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1.
The relationship between high glucose concentrations and arachidonic acid metabolism in uterine tissue from control and diabetic ovariectomized rats was evaluated. Uterine tissue from diabetic rats produced amounts of PGE2 and PGF similar to controls, while a lower production of 6-keto-PGF (indicating the production of prostacyclin) and a higher production of TXB2 (indicating the generation of TXA2) was found in the diabetic group. A group of diabetic rats was treated with phlorizin to diminish plasma glucose levels. Phlorizin treatment did not alter production of PGE2, PGF, and 6-keto-PGF in the diabetic group. A diminished production of TXB2 was found in the treated diabetic uteri when compared to the non-treated diabetic group. Moreover, a positive correlation between plasma glucose levels and uterine TXB2 generation was observed. When control uterine tissue was exposed in vitro to high concentrations of glucose (22 mM) and compared to control tissue incubated in the presence of glucose 11 mM alterations in the generation of PGE2, PGF, and 6-keto-PGF were not found, but a higher production of TXB2 was observed and values were similar to those obtained in the diabetic tissue. Alteration in the production of the prostanoids evaluated were not observed when diabetic tissue was incubated in the presence of high concentrations of glucose. These results provide evidence of a direct relationship between plasma glucose levels and uterine production of TXA2.  相似文献   

2.
Vehicle or 8 or 16 mg of PGF per 58 kg body weight was given intramuscularly to intact, hysterectomized or ovariectomized 90–100 day pregnant ewes in three separate experiments. Both doses of PGF increased PGF in ovarian venous plasma compared with controls at 72 hr post treatment in intact (P≤0.05) but did not in hysterectomized (P≥0.05) 90–100 day pregnant ewes. Concentrations of PGE in ovarian venous blood of intact ewes did not differ (P≥0.05) between treatment groups and were equivalent to concentrations of PGE determined in uterine venous plasma. PGE was decreased in ovarian venous plasma by PGF in hysterectomized ewes (P≤0.07). PGE in uterine venous plasma averaged 6 ng/ml over the 72-hr treatment period in intact and ovariectomized 90–100 day pregnant ewes and was 12 fold greater (P≤0.05) than PGF which averaged 500 pg/ml in uterine venous plasma. Both PGF and PGE increased (P≤0.05) by 64 hr in uterine venous plasma of the 8 mg PGF — treated intact pregnant ewes. A significant quadratic increase (P≤0.05) was observed for PGF and PGE in the vehicle and both PGF treatment groups of intact ewes at the end of the 72-hr sampling period. It is concluded that the uterus and ovaries secrete significant quantities of PGE but little PGF during midgestation. In addition, PGF increased uterine secretion of PGE . PGE may be a placental stimulator of ovine placental secretion of progesterone or PGE may protect placental steroidogenesis from actions of PGF.  相似文献   

3.
Four antiestrogens (anordiol, tamoxifen, RU 39411, ICI 182780) and the antiprogestin, mifepristone (RU 486), were administered to the following three animal models: (1) ovariectomized rats, (2) mated rats treated post-coitally; and (3) pregnant rats treated post-implantation. The antiestrogens were administered alone or in combination with mifepristone at doses effective in preventing and/or terminating pregnancy in rats. The objective of the study was to determine whether these drugs influenced uterine concentrations of prostaglandins (PGF and PGE2).Antiestrogens administered alone to ovariectomized rats did not effect uterine PGE2 or PGF concentrations; whereas the combination of anordiol/mifepristone increased uterine PGF concentration, resulting in an increase in the PGF/PGE2 ratio.Mated rats were treated post-coitally for three consecutive days with anordiol, tamoxifen, estradiol and mifepristone alone and with the combination of anordiol/mifepristone and tamoxifen/mifepristone. An increase in uterine PGF concentrations and in the PGF/PGE2 ratio occurred only in anordiol/mifepristone treated group. A decrease in uterine PGE2 concentrations occurred in animals treated with anordiol, tamoxifen and estradiol, resulting in an increase in the PGF/PGE2 ratio.Anordiol (5.0 mg/kg/day) and mifepristone (4.0 mg/kg/day) alone and the combination of anordiol/mifepristone (2.5/1.0 mg/kg/day) administered to pregnant rats on days 7, 8 and 9 of pregnancy induced an increase in PGF levels without affecting uterine PGE2 concentration. The changes in uterine PGF concentrations induced by anordiol and the combination of anordiol/mifepristone resulted in an increase in the PGF/PGE2 ratio.The antiestrogens tested except for ICI 182780 possessed agonist activity when assayed by measuring their capacity to increase the uterine weights in ovariectomized rats. Also, ICI 182789 was the only antiestrogen that did not influence uterine PG concentrations. It can be concluded that ICI 182780 is the only “pure” antiestrogen among those tested.The present results show that antiestrogens and the combination of mifepristone plus anordiol at doses preventing implantation and terminating pregnancy increase uterine PGF and/or decrease PGE2 concentrations, resulting in an alteration of PGF/PGE2 ratio. These findings suggest that there exists a critical balance of PGF to PGE2 concentrations in the uterus required for the normal passage of fertilized ova through the oviduct, initiating implantation of the blastocysts, development of embryos, and maintenance of pregnancy.  相似文献   

4.
Normal cyclic dairy cattle (n=7) underwent a midventral laparotomy on day 17 of the estrous cycle and were fitted, ipsilateral to the CL, with: an electromagnetic flow transducer around the uterine artery (UA; n=5); catheters within the ovarian vein (OV; n=7) via a uterine branch of the ovarian vein, uterine branch of the ovarian artery (UBOA; n=5) and facial artery (FA; n=7). On day 18, blood samples were collected at 30 min intervals for 1 h prior to injection of estradiol-17β (E2; 3 mg) and 12 h post-E2. Uterine blood flow (UBF) was monitored continuously and plasma samples analyzed for PGF and PGFM. Exact locations of catheters in reproductive tracts were verified post-slaughter. Data were analyzed by method of least squares analysis of variance. Uterine blood flow (ml/min) increased above pre-E2 flow rates within 30 min post-E2 injection, peaked between 2.5 to 3.5 h and declined between 4 to 8.5 h. A small secondary rise in UBF occurred between 9 and 12 h. Regression analysis for concentrations (pg/ml) of PGF and PGFM in the OV (i.e., [OV]-[FA]) demonstrate a similar response as PGFM concentration in the FA in that all increased at approximately 3 h, peaked between 5 and 7 h and returned to near baseline levels by 9 to 10 h post-E2. Facial artery PGFM concentrations were positively correlated with uterine production of PGF (r=.66) and PGFM (r=.30), whereas FA PGF concentrations were not. In three of five cows, a difference in PGF was detected between UBOA and FA (UBOA > FA); supportive of a local countercurrent exchange between the uterine venous drainage and the ovarian artery.  相似文献   

5.
We examined effects of protein kinase C (PKC) activation by phorbol dibutyrate (PDB) on prostaglandin production in astroglia. Astroglia were cultured from sheep fetal cortex and grown in Eagle's basal media supplemented with 10% fetal calf serum (BME-C). Prostaglandin F2a (PGF) levels in media were determined at 2–24 hours after exposure to PDB. PDB increased production of PGF at 10−8M and 10−6M. In addition, PDB increased the ratio of membrane to cytosolic PKC. Coapplication of H7 [1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine] (10−4M) with PDB (10−6M) inhibited PDB-induced PGF2a production. To investigate the role of protein synthesis in increased prostaglandin production by PDB, astroglia were coincubated with actinomycin D (1 mg/ml) or cycloheximide (10 mg/ml). At 4 hrs, both actinomycin D and cycloheximide inhibited increases in PGF2a in response to PDB application. In addition, COX-2 mRNA levels and COX activity levels were examined. PDB increased COX-2 mRNA levels by 2 hours, and COX activity tripled after 12 hr exposure to PDB. In addition, the increase in COX activity was blocked by cycloheximide. In summary, PKC activation promotes enhanced prostaglandin production via an increase in COX synthesis.  相似文献   

6.
The effect of bovine conceptus secretory proteins (CSP) on uterine prostaglandin (PG)-F production was evaluated in dairy cattle following injection of estradiol-17β. Intrauterine injections of dialyzed serum proteins (Control, n=5) or CSP (n=5) were administered from days 15 through 18 post-estrus. Following intrauterine treatments on day 18, all cows were injected with E2 (3 mg) to stimulate uterine PGF production. Plasma concentrations of progesterone (P4) and 15-keto-13,14-dihydro-PGF (PGFM) were determined by RIA. The PGFM responses following E2 challenge were decreased (p<0.01) for cows receiving CSP versus serum proteins into the uterine lumen. Individual PGFM, P4 and cycle length responses are discussed. Data suggest that proteins secreted by the bovine conceptus suppress uterine PGF production during pregnancy recognition in the cow.  相似文献   

7.
In rat luteal cells labeled with (3H]oleic acid, PGF-stimulated phospholipase D (PLD) activation was investigated. The PLD activity was detected by measuring the accumulation of [3H]phosphatidylethanol (PtdEt) in the presence of ethanol. PGF stimulated PtdEt accumulation at concentrations of more than 100 nM in the presence of ethanol. However, PtdEt accumulation did not change in the absence of ethanol. PGF (1 μM) increased PtdEt accumulation after 1 min, and the accumulation reached a plateau by 2–3 min. These results indicate that PGF activates PLD in rat luteal cells. U-73122, a phospholipase C (PLC) inhibitor, and staurosporine, a protein kinase C (PKC) inhibitor, did not inhibit PGF-stimulated [3H]PtdEt accumulation. These results suggest that PGF-induced PLD activation is different from PLC-PKC systems. We reported previously that PGF stimulated the release of arachidonic acid. The effects of indomethacin, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), inhibitors of arachidonic acid metabolism, on PGF-stimulated PtdEt accumulation were examined. Pretreatment with indomethacin enhanced PGF-induced PtdEt accumulation. In contrast, pretreatment with NDGA and ETYA inhibited PGF-induced PtdEt accumulation. It is suggested that PGF-stimulated PLD activation is mediated via lipoxygenase products.  相似文献   

8.
Effects of 10 ppm nitrogen dioxide (NO2) exposure on the contents of prostaglandins (PGs) and thromboxane (TX) B2 in broncho-alveolar lavage (BAL) of rats were studied. In the BAL of normal rats, the amounts of PGs and TXB2 in the whole lavage were 6-keto-PGF (38.0 ± 6.4 ng) > TXB2 (11.8 ± 4.0 ng) > PGF2α (5.7 ± 1.6 ng) PGE (0.5 ± 0.3 ng). Rats were exposed to NO2 for 1, 3, 5, 7 and 14 days. The NO2 exposure decreased in the level of 6-keto-PGF by about 35% throughout the exposure. The level of TXB2 was higher in the day 5 exposure group (155%). The contents of PGF and PGE first, decreased and then transiently increased on days 3 and 5. PG 15-hydroxy-dehydrogenase activity of lung homogenate decreased correspondingly on day 3 and 5. Then the contents PGF and PGE decreased on day 7 and 14.6-keto-PGF and TXB2 are stable metabolites of PGI2, a strong bronchorelaxant and TXA2, a strong bronchoconstrictor respectively. Therefore the results suggested that the decrease in 6-keto-PGF, a major prostanoid in the BAL and the increase in TXB2 may correlate with broncho constriction by NO2 exposure.  相似文献   

9.
We have measured by radioimmunoassay the production of leukotrienes (LTC4 and LTB4) and prostaglandins (PGE2 and PGF) in the rat uterus on Days 1 through 6 of pregnancy. The production is defined as the synthesis minus the degradation for a defined period. The production of LTC4 or LTB4 remained unaltered on days 1–3, but exhibited a marked increase on Day 4 showing a peak at noon. This was then followed by a sharp decline on Day-5 morning. A small but consistent peak in uterine LT production was also noticed on Day-5 noon prior to implantation and this was followed by a decline on Day-6 morning i.e. after initiation of implantation. The production profile of PGE2 and PGE showed a striking resemblance to that of LTs; one exception being that maximal PG production was noticed on Day-4 morning and preceded the peak production of LTs. These vasoactive arachidonate derivatives reached their peak production rates at around the time when a surge in estrogen level is noticed in the uterus on Day 4. Implantation is a local proinflammatory type of reaction that is associated with increased uterine vascular permeability. Vascular changes in inflammatory reactions are provoked by two kinds of chemical mediators: (1) vasodilators and (2) agents that increase vascular permeability. PGs (especially of the E series) are known as vasodilators, while LTs and histamine mediate increases in vascular permeability. Therefore, an interaction between LTs, PGs, and histamine could be important for uterine preparation for implantation and/or implantation .  相似文献   

10.
Endometrial concentrations of prostaglandins F2α (PGF2α) and E2 (PGE2) were measured by specific radioimmunoassay in sheep, on day 14 of estrous cycle or pregnancy, during luteolysis (Day 16 of the cycle), and after implantation (Day 23 of pregnancy) : concentrations observed on day 14 of cycle and pregnancy were similar. During luteolysis, on day 16 of cycle, a consistent drop was noticed. If luteal regression did not occur, as a consequence of the presence of an embryo, endometrial concentrations of PGF2α on day 23, were twice those of day 14, and PGE2 remained unchanged. 2 hour incubations of endometrial caruncular tissue from 14 days cyclic or pregnant ewes resulted in de novo synthesis of PG which could be increased by Arachidonic Acid and inhibited by Indomethacin; during the first 30 min of incubation, the PGF2α synthesis was comparable for both endometrial tissues, whereas PGE2 synthesis was twice as great in pregnant endometrium. Fourteen and 23 day conceptuses had high PGF2α and PGE2 concentrations which were not due to maternal PG sequestration : PG synthesis which could be inhibited by Indomethacin was observed in incubated 14 day old embryos. Treatment of pregnant ewes from day 7 to day 22 after mating, either with Indomethacin (300 mg s.c. daily) or with Acetylsalicylic Acid (1 g I.V. daily) resulted in a sharp diminution of endometrial PG concentration and release, with no apparent effect on the establishment of pregnancy. These results tend to ascribe a less important role to PG during early pregnancy in sheep as compared with rodents, in terms of embryonic growth and implantation.  相似文献   

11.
The physiological basis of uterine contractility in laying hens is not well understood, but a better understanding is important for understanding the mechanisms governing egg laying. The characteristics of uterine contractility arising spontaneously or by prostaglandin F (PGF) stimulation were therefore examined and the underlying mechanisms investigated. Uterine strips were isolated from laying hens 4 h before oviposition and force measured. These strips remained healthy in vitro and produced regular spontaneous contractions. The contractions were phasic and could be recorded for several hours. Exposure to nifedipine, the specific L-type Ca channel blocker, led to the abolition of force. The contraction amplitude and frequency were significantly increased when Bay K8644, an agonist of L-type Ca channels, was applied or when the concentration of extracellular Ca was elevated. Spontaneous contractions were also significantly inhibited by wortmannin, the specific inhibitor of myosin light chain kinase (MLCK). When 1 μM PGF was applied to spontaneously contracting uterus, it significantly increased their amplitude and frequency of the contractions. As with spontaneous contractions, PGF-induced force production was abolished by nifedipine and wortmannin. In the absence of extracellular Ca, a small but tonic force was generated upon application of PGF which was not affected by wortmannin. Thus, extracellular Ca entry and MLCK phosphorylation are essential for uterine force production occurring spontaneously or by PGF stimulation. Our data supports the conclusion that the pathway dependent on extracellular Ca entry and MLCK phosphorylation predominates during PGF stimulation but suggests some involvement of an alternative force-producing pathway, presumably Ca-sensitization.  相似文献   

12.
Objective: To test for differences in the amount and activity of peritoneal macrophages present in the peritoneal fluid of women with, and without endometriosis using prostaglandin release by macrophages in culture as a marker.Patients: Women of reproductive age undergoing laparoscopy for infertility or chronic pelvic pain with postoperative diagnosis of endometriosis and women undergoing laparoscopy for sterilization.Methods: Peritoneal fluid was aspirated during laparoscopy, volume was recorded, macrophages were isolated via a Ficoll Paque gradient and kept in primary culture. PGE2 and PGF release of the cells were measured before and after stimulation with zymosan.Results: Women with endometriosis had significantly more peritoneal macrophages than controls. Peritoneal macrophages of women with endometriosis released significantly more PGE2 than those of the control group: 8.4 ± 2.0 versus 1.4 ± 0.4 ng/ml/106cells (mean ± SEM, p=0.0005) and PGF : 10 ± 4.3 (endometriosis) versus 1.8 ± 0.4 (control) ng/ml/106cells (mean ± SEM, p = 0.045).Conclusion: There is a significant increase in the amount of prostaglandins released by peritoneal macrophages from women with endometriosis. These prostaglandins might alter uterine and tubal contractility, thereby affecting fertility.  相似文献   

13.
This study was conducted in vitro to examine factors that may regulate prostaglandin release by bovine trophoblast and endometrial slices. Trophoblastic tissues and endometrial slices were recovered from superovulating and normally-ovulating cattle on day 16 or 20 of pregnancy and incubated for 24 h. Release of PGF2α and 13,14-dihydro-15-keto-PGF2α (PGMF), and incorporation of [14C]-leucine into proteins were quantified and expressed per μg DNA, which gives a measure of cellular activity. Activity of trophoblastic tissue for synthesizing protein was decreased (P<.05) and for releasing PGMF was increased (P<.05) on day 20 compared to day 16 of pregnancy. Neither supercovulation nor day of pregnancy altered trophoblastic activity for releasing PGF2α. Supercovulation increased (P<.05) endometrial release of PGF2α. Endometrial release of PGF2α was less (P<.05) on day 20 than on day 16 of pregnancy. When arachidonic acid (0, 100, 200 or 400 μg) was added at the start of incubation, trophoblastic release of PGF2α changed (P<.05) quadratically with dose of arachidonic acid. When arachidonic acid was added 8 h after the start of incubation, triphoblastic release of PGF2α increased linearly (P<.01) with dose of arachidonic acid. Adding arachidonic acid to incubation medium did not affect trophoblastic or endometrial protein synthesis. Endometrial slices suppressed (P<.05) trophoblastic protein synthesis and release of PGF2α. Apparently, endometrium can modulate trophoblastic release of prostaglandins and synthesis of proteins in vitro, and trophoblastic tissue from supercovulated cattle 16 or 20 days pregnant can be used to study trophoblastic synthesis of prostaglandins and proteins.  相似文献   

14.
Prostacyclin was infused into the uterus of non-pregnant women either during early menstruation or in the secretory phase of the cycle. A dose of 5 μ/min produced little systemic effect and caused a significant decrease in uterine activity on Days 1 and 2 of the menses whereas 0.5 μg/min did not. However, when dysmenorrhoeic pain and increased uterine activity were produced by infusion of PGF during the secretory phase, PGI2 neither decreased the activity nor the pain. This indicates that PGI2 does not cause uterine relaxation by blocking the action of PGF.  相似文献   

15.
Prostaglandin biosynthesis was studied in the rat uterus during the oestrous cycle. Uterine homogenates were incubated for 20 minutes in the presence of exogenous substrate (2.10−5M). PGF and PGE2 were measured by R.I.A.. A sharp peak PGF and a smaller peak of PGE2 were observed at prooestrus, 20 h. Another small PGE2 peak occurred at dioestrus II, 15 h. The lowest values of both PGs were found on dioestrus, 15 h. Plasma oestradiol concentration were highest at proestrus, 15 h and 20 h. A sharp progesterone peak occurred at prooestrus, 20 h. The PGF peak is next to the oestradiol peak and is superimposable or lags slightly beyond the progesterone peak.Incubation with 14C arachidonic acid and subsequent analysis of extracts by TLC and scanning showed that the major metabolite is PGI2, identified as 6 keto PGF. The conversion rate of arachidonic acid into 6 keto PGF is 5 times higher than into PGF. 6 keto PGF was further identified by GC/MS. No significant difference was observed between 6 keto PGF production during oestrus and dioestrus.  相似文献   

16.
7β-hydroxy-epiandrosterone (7β-OH-EPIA) has been shown to be cytoprotective in various organs including the brain. It has also been shown that prostaglandin D2 (PGD2) and its spontaneous metabolite 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) are also cytoprotective. It is possible that these prostaglandins derived from circulating mononuclear cells may mediate the actions of 7β-OH-EPIA. The aim of this study, therefore, was to ascertain the effect of 7β-OH-EPIA (in the absence or presence of tumour necrosis factor-α (TNF-α)), a pro-inflammatory stimulus, on the biosynthesis of PGD2, PGE2 and 15d-PGJ2 from human mononuclear cells. Prostaglandins were measured by enzyme immunoassay (EIA). 7β-OH-EPIA alone induced a concentration-dependant increase in the production of PGD2. TNF-α increased PGD2 levels which were enhanced by 7β-OH-EPIA. 7β-OH-EPIA increased 15d-PGJ2 levels both in the absence and presence of TNF-α. 7β-OH-EPIA alone had no effect on PGE2 biosynthesis but suppressed TNF-α-induced PGE2 circa 50%. 7β-OH-EPIA also increased the level of free arachidonic acid and radiolabelled prostaglandins in cells pre-incubated with radiolabelled arachidonic acid, indicating that the increase may occur via the enhanced release of substrate arachidonic acid. 7β-OH-EPIA did not affect levels of the anti-inflammatory cytokine IL-10 indicating that this is an unlikely mechanism by which 7β-OH-EPIA induces its actions but more likely exerts its effects via the production of cytoprotective prostaglandins.  相似文献   

17.
Antibodies directed toward PGF were prepared in rabbits. The serologic specificity of the immune reaction was determined by inhibition of sodium borohydride-reduced (3H) PGE2 anti-PGF binding by several prostaglandins. The antibodies to PGF recognize the β-hydroxyl configuration in the cyclopentane ring of PGF. With the use of both anti-PGF and anti-PGF, the product of PGE2 reduction by 9-ketoreductase purified from chicken heart was identified as PGF. Guinea pig liver and kidney homogenates were examined for PGE 9-ketoreductase activity. Although enzyme activity was present, no evidence of PGF production was found.  相似文献   

18.
Pregnancies in hamsters may be terminated with 10 μg PGF administered b.i.d. on days 4, 5 and 6 of gestation. Small (250 μg and above) daily injections of progesterone on the same days will reverse this PG effect; in contradistinction, 10 mg of progesterone per day failed to maintain normal pregnancies in hamsters spayed on day 5. Daily administration of 3 mg of progesterone and 1 μg of estrone essentially normalized the gestation; administration of PGF at 10 mg on days 5, 6 and 7 of pregnancy in steroid-maintained rats, resulted in pregnancy termination in all animals, while 1 mg was partly effective. These data demonstrate an extra-ovarian site of action of prostaglandin F on pregnancy in hamsters.  相似文献   

19.
The effects of prostaglandin (PG)F and PGF, 1–15 lactone were compared in luteal phase, non-pregnant and in early pregnant rhesus monkeys. Animals treated with either PG after pretreatment with human chorionic gonadotropin (hCG) had peripheral plasma progesterone concentrations that were not statistically different from those in animals treated with hCG and vehicle. However, menstrual cycle lengths in monkeys treated with PGF, 1–15 lactone were significantly (P <0.02) shorter than those in vehicle treated animals. In the absence of hCG pretreatment, plasma progesterone concentrations were significantly (P <0.008) lower by the second day after the initial treatment with either PGF or PGF, 1–15 lactone than in vehicle treated monkeys. Menstrual cycle lengths in monkeys treated with either PG were significantly (P <0.04) shorter than those in animals treated with vehicle. There were no changes in plasma progesterone concentrations in early pregnant monkeys treated with PGF, and pregnancy was not interrupted. In contrast, plasma progesterone declined and pregnancy was terminated in 5 of 6 early pregnant monkeys treated with PGF, 1–15 lactone. These data indicate that PGF, 1–15 lactone decreases menstrual cycle lengths in non-pregnant rhesus monkeys. More importantly, PGF, 1–15 lactone terminates early pregnancy in the monkey at a dose which is less than an ineffective dose of PGF.  相似文献   

20.
The effects of the bisenoic prostaglandins on the uterine vasculature and uterine contractile activity have been evaluated in an unanesthetized chronically catheterized nonpregnant sheep preparation. Changes in uterine blood flow were monitored with electromagnetic flow probes while uterine contractile activity and tone were determined via an intra-uterine balloon connected to a pressure transducer. Prostaglandins A2, D2, E2, and prostacyclin (PGI2) were all found to be vasodilators. PGD2 and PGI2 were much more potent than PGA2 and PGE2 in dilating the uterine vasculature. The prostacyclin breakdown product 6-keto PGF, PGF, thromboxane B2, and the endoperoxide analogues U44069 and U46619 produced vasoconstriction of the uterine vasculature. Prostaglandins A2, D2 and F increased while PGI2 decreased uterine contractile activity. PGF also increased uterine tone suggesting that a portion of its vasoconstrictor activity may be due to mechanical compression of the uterine vasculature.  相似文献   

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