共查询到20条相似文献,搜索用时 9 毫秒
1.
Effects of PGE1 or PGE2 on luteal function were studied in 163 pseudopregnant rats. PGE1 (10, 100, or 300 micrograms) given intrauterine every 6 hr did not shorten pseudopregnancy (P greater than 0.05), however, the same doses of PGE2 given intrauterine every 6 hr advanced luteolysis (P less than 0.05). PGE1 (100 or 300 micrograms) given every 4 hr intramuscular maintained levels of progesterone in peripheral blood above controls (P less than 0.05) while 100 or 300 micrograms of PGE2 hastened the decline in progesterone (P less than 0.05). The antiluteolytic effect of PGE1 was not via an inhibition of PGF secretion (P greater than 0.05) by the uterus or by induction of ovulation in treated animals. Moreover, PGE1 (100, 200, or 500 micrograms) given intramuscular every 4 hr from day 4 of pseudopregnancy until the next proestrus delayed luteal regression around 3 days (P less than 0.05). PGE2 at doses of 100, 200, or 500 micrograms every 4 hr given intramuscular consistently shortened pseudopregnancy (P less than 0.05). Lower doses were without effect (P greater than 0.05). Based on the above data it is concluded that PGE2 is consistently luteolytic whereas PGE1 is not luteolytic in pseudopregnant rats and that PGE1 may be an antiluteolysin. 相似文献
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Four prostaglandins-PGE1, PGE2, 190H PGE1 and 190H PGE2-were quantified in human seminal fluid by GC-MS-SIM using only the internal standard, d4-PGE2. Methods and calculations were developed to minize errors inherent in using only one internal standard for quantifying four closely related prostaglandins. Preliminary data concerning the statistical significance of the differences found between PGE and 190H PGE levels in fertile, azospermic and oligospermic men are reported. 相似文献
5.
Yoshie S. Weems Aaron Raney John Pang Tracie Uchima Esther Lennon Drew Johnson Torrence M. Nett Ronald D. Randel Charles W. Weems 《Theriogenology》2013
The objective of this study was to determine whether prostaglandin E1 (PGE1) or prostaglandin E2 (PGE2) prevents premature luteolysis in ewes when progesterone is given during the first 6 days of the estrous cycle. Progesterone (3 mg in oil, im) given twice daily from Days 1 to 6 (estrus = Day 0) in ewes decreased (P < 0.05) luteal weights on Day 10 postestrus. Plasma progesterone concentrations differed (P < 0.05) among the treatment groups; toward the end of the experimental period, concentrations in jugular venous blood decreased (P < 0.05) compared with the other treatment groups. Plasma progesterone concentrations in ewes receiving PGE1 or PGE1 + progesterone were greater (P < 0.05) than in vehicle controls or in ewes receiving PGE2 or PGE2 or PGE2 + progesterone. Chronic intrauterine treatment with PGE1 or PGE2 prevented (P < 0.05) decreases in plasma progesterone concentrations, luteal weights, and the proportion of luteal unoccupied and occupied LH receptors on Day 10 postestrus in ewes given exogenous progesterone, but did not affect (P > 0.05) concentrations of PGF2α in inferior vena cava blood. Progesterone given on Days 1 to 6 in ewes advanced (P < 0.05) increases in PGF2α in inferior vena cava blood. We concluded that PGE1 or PGE2 prevented progesterone-induced premature luteolysis by suppressing loss of luteal LH receptors (both unoccupied and occupied). 相似文献
6.
D. M. Grennan I. J. Zeitlin W. S. Mitchell W. W. Buchanan W. C. Dick 《Prostaglandins & other lipid mediators》1975,9(5):799-816
In these experiments we have examined the effects of PGE1, PGE2, PGF1α and PGF2α on synovial perfusion in the normal canine synovial microcirculation. The effects of the drugs on synovial perfusion were determined indirectly from the changes produced in the rate of clearance of 133Xenon from the joint by their intra-articular injection. Prostaglandins PGE1 and PGE2 were found to be strongly vasodilator with PGE1 being the more active. PGF1α appeared to have little or no vasoactive properties in doses up to 1 ugm. (2.8 × 10−5M) in our I preparation while PGF2α was vasodilator at this high dosage only. Neither SC19920 nor diphloretin phosphate antagonised the effects of PGE1 in these experiments. 相似文献
7.
The effects of a wide range of PGE1 and PGE2 concentrations on the isometric developed tension of isolated rat atria beating spontaneously or paced at a fixed rate, were explored. PGE1 only produced a negative inotropic effect (NIE), whereas PGE2 elicited a biphasic inotropic action; negative at low concentrations and positive (PIE) at higher ones. Phenoxybenzamine and phentolamine failed to modify either the NIE or the PIE, but subthreshold exogenous norepinephrine abolished the NIE, suggesting a presynaptic inhibitory effect of PGEs on the adrenergic neurotransmitter release. Auricles pretreated with subthreshold norepinephrine react with a PIE to PGE1, but not to PGE2. On the contrary in the presence of subthreshold methoxamine the PIE of PGE2 was increased whereas the action of PGE1 was not modified. 相似文献
8.
Michel Lagarde Marc Dechavanne Michel Rigaud Jacqueline Durand 《Prostaglandins & other lipid mediators》1979,17(5):685-705
Radioimmunoassays of platelet prostaglandins E1 and F1α in platelet rich plasma or platelet suspension, demonstrate that both PGE1 and PGF1α are present at higher concentrations than prostaglandins E2 and F2α. Gas chromatography — mass spectrometry determinations of prostaglandins E1 and E2 in resting washed platelets confirm this difference. Lastly, there is a greater incorporation of [1-14C] acetate into prostaglandins E1 and F1α compared to that into prostaglandins E2 and F2α. 相似文献
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The phenylephrine-stimulated perfused oviduct of the rabbit was evaluated as a model for studying the activity of prostaglandins that produce inhibition of the oviducal smooth muscle. Elevation of the normal “tone” of the oviduct by perfusing phenylephrine through the lumen permitted quantitation of the responses to PGA2, PGE1 and PGE2 by measuring the magnitude of the inhibitory response produced by the agents. PGE2 was relatively more potent, efficacious and specific for the oviduct than PGA2 or PGE1. It was concluded that the model was suitable for comparative dose-response studies of PGA2, PGE1 and PGE2 and their analogs. 相似文献
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Numerous biochemical pathways influence the synthesis and release of anterior pituitary hormones. Releasing factors extracted from the hypothalamus and prostaglandins (PGs) appear to alter a common biochemical activity, adenyl cyclase, in pituitary cells. Luteinizing hormone releasing hormone (LRH), prostaglandin (PGE1), 7 oxa-13-prostynoic acid and cycloheximide were tested for individual and interacting effects on the in vitro release of FSH, LH and prolactin from hemipituitaries of 15 day old female rats. LRH (10 ng/ml) consistently released both LH and FSH in all in vitro experiments and inhibited prolactin release in 1 of 2 experiments. Lower concentrations (5 and 1 ng/ml) also stimulated LH and FSH release but did not influence prolactin release. Concurrent depletion of stored LH and FSH in the gland was observed. PGE1 in a 6.5 hour incubation increased the storage of LH within the gland in the absence of LRH. In a 1.5 hour incubation in the presence of LRH, storage of LH was also increased. PGE1 had no effect on LH and FSH release; however, in 1 of 2 experiments it stimulated prolactin release in the absence of LRH. Prostynoic acid stimulated LH and FSH release but did not synergize with LRH action in the same tissue. Cycloheximide did not affect LH release during the first 30 minutes of incubation; however, the release during the subsequent 1 hour was significantly inhibited. Similar tissue also exposed to cycloheximide was still responsive to LRH during the latter 1 hour incubation period. Cycloheximide had no effect on prolactin storage and release from the same tissue. 相似文献
11.
Numerous biochemical pathways influence the synthesis and release of anterior pituitary hormones. Releasing factors extracted from the hypothalamus and prostaglandins (PGs) appear to alter a common biochemical activity, adenyl cyclase, in pituitary cells. Luteinizing hormone releasing hormone (LRH), prostaglandin (PGE1), 7 oxa-13-prostynoic acid and cycloheximide were tested for individual and interacting effects on the release of FSH, LH and prolactin from hemipituitaries of 15 day old female rats. LRH (10 ng/ml) consistently released both LH and FSH in all experiments and inhibited prolactin release in 1 of 2 experiments. Lower concentrations (5 and 1 ng/ml) also stimulated LH and FSH release but did not influence prolactin release. Concurrent depletion of stored LH and FSH in the gland was observed. PGE1 in a 6.5 hour incubation increased the storage of LH within the gland in the absence of LRH. In a 1.5 hour incubation in the presence of LRH, storage of LH was also increased. PGE1 had no effect on LH and FSH release; however, in 1 of 2 experiments it stimulated prolactin release in the absence of LRH. Prostynoic acid stimulated LH and FSH release but did not synergize with LRH action in the same tissue. Cycloheximide did not affect LH release during the first 30 minutes of incubation; however, the release during the subsequent 1 hour was significantly inhibited. Similar tissue also exposed to cycloheximide was still responsive to LRH during the latter 1 hour incubation period. Cycloheximide had no effect on prolactin storage and release from the same tissue. 相似文献
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G.J. Wiepz M.C. Wiltbank S.B. Kater G.D. Niswender H.R. Sawyer 《Prostaglandins & other lipid mediators》1993,45(2)
When ovine large luteal cells are placed in culture and exposed to PGF2α, there is a rapid and sustained increase in the concentration of free intracellular calcium which is believed to play a major role in the luteolytic and cytotoxic effects of PGF2α. Since administration of exogenous PGE2 can prevent spontaneous and PGF2α-induced luteolysis in vivo, and the cytotoxic effects of PGF2α on large luteal cells in vitro, the objective of this study was to determine if one mechanism by which PGE2 acts is to attenuate increases in free intracellular calcium induced by PGF2α. At concentrations of 10 nM or greater, PGF2α caused a significant and sustained increase in free intracellular calcium in large luteal cells. Similarly, PGE2 also induced increases in free intracellular calcium but required doses 20-fold greater than PGF2α. When PGE2 (1, 10 or 100 nM) was incubated with PGF2α (100 nM) increases in free intracellular calcium induced by PGF2α were attenuated (P<0.05) when measured 5 min, but not at 30 min, after initiation of treatment. The observed decrease in the concentration of free intracellular calcium at 5 min in response to PGF2α was the result of fewer cells responding to PGF2α. In addition, the concentrations of free intracellular calcium attained in the cells that did respond was reduced 25% compared to cells treated with PGF2α alone. Thus, part of the luteal protective actions of PGE2 appears to involve an inhibition of the early (5 min) increase in free intracellular calcium induced by PGF2α. 相似文献
13.
Roberto P. Rosenkranz 《Prostaglandins & other lipid mediators》1978,15(6):925-942
Intracerebroventricular administration of prostaglandins E1 or E2 was shown to block, while PGF2α increased the incidence of tonic convulsion due to electroshock in mice. The Prostaglandins were administered intracerebroventricularly (i.c.v.) to conscious mice by a modification of Haley and McCormick's method (1) prior to a transcorneal maximal electroshock (MES) or a transcorneal supra-maximal electroshock (SMES). PGE1 and PGE2 i.c.v. blocked the tonic hindlimb extension (THE) and protected the animals from death induced by MES with ED50's for PGE1 and PGE2 for inhibition of the THE of 6.6 (4.3–12.0) μg/mouse i.c.v. and 13.3 (8.9–22.4) μg/mouse i.c.v. respectively. When PGE2 was administered intraperitoneally (i.p.) in doses as high as 4.0 mg/kg it did not block the THE. However, the duration of the THE as well as the mortality were reduced by doses of 0.5–4.0 mg/kg PGE2 i.p.. Both PGE1 and PGE2 were shown to cause a dose related significant (p<.001) decrease in the duration of the THE with SMES in doses of 1–10 μg/mouse i.c.v. for PGE1 and 2–40 μg/mouse i.c.v. for PGE2. PGF2α, administered i.c.v. prior to a transcorneal electroshock equivalent to a current at the ED1 level, increased the incidence of the THE as well as the mortality in doses of 20–50 μg/mouse. 相似文献
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Prostaglandins are well known for their ability to stimulate contraction in gastrointestinal smooth muscle, yet very little information is available on how their activity affects propulsion
. Thus, studies were undertaken to determine the effect of various prostaglandins on qastric emptying (GE) and small intestinal transit (SIT) in unanesthetized fasted rats. Rats were treated with intravenous, subcutaneous, or oral PGF2α, PGE2, or 16,16 dimethyl PGE2 at various doses, followed 1 (intravenous), 20 (subcutaneous) or 10 (oral) mins later by intragastric 51Cr oxide in black ink. Forty-five mins later, rats were sacrificed by CO2 asphyxiation, the pylorus clamped, and the gut excised. SIT was expressed as the percent of intestinal length traveled by the most distal portion of ink. GE was expressed as the percent of the 51Cr emptied into the intestines. If GE was affected by prostaglandin treatment, the experiments were repeated with rats pre-implanted with duodenal cannula. This preparation allowed the visual transit marker to be deposited directly into the dueodenum, thus avoiding acceleration or delay of SIT caused by fluctuations in GE. The results of these studies show that: (1) intravenous 16,16 dimethyl PGE2 (5–50 μg/kg), but not PGF2α or PGE2, accelerates GE and delays SIT; (2) oral prostaglandin administration increases SIT; (3) oral 16,16 dimethyl PGE2 delays GE; (4) subcutaneous 16,16 dimethyl PGE2 accelerates, has no effect upon, or delays GE depending upon dose, but accelerates SIT at all doses tested; and (5) subcutaneous PGE2 accelerates SIT while PGF2α does not. Thus, the effect of prostaglandins on GE and SIT depends upon the dosage and route of administration as well as type of prostaglandin used. 相似文献
15.
E. Schillinger G. Prior A. Speckenbach S. Wellershoff 《Prostaglandins & other lipid mediators》1979,18(2):293-302
Sulprostone is a tissue-specific PGE2-derivative with high abortifacient activity in various species including man. The dissociation constant KD of the receptor binding of this compound was compared with PGE2 and PGF2α in various tissue preparations of different species. A structure-binding relationship was developed from competition curves after a logit/log transformation. It is demonstrated that the relative affinities of Sulprostone, PGE2 and PGF2α remain essentially constant in all the tissues investigated. It is concluded that the tissue-specificity of Sulprostone cannot be ascribed to structural differences of the receptor molecule. 相似文献
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R.N.V. Prasad A.C. Roy S.R. Kottegoda S.S. Ratnam S.M.M. Karim 《Prostaglandins & other lipid mediators》1985,29(2):269-272
To determine the release and absorption profile of prostaglandin E2 from a new vaginal film formulation containing 850 μg PGE2, serial plasma levels of 13,14-dihydro-15-keto PGE2 were measured by radioimmunoassay in pregnant women between 16 and 18 weeks gestation. A control group, using placebo vaginal film was included in the study. There was a somewhat uniform increase in the plasma levels of the PGE2 metabolite, reaching peak levels between 4 and 6 hours after application of the film. The findings suggest that this drug formulation could be used clinically when slow constant release of the prostaglandin is required over a period of hours such as in pre-induction cervical ripening of term pregnancy. 相似文献
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Uffe Bang Olsen 《Prostaglandins & other lipid mediators》1981,21(4):591-597
Normal conscious female Sprague-Dawley rats were treated with chlorazanil (3 mg/kg i.p.), and urine was collected for 3 hours. Urine prostaglandin E2-excretion increased from 25±3 to 271±32 ng/kg/3 h. The enhancement of urine PGE2-excretion was inhibited by pretreatment with bumetanide (75 mg/kg p.o.). In separate experiments the papillary quantity of PGE2 was determined in freshly homogenized tissue. The basal level (14±2 ng PGE2/papilla) was increased by chlorazanil to 51±11 ng PGE2/papilla and 24±7 ng PGE2/papilla at one and two hours respectively after drug administration. The capacity of chlorazanil to increase medullary PGE2 accumulation was unaffected by bumetanide dissociated the medullary PGE2 level from the excretion of PGE2 in urine, when the former was elevated by chlorazanil. 相似文献
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C. Weems G. Hoyer R. Magness G. Whysong M. Huie 《Prostaglandins & other lipid mediators》1985,29(2):233-241
Fifteen ewes were assigned as they came into estrus to the following randomized treatment groups: 1) Vehicle (1 ml corn oil + vehicle Na2CO3 buffer), 2) Estradiol-17β + vehicle and 3) Estradiol-17β + PGE2 (500 μg) in Na2CO3 buffer (5 ewes/treatment group). Prostaglandin E2 was given through an intrauterine cannula every four hours from days 8 through 15 postestrus. PGE2 prevented a luteolytic dose of estradiol-17β given on days 9 and 10 from causing a precious luteolysis. PGE2 maintained concentrations of progesterone in peripheral blood (days 8 through 15) and weights and concentrations of progesterone in corpora lutea on day 15 postestrus of ewes receiving estradiol-17β. It is concluded that chronic intrauterine infusions of PGE2 can prevent an estradiol-17β-induced premature luteolysis. 相似文献
20.
Using perfused livers of rats fasted for 48 hours, glucose production and incorporation of 2-14C pyruvate (trace dose) into perfusate glucose were studied. Both were found to be inhibited by PGE1 (infused at a concentration of 0.5 μg/min) by about 60 %. The incorporation of 1-14C glycerol into perfusate glucose and into glycerol-glyceride part of the liver glycerides were also studied, using the same test conditions. The former incorporation was significantly inhibited (56%) and the latter strongly stimulated (360 %) by PGE1. PGE1 had no effect on glucose production in a perfusate overloaded with sodium pyruvate, nor on pyruvate carboxylase and phospho-enolpyruvate carboxykinase activity. This was in contrast with the results obtained in perfusions with a trace dose of 2-14C pyruvate. The results showed that PGE1, at the physiological concentration used, stimulated the incorporation of 1-14C glycerol into glycerol-glyceride part of liver glycerides and, when there was no overload of pyruvate present in the perfusion medium, inhibited gluconeogenesis at some point, possibly, but perhaps not exclusively, between the glycerol and glucose steps. 相似文献