conditions. These findings indicate that the differential pattern of prostaglandin E and thromboxane B2 release from human monocytes is not related to a time-dependent shift in the release of prostaglandin E1 relative to prostaglandin E2. Because thromboxane B2 and prostaglandin E2 are produced through cyclooxygenase mediated conversion of arachidonic acid, these results further suggest that prostaglandin E2 and thromboxane B2 are independently metabolized in human monocyte populations.  相似文献   

9.
We determined the effect of 2 mg/kg intravenous furosemide on the production and metabolism of prostaglandin E2 in the utero-placental unit of pregnant dogs. Uterine venous prostaglandins E2 and 15-keto-13,14-dihydro E2 were measured by gas chromatography-mass spectrometry. Even though the dose of furosemide was adequate to effect a good diuresis, neither the production nor the metabolism of prostaglandin E2 by the uterus was altered by that dose of the drug. Using radioactive microspheres to measure hemodynamic parameters, we observed no change in uterine vascular resistance while renal vascular resistance decreased. Although the renal concentration of furosemide may be higher than the uteroplacental concentration, there is so far no evidence in vivo that usual doses of furosemide enhance the production or inhibit the metabolism of prostaglandin E2.  相似文献   

10.
The oxytocic properties of prostaglandin 16,16 dimethyl E2 methyl ester were investigated during the second trimester of pregnancy. As an abortifacient, this compound compared unfavorably to the 15 methyl analogs of prostaglandin E2, with a lower rate of effectiveness and a relatively high incidence of side effects.  相似文献   

11.
Human erythrocytes were found to contain two prostaglandin metabolizing enzymes: a prostaglandin E 9-ketoreductase catalyzing the reduction of prostaglandin E2 to form prostaglandin F and a 15-hydroxyprostaglandin dehydrogenase that catalyzes the oxidation of prostaglandin F to form 15-ketoprostaglandin F. Both enzymes are found in the cytoplasmic fraction of erythrocytes and both enzymes use the triphosphopyridine nucleotides as cofactors more effectively than the diphosphopyridine nucleotides. These two enzymes were partially purified from erythrocyte homogenates and some of their properties were studied.  相似文献   

12.
The effects of endotoxic shock on the synthesis of PAF-acether by the stomach, duodenum and lung were examined in the rat. Furthermore, the effect of pretreatment with prostaglandin E2 on endotoxin induced PAF-acether synthesis and changes in vascular permeability were examined. Administration of endotoxin resulted in significant increases in PAF-acether synthesis in all tissues studied. Such increases were apparent within 5–15 minutes of the administration of endotoxin, corresponding to the time when significant hypotension, hemoconcentration and increases in gastrointestinal vascular permeability were first observed. Pretreatment with prostaglandin E2 resulted in a significant reduction of endotoxin-induced hypotension, hemoconcentration and changes in vascular permeability in the gastrointestinal tract. However, prostaglandin pretreatment did not significantly alter endotoxin-induced PAF-acether release from the gastrointestinal tissues studied. These results demonstrate that prostaglandin E2 can significantly attenuate several of the systemic and gastrointestinal manifestations of endotoxic shock. The mechanism responsible for these beneficial actions appears to be unrelated to effects of prostaglandin E2 on PAF-acether synthesis.  相似文献   

13.
Use of (125I)-labeled histamine-prostaglandin tracer increases the sensitivity of the radioimmunoassays of prostaglandin derivatives. Six different antisera were produced for prostaglandins and their derivatives (prostaglandins E1, E2, F, F, 13,14-dihydro-15-ketoprostaglandin E2, and 13,14-dihydro-15-ketoprostaglandin F) and were investigated with the corresponding tritiated and lodinated tracers. Displacement of iodinated tracers by the methyl esters of the prostaglandin compounds resulted, in most cases, in a three- to fivefold increase in sensitivity compared to unesterified inhibitors. Esterification also caused some alteration in the specificities observed. Our results suggest that conformational changes in the esterified prostaglandins (tracer and inhibitor) could explain these charges.  相似文献   

14.
Prostaglandins E2 and F2α were administered by mouth to induce labour in 24 patients at or past term. The drugs were administered at two-hourly intervals in doses ranging from 0·5 to 1·5 mg for prostaglandin E2 and from 5 to 15 mg for prostaglandin F2α. Of the 10 cases in which prostaglandin E2 was used, labour was successfully induced in eight and there were no side effects. With prostaglandin F2α labour was induced in 12 of 14 patients nine of whom had gastrointestinal disturbance, mostly of mild degree. With both drugs the infant was apparently unaffected and Apgar scores were satisfactory. Uterine hypertonus was not observed and the postpartum blood loss was within normal limits.  相似文献   

15.
Prostaglandin E2 and F were measured in ejaculates from 10 fertile and 55 infertile men. Prostaglandin F was negatively correlated with motility (r=0.77; p<0.01) in normal men. In patients with disturbed fertility, prostaglandin F was always higher than in the controls, while prostaglandin E2 was elevated only in patients with persisting varicocele and in those with very low sperm counts and severely impaired motility. There was neither synthesis of prostaglandins in spermatozoa nor were binding sites for prostaglandin E2 and F detectable. Inactivation of seminal prostaglandins by incubation with prostaglandin 15-hydroxydehydrogenase resulted in a dramatic fall in motility. The results suggest that prostaglandin F act on motility, but the action is not mediated by receptors.  相似文献   

16.
Prostacyclin (Prostaglandin I2) effects on the rat kidney adenylate cyclase-cyclic AMP system were examined. Prostaglandin I2 and prostaglandin E2, from 8 · 10?4 to 8 · ?7 M stimulated adenylate cyclase to a similar extent in cortex and outer medulla. In inner medulla, prostaglandin I2 was more effective than prostaglandin E2 at all concentrations tested. Both prostaglandin I2 and prostaglandin E2 were additive with antidiuretic hormone in outer and inner medulla. Prostaglandin I2 and prostaglandin E2 were not additive in any area of the kidney, indicating both were working by similar mechanisms. Prostaglandin I2 stimulation of adenylate cyclase correlated with its ability to increase renal slice cyclic AMP content. Prostaglandin I2 and prostaglandin E2 (1.5 · 10?4 M) elevated cyclic AMP content in cortex and outer medulla slices. In inner medulla, with Santoquin® (0.1 mM) present to suppress endogenous prostaglandin synthesis, prostaglandin I2 and prostaglandin E2 increased cyclic AMP content. 6-Ketoprostaglandin F, the stable metabolite of prostaglandin I2, did not increase adenylate cyclase activity or tissue cyclic AMP content. Thus, prostaglandin I2 activates renal adenylate cyclase. This suggests that the physiological actions of prostaglandin I2 may be mediated through the adenylate cyclase-cyclic AMP system.  相似文献   

17.
The effect of orally administered prostaglandin E2 and its synthetic 15-methyl analogues on gastric secretion in man was studied. The parent E2 compound did not inhibit basal secretion, whereas both the 15 (S) 15-methyl-E2 methyl ester and its isomer, 15 (R) 15-methyl-E2 methyl ester inhibited basal acid secretion. This action is likely to be a direct one on the parietal cell, and it could prove of value in the treatment of peptic ulcer.  相似文献   

18.
Prostaglandins E1 and E2 caused a 5–10 fold stimulation of ornithine decarboxylase activity in granulosa cells isolated from porcine ovarian follicles. The minimally effective concentration of prostaglandin E2 was 10 ng/ml and the plateau of activity was reached at 500 ng/ml. Prostaglandin F was ineffective. 1-Methyl,3-isobutyl-xanthine, a phosphodiesterase inhibitor, potentiated the effect of both submaximal and maximal effective doses of prostaglandin E2, suggesting that the effect of prostaglandin E2 is mediated by cAMP. The effect of prostaglandin E2 was similar to that of luteinizing hormone and a cAMP analogue, 8-Bromo-cAMP.  相似文献   

19.
Saline washed red blood cells of the toadfish convert [1-14C] arachidonic acid to products that cochromatograph with prostaglandin E2 and prostaglandin F. This synthesis is inhibited by indomethacin (10 μg/ml). Conversion of arachidonic acid to prostaglandin E2 was confirmed by mass spectrometry. When saline washed toadfish red blood cells were incubated with a mixture of [1-14C]-arachidonic acid and [5,6,8,9,11,12,14,15,-3H]-arachidonic acid, comparison of the isotope ratios of the radioactive products indicated that prostaglandin F was produced by reduction of prostaglandin E2. The capacity of toadfish red blood cells to reduce prostaglandin E2 to prostaglandin F was confirmed by incubation of the cells with [1-14C] prostaglandin E2.  相似文献   

20.
We have examined the role of phospholipid-sensitive calcium-dependent protein kinase (protein kinase C) in prostaglandin E2 synthesis by monolayer cultures of swine granulosa cells. Specific phorbol ester derivatives known to activate protein kinase C significantly augmented the production of prostaglandin E2. These stimulatory actions were dose and time-dependent, and could be abolished by the cyclooxygenase inhibitor, indomethacin, or the protein synthesis inhibitor, cycloheximide. Moreover, the rank order of potency of phorbol esters in enhancing prostaglandin E2 production was concordant with that demonstrated for activation of protein kinase C. Phorbol ester in conjunction with the divalent cation ionophore, A23187, increased prostaglandin E2 production synergistically. In addition, a non-phorbol stimulator of protein kinase C, 1-octanoyl-2-acetylglycerol, also significantly enhanced prostaglandin E2 biosynthesis. The stimulated synthesis of prostaglandin E2 was confirmed by high-pressure liquid chromatographic purification of this radiolabeled metabolite of 3H-arachidonic acid, and by capillary gas chromatography high-resolution mass spectrometry. Thus, the present studies indicate that the protein kinase C effector pathway is functionally coupled to prostaglandin E2 production in the swine granulosa cell.  相似文献   

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