Role of prostaglandin F2alpha in ovulation.

Using radioimmunoassay procedures, the levels of plasma, uterine and ovarian prostaglandin (PG) F2alpha, and those of plasma estradiol and progesterone were measured in intact, hysterectomized or ovariectomized immature female rats pretreated with PMS and subsequent HCG. Occurrence of ovulation was confirmed at 8 hours after the HCG administration not only in the intact rats but also in the hysterectomzied rats. The levels of plasma estradiol and progesterone, and of uterine and ovarian PGF2alpha rose with the PMS injection alone, but they did not reach the peaks before the HCG administration. Both plasma estradiol and uterine PGF2alpha showed a peak at 2 hours after the HCG injection. These peaks were antecedent 2 or 6 hours before the peaks of ovarian and plasma PGF2alpha, respectively. However, such increase of uterine PGF2alpha does not seem to be indispensable for ovulation, because ovulation could occur in the hysterectomized rats. The levels of ovarian PGF2alpha showed a high plateau from 4 to 8 hours after the HCG injection, and then rapidly decreased after ovulation. The levels of plasma PGF2alpha peaked not only in the intact rats but also in the hysterectomized rats at 8 hours after the HCG treatment. But in the ovariectomized rats, this plasma PGF2alpha peak at 8 hours disappeared and there was no statistical change of plasma PGF2alpha throughout the PMS-HCG treatment. Plasma progesterone gradually increased and reached the maximum at 10 hours after the HCG injection. These results conclude that the main source of increased plasma PGF2alpha during the ovulatory process induced with the PMS-HCG treatment is the ovary, and it is strongly suggested that a rapid increase of PGF2alpha in the ovary may play some important role(s) in the ovulatory process.     

Structural specificity for prostaglandin effects on hepatocyte glycogenolysis.

Prostaglandins (PGs) are known to have effects on hepatic glucose metabolism. Some actions of PGs in intact liver systems may not involve PG effects directly at the level of the hepatocyte. To define the ability of structurally distinct prostaglandins to affect hepatocyte metabolism directly, the regulation of glycogenolysis was studied in hepatocytes isolated from male Sprague-Dawley rats. PGF and PGB2 inhibited glucagon-stimulated glycogenolysis in the hepatocyte system. Pinane thromboxane A2 (PTA2) and PGD2 had no effect on glucagon-stimulated glycogenolysis. Consistent with their inhibition of glucagon-stimulated glycogenolysis, PGF2 and PGF2 alpha inhibited glucagon-stimulated hepatocyte cyclic AMP accumulation. These actions of PGB2 and PGF2 alpha are identical with those previously reported for PGE2. Additionally, PGE2, PGF2 alpha and PGB2 inhibited glucagon-stimulated adenylate cyclase activity in purified hepatic plasma membranes. In contrast, PGF2 alpha, PGD2 and PTA2 were all without affect on basal rates of hepatocyte glycogenolysis or hepatocyte cyclic AMP content. PGE2 also inhibited glycogenolysis stimulated by the alpha-adrenergic agonist phenylephrine. Exogenous arachidonic acid was not able to reproduce the affects of PGE2 or PGF2 alpha on hepatocyte glycogenolysis, consistent with an extra-hepatocyte source of the prostaglandins in the intact liver. Thus PGE2 and PGF2 alpha act specifically to inhibit glucagon-stimulated adenylate cyclase activity. No prostaglandin tested was found to stimulate glycogenolysis. PGE2 and PGF2 alpha may represent intra-hepatic modulators of hepatocyte glucose metabolism.     

Regulation of estrous cycle in hysterectomized albino rats by activation of follicular development.

Wistar strain albino rats were hysterectomized and the estrous cycle was compared with sham operated controls. Duration of estrous cycle in hysterectomized rats increased markedly with significant delay in the luteal phase and this was correlated to the inhibited follicular development of ovary. When these rats were treated with PGF2 alpha and PMSG and subjected to physical exercises, the estrous cycle was synchronised and the ovaries of such animals had active follicular development. Thus the deranged operation of sexual cycle in hysterectomized rats was regulated through physical exercises.     

Effect of prostaglandin F2 alpha (PGF2 alpha) on sources of progesterone and pregnancy in intact, ovariectomized and hysterectomized 90-100 day pregnant ewes.

A single dose of 8 or 16 mg of PGF2 alpha per 58 kg body weight was injected intramuscular into intact, ovariectomized or hysterectomized 90-100 day pregnant sheep in three separate experiments. Both doses of PGF2 alpha decreased the weights of the corpora lutea (P less than or equal to 0.05) and the concentration of progesterone in ovarian venous plasma at 72 hr (P less than or equal to 0.05) compared to the 0 hr sample within treatment groups and to control ewes at 72 hr in intact and hysterectomized pregnant ewes. In hysterectomized pregnant ewes, progesterone in jugular plasma declined (P less than or equal to 0.05) from 0 to 72 hr but never fell below 4 mg/ml and this decrease in progesterone after 8 or 16 mg PGF2 alpha was greater than in control hysterectomized ewes (P less than or equal to 0.05). There was a significant decrease in progesterone over time in jugular or uterine venous plasma in the presence of absence of the ovaries in 90-100 day pregnant ewes (P less than or equal to 0.05) but the profiles of progesterone were not different between vehicle and PGF2 alpha-treated ewes (P greater than or equal to 0.05). Uterine venous progesterone never declined below 30 ng/ml in the presence or absence of the ovaries and there was a significant quadratic increase (P less than or equal to 0.05) in uterine venous progesterone toward the end of the 72 hr sampling period indicating an increase in steroidogenic activity of the placenta. PGF2 alpha did not affect the number of abortions in intact or ovariectomized pregnant ewes (P greater than 0.05). Thus, the corpus luteum of sheep at 90-100 days of pregnancy is functional and responsive to PGF2 alpha, placentomes are functional but do not appear to be responsive to the doses of PGF2 alpha tested and PGF2 alpha was not an abortifacient over the 72 hr treatment period.     

Effects of hysterectomy and uterine decidualization on in vivo levels of prostaglandins in the corpus luteum of adult pseudopregnant rats

A possible role of the uterus in regulating content of luteal prostaglandins (PGs) was investigated. Pseudopregnancy was induced in adult virgin female rats by mating them with vasectomized male rats. On Day 5 of pseudopregnancy, decidualization of the uterus was induced or hysterectomy was performed. As controls, intact pseudopregnant animals with a luteal phase of 13 +/- 1 days were used. Measurements of in vivo tissue levels of PGF2 alpha, PGE2, and 6-keto-PGF1 alpha were performed by RIA after homogenization and extraction procedures in CL of pseudopregnancy and remainder of ovaries on Days 5, 13, and 19. Serum levels of progesterone and 20 alpha-dihydroprogesterone were determined by RIA. In hysterectomized animals, PGF2 alpha levels increased 2.5-fold in corpora lutea on Day 13 compared with levels on Day 5 of pseudopregnancy, but were still lower than in control rats undergoing functional luteolysis on Day 13. Decidual-tissue-bearing rats exhibited low levels of PGF2 alpha on Day 13 of pseudopregnancy. On Day 19, when luteolysis had occurred in decidual-tissue-bearing and hysterectomized rats, as judged by plasma levels of progestins, luteal content of PGF2 alpha was elevated to a similar level as that in control animals undergoing functional luteolysis on Day 13. When data pooled from control, decidual-tissue-bearing and hysterectomized rats were analyzed, a highly significant inverse correlation (r = -0.72, n = 46, p less than 0.001) between luteal PGF2 alpha content and ratio of plasma progestins was found.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prostaglandin F2 alpha-stimulated release of ovarian oxytocin in the sheep in vivo: threshold and dose dependency

To determine the threshold of prostaglandin F2 alpha (PGF2 alpha)-stimulated oxytocin secretion from the ovine corpus luteum, low levels of PGF2 alpha (5-100 pg/min) were infused into the ovarian arterial blood supply of sheep with ovarian autotransplants. PGF2 alpha was infused for six sequential 10-min periods at hourly intervals, 6, 12, or 24 days after estrus (n = 3 for each day). Each cycle day was studied during a separate cycle. Oxytocin and progesterone in ovarian venous and carotid arterial plasma was measured by radioimmunoassay, and secretion rates were determined (venous-arterial concentration x plasma flow). In animals treated on Day 6, 5 pg/min PGF2 alpha caused a significant release of oxytocin (p less than 0.01), whereas in animals treated on Day 12, this threshold was 40 pg/min (p less than 0.05). In animals treated on Day 24, the threshold for oxytocin release was greater than 100 pg/min. PGF2 alpha did not significantly change ovarian blood flow or progesterone secretion rate on any day (p greater than 0.05). To determine residual luteal oxytocin after each threshold experiment, 5 mg PGF2 alpha was given i.m. to all animals. Significantly more oxytocin was released by Day 6 than by Day 12 and Day 24 corpora lutea, and by Day 12 than by Day 24 corpora lutea (1.2 micrograms, 0.7 microgram, and 0.3 microgram, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Immunohistochemical localization of PGF2 alpha receptor in the rat ovary.

As a step towards understanding the role of prostaglandin F2 alpha (PGF2 alpha) in ovarian function, a rabbit antiserum against purified PGF2 alpha receptor (PGF2 alpha-R) was produced. This report details the use of this antiserum in immunohistochemical staining of ovaries of non-pregnant and pregnant rats to ascertain which cell types, in vivo, possess PGF2 alpha-R. In non-pregnant rats, three ovarian cell subpopulations contain immunoreactive PGF2 alpha-R. These include: a subpopulation of the cells found in corpora lutea, a subpopulation of the thecal cells surrounding secondary and mature (Graafian) follicles, and a subpopulation of primary and secondary interstitial cells. The ovarian tissues and cell types in which immunoreactive PGF2 alpha-R cannot be demonstrated include: the serosa overlying the ovary and its vessels, the coelomic epithelium and its underlying cortical stroma, medullary stroma and vessels, granulosa cells of primary, secondary and mature follicles, the oocyte, and the blood vessels and stroma within corpora lutea. PGF2 alpha-R immunohistochemical staining of corpora lutea from non-pregnant animals was examined both prior to the start of luteolysis and during luteolysis. During luteolysis, cells undergoing apoptosis stained for the presence of PGF2 alpha-R. PGF2 alpha-R immunohistochemical staining was also examined in corpora lutea during pregnancy and until 4 days postpartum. The major findings here were the apparent large increase in staining intensity of granulosa-lutein cells during pregnancy, and the loss of PGF2 alpha-R immunopositivity of the granulosa-lutein cells during the postpartum period. In summary, three ovarian cell subpopulations, all of which can secrete steroids, possess immunoreactive PGF2 alpha-R.     

The possible mode of action of prostaglandins IX-prostaglandin F2alpha involvement in the reversal of ovulation blockade by ergocornine in rats.

A single injection of 1 mg ergocornine methanesulphonate to semispayed rat on day 3 of the cycle was found to block ovulation. However, the animals showed regular compensatory hypertrophy of the remaining ovary. Prostaglandin F2alpha (PGF2alpha) of 2.0 mg/kg bw on days 3 and 4 in the ergocornine-blocked semispayed rats consistently reversed the blocking effect and the animals showed compensatory ovulation and ovarian hypertrophy. It was moreover observed that the ergocornine-treated mated animals did not become either pregnant or pseudopregnant, but returned to normal cycle as usual. Conversely, the animals which had combined regimen of ergocornine and PGF2alpha became pregnant and the number of embryonic swellings in a single horn and their average weight were statistically identical to their experimental controls. The possible involvement of PGF2alpha in the mechanism of follicular rupture has been discussed.     

The effects of ovarian steroids in controlling rat uterine prostaglandin F2-alpha during the peri-implantation period

Rats with delayed implantation, induced by ovariectomy or hypophysectomy, as well as those with normal pregnancy were used to examine the changes in uterine prostaglandin F2 alpha (PGF2 alpha) associated with implantation. In normal pregnant rats, while maximal uterine production of PGF2 alpha was found at 09:00, maximal catabolic enzyme activity (CEA) was seen at 17:00 of day 4. Uterine content of PGF2 alpha was high at 17:00 of day 4, but decreased by 80% within the next 24 h. There was no change in PGF2 alpha production during the first 6 h after injection of estradiol to hypophysectomized animals. There was, however, a dramatic decrease in production within the next 6 h. In contrast, CEA was not different in animals treated with estrogen than in those receiving only progesterone. In ovariectomized animals, uterine PGF2 alpha production also was lowered by estrogen but in these animals CEA was significantly elevated 18 h after injection of estradiol. Estrogen caused a greater increase in PGF2 alpha content in the hypophysectomized, compared to the ovariectomized, rats. The results are consistent with the view that ovarian steroids play an important role in controlling the changes in uterine PGF2 alpha around the time of implantation in rat.     

Secretion and metabolism of prostaglandin F2 alpha by endometrial tissue obtained at different days of the oestrous cycle in cattle

Two mature heifers were slaughtered on days 3, 6-7, 10-11, 16, 18-19 or on day 21 of the oesterus cycle. Endometrium was incubated in quadruplicates with medium-199 at 37 C and a water saturated gas phase of 95% O2 + 5% CO2. Half ml medium samples were taken after 6, 12 and 24 h of incubation for determination of PGF2 alpha and PGFM. PGF2 alpha was secreted by endometrium at each stage of the oestrous cycle. Maximal secretion was measured around oestrus (p less than 0.01) compared with days 6-16 of the cycle. Concentration of PGFM in medium had a similar trend. Highest ability of endometrium for PGF2 alpha metabolism (indicated by the ratio PGF2 alpha:PGFM) was on days 6-16 of the cycle. Data suggest that PGF2 alpha metabolism by the endometrium may depend on ovarian steroids and that this metabolism may also protect the corpus luteum from the luteolytic action of PGF2 alpha besides reduced production of this prostaglandin during the luteal phase.     

The effect of inhibition of prostaglandin synthesis on ovarian hypertrophy in the rat.

Aspirin and indomethacin, inhibitors of prostaglandin biosynthesis, were utilized to determine the role of prostaglandins (PGs) in ovarian weight gain in rats following unilateral ovariectomy or treatment with PMSG. After unilateral ovariectomy, the compensatory ovarian hypertrophy was 185-0% compared with 139-8% and 97-5% in rats treated with indomethacin and aspirin, respectively. The adrenal weights in rats treated with aspirin were also reduced significantly. Administration of PGE2 or PGF2alpha with aspirin reversed the effect of aspirin on the adrenals but had no effect on the ovarian weight. Indomethacin and aspirin treatment of animals injected with PMSG also reduced the ovarian weight gain. If 100 mug PGE2 were given twice daily, this effect was reversed in both groups but thrice daily administration had no effect on rats receiving aspirin. In PMSG-treated rats, 100 mug PGF2alpha twice daily did not reverse the effect of indomethacin and aspirin, and actually enhanced the effect of aspirin.     

Transport of uterine PGF2 alpha to the ovaries by systemic circulation and local lymphovenous-arterial diffusion during luteolysis in sheep.

The theory of countercurrent vascular transfer of PGF2 alpha during luteolysis was examined. In the first experiment, pulmonary clearance of PGF2 alpha was determined to re-examine whether the total amount of PGF2 alpha was degraded in the lungs after one passage. Cardiac output was measured by the Fick method and PGF2 alpha by radio-immunoassay before and after vascular lung supply, using pulmonary catheterization and the interventional radiology method in ten anaesthetized ewes on day 16 of the oestrous cycle. Cardiac output remained stable (7156 +/- 439 ml min-1). Infusion of 5 iu oxytocin resulted in an increase in plasma PGF2 alpha concentrations at 30 min in the uterine vein and the pulmonary and femoral arteries (3811 +/- 806, 224 +/- 55 and 18 +/- 4 pg ml-1, respectively). The PGF2 alpha concentrations decreased exponentially and the half-time decreases were 27 (r = 0.99), 16 (r = 0.99) and 18 (r = 0.98) min, respectively. Pulmonary clearance of PGF2 alpha was estimated at 6338 +/- 451 ml min-1. In a second experiment, an arterio-arterial gradient of plasma PGF2 alpha concentrations was analysed between the proximal and distal segments of the ovarian artery to verify whether the total amount of PGF2 alpha flowing to the ovary was from the local venous-arterial countercurrent pathway. Surgical catheterization techniques were performed on 11 ewes on day 16 of the oestrous cycle. The ovarian arterial blood flow was measured by the implantable Doppler method (8 +/- 1 ml min-1). The maximum plasma PGF2 alpha concentrations in the femoral and distal ovarian arteries were 23 +/- 6 and 42 +/- 11 pg ml-1 (P < 0.05), respectively. Plasma PGF2 alpha decreased exponentially in the femoral artery and the half-time decrease was 26 min (r = 0.98), and in the distal ovarian artery close to the ovary PGF2 alpha decreased linearly and the half-time decrease was 108 min (r = 0.96). Consequently, the arterio-arterial diffusion gradient of PGF2 alpha concentrations was extended to 3 h. These experiments showed that the PGF2 alpha flow rate in the pulmonary artery was 42.275 +/- 10.793 micrograms per 150 min (n = 10) and the systemic arterial PGF2 alpha flow rate was 5.359 +/- 1.658 micrograms per 150 min (n = 10). Therefore, 12% of the PGF2 alpha was not oxidized by the lungs. The proximal ovarian PGF2 alpha flow rate was 6.909 +/- 2.341 ng per 150 min, while the distal flow rate was 21.003 +/- 5.703 ng per 150 min (n = 11). Thus, 33% of the PGF2 alpha was transported rapidly to the ovary via the systemic route, while 67% was transported by slow local countercurrent diffusion, which extended the duration of luteolytic activity to four times that of the PGF2 alpha surge. These results indicate both rapid systemic transport of PGF2 alpha to the ovaries and a slower buffer mechanism involving a local diffusion pathway, rather than a direct countercurrent system.     

Changes in serum lipids in rats treated with PGF2 alpha

Serum lipid concentrations were determined in rats treated with PGF2 alpha, PGE1, and controls. Administration of PGF2 alpha in rats influenced only the HDL lipid composition. HDL-cholesterol decreased while HDL-triglycerides increased. No significant difference was observed in the levels of serum total cholesterol, triglycerides, and phospholipids between animals treated with PGF2 alpha and controls. Reduced concentrations of serum lipid levels and especially of HDL-cholesterol, HDL-triglycerides, and HDL-phospholipids were found in the rats treated with PGE1. These results suggest that PGF2 alpha and PGE1 could modify serum lipid levels influencing lipoprotein metabolism.     

On the influence of prostaglandin F2alpha-induced labor at term on the metabolism and coagulation of mother and fetus.

11 pregnancies at term were terminated by dilatation of the uterine cervix, low amniotomy, and by intravenous administration of PGF2alpha. The average infusion time was 3 hours 55 minutes, and the average total dose of PGF2alpha amounted to 2.0 mg. Parameters of acid-base changes, carbohydrate and energic state changes, gas metabolism, and changes in coagulation and fibrinolysis in mother and in fetus were analyzed during labor and after birth. Labor activity and fetal cardiac action were monitored cardiotocographically. Checked against 50 uncomplicated spontaneous deliveries, we found no disadvantageous changes in the parameters investigated.     

Destruction of bovine ovarian follicles: effects on the pulsatile release of luteinizing hormone and prostaglandin F2 alpha-induced luteal regression

Destruction of ovarian follicles during diestrus prolongs the lifespan of corpora lutea in cows, but the site(s) of action is unclear. Thus, ovarian follicles were destroyed in 10 beifers (X-IRRAD) on Day 9 postestrus, while 10 additional beifers (SHAM) served as a control group. To investigate changes in luteotropic support resulting from destruction of ovarian follicles, pulses of luteinizing hormone (LH) were characterized on Days 8, 13, and 15 postestrus. To study the interaction between products from ovarian follicles and prostaglandin F2 alpha (PGF2 alpha) in luteolysis, changes in serum concentrations of progesterone were monitored after an injection of saline or PGF2 alpha on Day 14 postestrus. Frequency and amplitude of pulses of LH increased by Day 13 in X-IRRAD beifers. An increase of similar magnitude in amplitude but not frequency of pulses of LH occurred between Day 13 and Day 15 postestrus in SHAM beifers. Exogenous PGF2 alpha was significantly less efficacious in causing luteolysis in X-IRRAD animals. We suggest that increased luteotropic support may be involved in but is not the only cause for lengthening the lifespan of corpora lutea following destruction of ovarian follicles. Additionally, we suggest that regression of bovine corpora lutea involves a synergistic action between products from ovarian follicles and PGF2 alpha.     

Identification of metabolites from type III F2-isoprostane diastereoisomers by mass spectrometry

F(2)-isoprostanes (F(2)-iPs) are prostaglandin (PG)-like products of non-enzymatic free radical-catalyzed peroxidation of arachidonic acid that are now widely used as indices of lipid peroxidation in vivo. Knowledge of the metabolic fate of F(2)-iPs in vivo is still scant, despite its importance for defining their overall formation and biological effects in vivo. Type III F(2)-iPs, which are diastereoisomers of cyclooxygenase-derived PGF(2alpha), may be metabolized through the pathways of PG metabolism. We therefore studied the in vitro metabolism of eight synthetic Type III F(2)-iP diastereoisomers in comparison with PGF(2alpha). We used gas chromatography-mass spectrometry and high performance liquid chromatography-electrospray-tandem mass spectrometry for structural identification of metabolites formed after incubation of the various compounds with isolated rat hepatocytes. PGF(2alpha) was metabolized to several known products, resulting from a combination of beta-oxidation, reduction of Delta(5) and/or Delta(13) double bonds, and 15-OH oxidation, plus other novel products deriving from conjugation with taurine of PGF(2alpha) and its metabolites. Of the eight F(2)-iP diastereoisomers, some were processed similarly to PGF(2alpha), whereas others showed peculiar metabolic profiles according to specific stereochemical configurations.These data represent the first evidence of biodegradation of selected Type III F(2)-iP isomers other than 8-epi-PGF(2alpha), through known and novel pathways of PGF(2alpha) metabolism. The analytical characterization of these products may serve as a basis for identifying the most significant products formed in vivo.     

Oxytocin-stimulated production of prostaglandin F2alpha by isolated endometrium of rabbit: modulation by ovarian steroids

To test the hypothesis that ovarian steroid hormones modulate oxytocin-induced release of prostaglandin F2alpha (PGF2alpha) from uterine endometrium, 2 ovariectomized rabbits were pretreated with progesterone (5 mg/day for 10 days), 2 with estradiol-17 beta (25 microgram/day for 10 days), 2 with both steroids, and one with sesame oil only. On the last day of treatment, endometrial fragments were excised and incubated in vitro with or without oxytocin (100 muU/ml). Although endometrium from rabbits pretreated with combined steroids released more PGF2alpha immediately after excision than did tissue from animals pretreated with either steroid by itself, endometrium from animals pretreated with estradiol-17 beta alone released the most PGF2alpha during sustained incubation in vitro. Moreover, only this tissue exhibited significant oxytocin-dependent release of PGF2alpha. At the dosages used, progesterone completely antagonized both of these effects of estradiol-17 beta. The results support the hypothesis that ovarian steroid hormones regulate oxytocin-dependent release of PGF2alpha from endometrial cells. A posible mechanism of action is suggested.     

Effects of an agonist of gonadotropin-releasing hormone on ovarian follicles in cattle.

Three experiments were conducted to examine effects of Buserelin, a potent agonist of gonadotropin-releasing hormone, on characteristics of ovarian follicles in cycling cows and heifers. In experiment 1, heifers were injected once with 10 micrograms Buserelin on Day 11, 12, or 13 of the estrous cycle (estrus = Day 0), or once with 20 micrograms of Buserelin on Day 12. Additionally, two groups were injected with a luteolytic dose of prostaglandin F2 alpha (PGF2 alpha) on Day 13 preceded with or without a Buserelin injection (10 micrograms) on Day 12. A control group did not receive a Buserelin injection. Ovaries were recovered and weighed after animals were slaughtered on Day 15. Follicle diameters were measured with calipers. Follicles for all experiments were classified as small (class 1: 3-5 mm diameter), medium (class 2: 6-9 mm), or large (class 3: greater than 9 mm). Heifers receiving only Buserelin had an increased number of medium-sized follicles compared to controls. Buserelin injection administered 24 h before PGF2 alpha reduced the decline in the average weight of the ovaries containing the corpus luteum (7.8 g for Buserelin before PGF2 alpha vs. 6.7 g for no Buserelin before PGF2 alpha). Buserelin pretreatment appeared to delay or prevent complete luteolysis by the injected PGF2 alpha. In experiment 2, 0, or 10 micrograms Buserelin was injected on Day 12 and follicle development was monitored by ultrasonography in situ from Day 12 to estrus. Follicles also were classified as clear or cloudy; cloudy was associated with flocculent material in the follicular fluid or with an indistinct follicular wall.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of prostaglandin F2alpha on ovarian and pituitary function in the mid-luteal phase.

The effects of PGF2alpha infusion in a dose of 25 micrograms/min for 5 hours on serum levels of estradiol-17beta, progesterone, LH, FSH, TSH and prolactin, and on the pituitary hormone responsiveness to LRH and TRH were studied in 10 apparently healthy cycling women in the mid-luteal phase. No systematic alteration was seen in the pituitary and ovarian hormone levels during PGF2alpha infusion, and the pituitary hormone responses to releasing hormones were unaffected. Ovarian steroid production increased in response to increased gonadotropin levels after LRH injection during PGF2alpha administration. These results confirm that PGF2alpha is not luteolytic in humans and no apparent relationship between PGF2alpha and pituitary hormone secretion exists.     

Biosynthesis of prostaglandins in ovarian follicles and corpus luteum of sheep ovary

The biosynthetic potential of prostaglandins (PGs) was measured in ovarian follicles and corpus luteum of sheep ovary. The total prostaglandins formed under non-enzymatic conditions were much lower in comparison to that formed using native GSTs. When the GSTs of ovarian follicles were employed, the major prostaglandin formed was PGE2 (81.22%) followed by PGD2 (16.9%) and PGF2 alpha (1.87%). In case of corpus luteum, prostaglandin formed was PGF2 alpha (59.01%). Since PGF2 alpha was demonstrated to be the luteolytic factor, the present study indicates the formation of luteolytic factor in the ovarian tissue itself.