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1.
The cerebral cortical action of prostaglandin F (PGF) has been determined by recording the effects of intracarotid injections of PGF on cerebral evoked potentials. PGF differentially reduced cortical evoked potentials. The cortical action of PGF appeared to be qualitatively identical with that of norepinephrine (NE) but weaker. A protection of the cortex from the inhibitory action of NE by a preceding dose of PGF was demonstrated. The actions of both PGF and NE appear to be on the same or related postsynaptic receptors. The actions described were at doses that did not reduce oxygen availability. PGF may act as a modulator of adrenergic transmission in the cortex. The intracellular recording in the companion paper supplies the further critical evidence that PGF has a synaptic inhibitory action.  相似文献   

2.
Prostaglandin F2α (5μg/kg, i.v.) causes an increase in pulmonary arterial pressure, decrease in systemic arterial pressure, and reflex bradycardia in the anesthetized cat. The same dose of the 15-methyl analogue of PGF2α produces the same triad of effects but of greater magnitude and duration. Although prostaglandins F1α, F2β and F1β also cause the same cardiovascular effects as F2α, there is a decrease in potency for all parameters measured, with PGF2α>PGF1α>PGF2β>PGF1β. When compared to the actions of PGF2α in producing an increase in pulmonary arterial pressure, PGs F1α, F2β and F1β were less potent by approximately 10, 100, and 1000 fold respectively.  相似文献   

3.
To evaluate the details of the adrenergic stimulation of urinary prostaglandins in man, ten normal volunteers were given various agonists and antagonists. The effect of 4 hour IV infusions of norepinephrine (NE), NE + phentolamine (PHT), NE + phenoxybenzamine (PHB), NE + prazosin (PZ), isoproterenol (ISO), and PHT alone on urinary PGE2 and PGI2 (6 keto PGF) were determined. PGE2 and 6 keto PGF were measured by radioimmunoassay from 4 hour urine samples. NE stimulated both PGE2 (196±40 to 370±84 ng/4 hrs/g creatinine and 6 keto PGF1α(184±30 to 326±36), both p<0.01. In contrast, ISO had no effect on either PGE2 or 6 keto PGF excretion. Alpha blockade with PHT. PHB, or PZ inhibited the NE induced systemic pressor effect. However, the effect of the alpha blockers on the NE induced stimulation of PGE2 and 6 keto PGF varied. PHT did not alter the NE stimulated PGE2 or 6 keto PGF release (370±84 vs. 381±80) PGE2 and (326±50 vs. 315±40) 6 keto PGF, both p>0.2). PHT alone stimulated only 6 keto PGF. PHB and the specific α1 antagonist PZ similarly eliminated the NE induced prostaglandin release. These results suggest that adrenergically mediated urinary prostaglandin release in man is via an alpha receptor with α1 characteristics.  相似文献   

4.
The susceptibility of induced corpora lutea (CL) of prepuberal gilts and spontaneously formed CL of mature gilts to prostaglandin F (PGF) luteolysis was studied. Prepuberal gilts (120 to 130 days of age) were induced to ovulate with Pregnant Mare Serum Gonadotropin and Human Chorionic Gonadotropin (HCG). The day following HCG was designated as Day 0. Mature gilts which had displayed two or more estrous cycles of 18 to 22 days were used (onset of estrus = Day 0). Gilts were laparotomized on Day 6 to 9, their CL marked with sterile charcoal and totally hysterectomized. On Day 20, gilts were injected IM with either distilled water (DW), 2.5 mg PGF or 5.0 mg PGF. An additional group of prepuberal gilts was injected with 1.25 mg PGF, a dose of PGF equivalent, on a per kilogram body weight basis, to the 2.5 mg PGF dose given to the mature gilts. The percentages of luteal regression on Day 27 to 30 for mature and prepuberal gilts given DW, 2.5 mg PGF and 5.0 mg PGF were 0.0 vs 4.4, 43.5 vs 96.8 and 47.7 vs 91.6, respectively; the percentage of luteal regression for the prepuberal gilts given 1.25 mg PGF was 75.1. These results indicate that induced CL of the prepuberal gilt were more susceptible to PGF luteolysis than spontaneously formed CL of the mature gilt and that pregnancy failure in the prepuberal gilt could be due to increased susceptibility of induced CL to the natural luteolysin.  相似文献   

5.
Radioimmunoassays for measuring prostaglandin F (PGF) and 5α, 7α-dihydroxy-11-keto tetranorprosta-1,16-dioic acid, PGF-main urinary metabolite (PGF-MUM), with 125I-tyrosine methylester amide (TMA) of PGF and PGF-MUM were developed.Antibody to PGF was produced in rabbits immunized with conjugates of PGF coupled to bovine serum albumine. Antibody to PGF-MUM was also produced in rabbits immunized with conjugates of PGF-MUM coupled to bovine serum albumin.PGF-125I-TMA had an affinity to antiserum to PGF. PGF-MUM-125I-TMA also responded to antiserum to PGF-MUM.  相似文献   

6.
When ovine large luteal cells are placed in culture and exposed to PGF, 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 PGF. Since administration of exogenous PGE2 can prevent spontaneous and PGF-induced luteolysis in vivo, and the cytotoxic effects of PGF 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 PGF. At concentrations of 10 nM or greater, PGF 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 PGF. When PGE2 (1, 10 or 100 nM) was incubated with PGF (100 nM) increases in free intracellular calcium induced by PGF 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 PGF was the result of fewer cells responding to PGF. In addition, the concentrations of free intracellular calcium attained in the cells that did respond was reduced 25% compared to cells treated with PGF 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 PGF.  相似文献   

7.
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   

8.
In humans eicosapentaenoic acid can be converted to 3-series prostaglandins (PGF, PGI3, and PGE3). Whether 3-series prostaglandins can protect the gastric mucosa from injury as effectively as their 2-series analogs is unknown. Therefore, we compared the protective effects of PGF and PGF against gross and microscopic gastric mucosal injury in rats. Animals received a subcutaneous injection of either PGF or PGF in doses raning from 0 (vehicle) to 16.8 μmol/kg and 30 min later they received intragastric administration of 1 ml of absolute ethanol. Whether mucosal injury was assessed 60 min or 5 min after ethanol, PGF was significantly less protective against ethanol-induced damage than PGF. These findings indicate that the presence of a third double bond in the prostaglandin F molecule between carbons 17 and 18 markedly reduces the protective effects of this prostaglandin on the gastric mucosa.  相似文献   

9.
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   

10.
Potential interactions between PGD2 and PGF in the mesenteric and renal vascular beds were investigated in the anesthetized dog. Regional blood flows were measured with electromagnetic flow probes. PGD2, PGF and Norepinephrine (NE) were injected as a bolus directly into the appropriate artery, and responses to these agents were obtained before, during and after infusion of either PGD2 or PGF into the left ventricle. In each case, the infused prostaglandin caused vascular effects of its own. Left ventricular infusion of PGD2 reduced responses to local injections of PGD2 in the intestine, and a similar effect was observed for PGF, suggesting significant receptor or receptor-like interactions for each of the prostanoids. However, systemic infusion of prostaglandin F (20–100 ng/kg/min) had no effect on renal or mesenteric vascular responses to local injection of prostaglandin D2. Similarly, PGD2 administration (100 ng/kg/min) did not affect responses to PGF in the intestine. The present results therefore suggest that these prostaglandins, i.e., D2 and F, act through separate receptors in the mesenteric and renal vascular beds. In addition, increased prostaglandin F levels produced by infusion of F reduced mesenteric but not renal blood flow, suggesting that redistribution of cardiac output might participate in side effects often observed with clinical use of this prostaglandin, such as nausea and abdominal pain.  相似文献   

11.
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   

12.
Prostaglandin F (PGF) at 14, 30 or 50 μg/hamster/day from Days 3–5 of pseudopregnancy (PSP) shortens PSP from a mean length of 9.1 to 5.6–7.9 days, depending on the dose of PGF administered. Bilateral intrauterine device (BIUD) bearing hamsters exhibit a mean length of PSP of 9.2 days, which is comparable to that in normal saline controls. Combination of PGF (14 μg/day on Days 3–5 of PSP) and BIUD also resulted in shortening of PSP although the mean length of PSP resulted from the combined treatment was not significantly different from those PSP animals treated with 14 μg/day of PGF alone. It is concluded that the antifertility effect of intrauterine device possibly is attributed to a small and continuous release of PGF which interferes with the normal implantation processes but does not curtail PSP.  相似文献   

13.
Prostaglandin F (PGF) was measured by immunoassay in plasma and milk of four cows (six experiments). After 30 mg PGF im, plasma PGF peaked at 15 minutes (2.4 ± 0.7 ng/ml) and declined toward basal values by 3 hours; maximum milk PGF (0.91 ± 0.12 ng/ml) occurred at 1 hour. The average excretion rate in milk was 2.9 μg/day 0.9 μg (0.003%) of which was due to the 30 mg PGF injected. In six non-pregnant control cows, daily changes of milk PGF and progesterone were not consistently related.  相似文献   

14.
The present study has been performed to investigate how PGs would participate the hatching process. Effects of indomethacin, an antagonist to PGs biosynthesis, on the hatching of mouse blastocysts were examined in vitro. Furthermore, it was studied that prostaglandin E2 (PGE2), prostaglandin F (PGF) or 6-keto-prostaglandin F (6-keto-PGF) were added to the culture media with indomethacin. (1) The hatching was inhibited by indomethacin yet the inhibition was reversible. (2) In the groups with indomethacin and PGE2, no improvement was seen in the inhibition of hatching and the inhibition was irreversible. (3) In the groups with indomethacin and PGF, inhibition of hatching was improved in comparison with the group with indomethacin. (4) In the groups with indomethacin and 6-keto-PGF, no improvement was seen. The above results indicated that PGF possibly had an accelerating effect on hatching and a high concentration of PGE2 would exert cytotoxic effect on blastocysts.  相似文献   

15.
Seven rabbits were ejaculated four times once weekly, and saline or 2.5 mg PGF tromethamine salt was injected sc at 4 and 2 hours or at 8 and 4 hours before ejaculation. First ejacula taken at 2 hours after the second injection of PGF contained 150% more (P.07) sperm than those after injections of saline. The comparable difference (60%) at 4 hours after PGF was not significant. PGF did not influence sperm output in second, third or fourth ejacula. After 28 daily sc injections of 5 mg PGF in another experiment, the fertility of four treated rabbits was as high as that for four controls. Without sexual preparation in seven bulls, im injections of 40 or 80 mg PGF 30 minutes before ejaculation resulted in 33% greater (P<.05) sperm output than that after injection of 0, 7 or 20 mg PGF, but the highest sperm output after PGF was 30% less (P<.05) than that after sexual preparation in the same bulls. We conclude that injections of PGF result in increased sperm output in ejacula taken without sexual preparation within 2 hours in rabbits and in bulls.  相似文献   

16.
Fully convulsant doses of pentamethylenetetrazole cause marked increase in rat brain cortical PGF, PGE2, cGMP and cAMP during seizures, whereas subconvulsant doses cause an increase of rat brain cortical PGF without affecting the other biochemical parameters considered. Rat cerebellar prostaglandins were not modified by the convulsant agent at either dosage.  相似文献   

17.
The efficiency and acceptability of a single-dose, long-acting vaginal suppository containing 3.0 mg of 15-methyl PGF methyl ester was compared with intra-amniotic administration of 50 mg of PGF in 100 patients with a second trimester pregnancy termination. Within 24 hours, 78 per cent of the patients in the vaginal group and 92 per cent in the intra-amniotic group had aborted. The mean induction-abortion interval was 17.9 hours in the vaginal group and 15.8 hours in the intra-amniotic group.Gastrointestinal side-effects were more frequent, but the procedure was less painful, with vaginal 15-methyl PGF methyl ester than with intra-amniotic PGF.The vaginal route is technically simple for adaptation to large-scale use, but the high frequency of gastrointestinal side-effects still limits the acceptability of 15-methyl PGF methyl ester in vaginal administration.  相似文献   

18.
Three 16-aryloxy analogues of PGF are potent, full agonists on the isolated rabbit jejunum. Their actions are more prolonged than that of PGF, and radioactive tracer studies with one of the analogues reveal a slower wash-out of the analogue compared to PGF, under superfusion conditions. During the prolonged contractile response diminished responses to PGF were obtained: this effect was investigated in terms of receptor desensitization. The actions of these analogues were also investigated on the isolated guinea-pig ileum and the rabbit oviduct .  相似文献   

19.
Prostaglandin F (PGF) 20 mg combined with urea 80 g was injected intra-amniotically in 20 patients to induce mid-trimester abortion. Abortion resulted in all subjects within 24 hours in a mean time of 12 hours 38 minutes (range 5 hours 50 minutes to 20 hours 45 minutes).Plasma sex steroids were evaluated before and hourly for 5 hours after the injection. A progressive decline in levels occurred with time. Decreases in plasma progesterone, estrone, estradiol and estriol were significant as soon as one hour after injection.Gastrointestinal side effects occurred with a greater frequency than when a comparable dose of PGF is given alone and 2 patients had small cervical lacerations requiring suture. Further studies are indicated to establish whether a lower dose of PGF will be associated with fewer side effects and be as effective.  相似文献   

20.
Two types of experiments were conducted to determine the relationship of changes in blood luteinizing hormone (LH) and testosterone in bulls given prostaglandin F (PGF). Episodic surges of LH and testosterone occurred in tandem, apparently at random intervals, on the average once during the 8-hr period after bulls were given saline. In contrast, after sc injection of 20 mg PGF, blood serum testosterone increased synchronously to a peak within 90 minutes four-fold greater than pre-injection values, and the testosterone surges were prolonged about three-fold compared to those in controls. Each of the PGF-induced surges of testosterone was preceded by a surge of blood serum LH which persisted for about 45 minutes and peaked at about 3 ng/ml. In a second experiment, PGF was infused (iv, 0.2 mg/min) for 20 hr; blood plasma testosterone increased from 7.0 ± 0.6 to 16.0±1.5 ng/ml within 2.5 hr and remained near this peak for 10 hr. Then testosterone gradually declined to about 9 ng/ml at the conclusion of the 20-hr infusion. These changes in testosterone were paralleled by similar changes in blood plasma LH, although LH declined 3 hr earlier than testosterone. Random episodic peaks of blood plasma LH and testosterone typical of untreated bulls resumed within 8 hr after conclusion of PGF infusion. In both experiments, the surge of testosterone after PGF was preceded by increased blood LH. We conclude that increased LH after administration of PGF probably caused the increased testosterone. However the mechanisms of these actions of PGF remain to be determined.  相似文献   

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