Prostaglandin concentrations in peripheral plasma and ovarian and uterine plasma and tissue in relation to oviposition in hens

An increase in the plasma concentrations of prostaglandins (PGs) is associated with uterine contractile activity and with oviposition in the hen. In order to assess the contribution of potential sources of prostaglandins to the increase in prostaglandin levels observed at oviposition, prostaglandins E2, F2 alpha, and 13,14-dihydro-15-keto PGF2 alpha (PGFM, the stable but biologically less active metabolite of PGF2 alpha) were measured in plasma from the brachial vein, ovarian follicular vein and uterine vein, and in tissues from ovarian follicles and the uterus 12 h before and at midsequence oviposition or a terminal oviposition. These two ovipositions differ in that a midsequence oviposition is followed within 0.25-1.0 h by the next ovulation of the sequence, whereas the terminal oviposition is followed by an ovulation 14 h later. The concentration of PGFM in plasma from the brachial vein increased at midsequence oviposition, while the levels of PGE2 were unchanged. Prostaglandin E2, F2 alpha, and FM levels were each similar in the plasma from the brachial and uterine veins at the time of midsequence oviposition. In plasma from the largest preovulatory follicle, the concentration of PGF2 alpha and PGFM increased 19- and 7-fold, respectively, from 12 h before midsequence oviposition to midsequence oviposition, although no changes were observed in the concentrations of PGE2 during this interval. The levels of PGF2 alpha increased in the tissues of the two largest preovulatory follicles and the two most recently ruptured follicles during the 12-h period before a midsequence oviposition, while there was no change or a decrease in PGE2 levels in these tissues during the same interval. In contrast, the concentration of PGF2 alpha did not increase during the 12-h period preceding the terminal oviposition of the sequence in plasma from the brachial, uterine, or follicular veins.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prostaglandin levels in peripheral and follicular plasma, the isolated theca and granulosa layers of pre- and postovulatory follicles, and the myometrium and mucosa of the shell gland (uterus) during a midsequence-oviposition of the hen (Gallus domesticus)

Prostaglandins (PG) F and E were measured by radioimmunoassay in peripheral, uterine and follicular plasma and in the theca and granulosa layers of the five largest preovulatory and the three largest postovulatory follicles, and in the myometrium and mucosa. Plasma and tissues were collected 16, 12, 8 and 4 h before and immediately after a midsequence oviposition that was accompanied by the next ovulation. PGF concentrations in the peripheral and uterine plasma increased at oviposition with a concomitant, 16-fold increase in plasma PGF concentrations of the largest preovulatory (F1) follicle. There was a gradual increase in PGF concentrations in the theca layers during follicular maturation, with the large increases occurring 12 h before oviposition in most follicles. The highest and the second highest concentrations were observed at oviposition in the F1 and the largest postovulatory (R1) follicles. In contrast, there were no specific changes in PGF concentrations in the granulosa layers of the follicles in relation to oviposition or follicular maturation. PGE concentrations in the theca layers of the F2 and F1 follicles were greater than in other follicles, while concentrations in the granulosa layer of all the follicles remained low. PGF concentrations in the myometrium and mucosa increased 8 h before oviposition but abruptly decreased at oviposition. These results suggest that the primary source of the increase in plasma PGF at oviposition are the theca layers of the F1 and R1 follicles and that PGs may be involved in uterine contractions for oviposition and in the ovulation process.     

Prostaglandin production by the largest preovulatory follicles in the domestic hen (Gallus domesticus)

An injection of 5 micrograms of gonadotropin-releasing hormone (GnRH) into hens 8 h prior to oviposition advanced the expected time of oviposition by approximately 1 h. The plasma concentration of progesterone increased approximately 1 h earlier in GnRH-injected hens in comparison to saline-injected hens. The plasma concentration of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) increased significantly (p less than 0.05) at the time of oviposition in both the GnRH- and saline-injected hens. Significantly (p less than 0.05) greater concentrations of prostaglandin F2 alpha (PGF2 alpha) were assayed in media containing the largest preovulatory follicles collected at oviposition than in media containing the second and fifth largest preovulatory follicles collected at the same time. No prostaglandin was detected in media containing small, nonhierarchial follicles. The concentration of PGF2 alpha in media containing granulosa cells from the largest preovulatory follicle was significantly greater (p less than 0.05) than in media containing 4 times as many theca cells. Ovine luteinizing hormone (oLH) alone or in combination with arachidonic acid had no effect on PGF2 alpha output from granulosa cells collected 6 h before oviposition, whereas A23187 caused a small stimulation of PGF2 alpha output. However, treating cells first with oLH and then with A23187 stimulated a 15- to 20-fold increase in PGF2 alpha. None of these stimuli enhanced the already high output of PGF2 alpha when added to incubations of granulosa cells collected within 5 min after oviposition. These data suggest that the granulosa cells of the largest preovulatory follicle are the major intraovarian source of prostaglandin and that production of PGF2 alpha is associated with the preovulatory surges of gonadotropins and steroid hormones preceding oviposition.     

Differential effects of progesterone treatment on the oxytocin-induced prostaglandin F2 alpha response and the levels of endometrial oxytocin receptors in ovariectomized ewes.

The oxytocin-induced uterine prostaglandin (PG) F2 alpha response and the levels of endometrial oxytocin receptors were measured in ovariectomized ewes after they had been given steroid pretreatment (SP) with progesterone and estrogen to induce estrus (day of expected estrus = Day 0) and had subsequently been treated with progesterone over Days 1-12 and/or PGF2 alpha over Days 10-12 postestrus. The uterine PGF2 alpha response was measured after an i.v. injection of 10 IU oxytocin on Days 13 and 14, using the PGF2 alpha metabolite, 13,14-dihydro-15-keto-PGF2 alpha (PGFM), as an indicator for PGF2 alpha release. The levels of oxytocin receptors in the endometrium were measured on Day 14. During the treatment with progesterone, the peripheral progesterone concentrations were elevated and remained above 1.8 ng/ml until the morning of Day 14. The PGFM responses to oxytocin in untreated controls and SP controls were low on both Days 13 and 14 whereas the levels of endometrial oxytocin receptors in the same ewes were high. Treatment with progesterone either alone or in combination with PGF2 alpha significantly (p less than 0.04) increased the PGFM response on Day 14 and reduced the levels of endometrial oxytocin receptors; treatment with PGF2 alpha alone had no effect. It is concluded that progesterone promotes the PGFM response to oxytocin while simultaneously suppressing the levels of endometrial oxytocin receptors. PGF2 alpha treatment had no effect on either the uterine secretory response to oxytocin or the levels of oxytocin receptors in the endometrium.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mouse placental prostaglandins are associated with uterine activation and the timing of birth

We explored a potential mechanism linking placental prostaglandins (PGs) with a fall in plasma progesterone and increased expression of uterine activation proteins in the mouse. PG endoperoxide H synthase 2 (PGHS-2) mRNA expression increased in placenta in late gestation in association with an 8-fold increase in PGF(2alpha) concentration, reaching a peak on Gestational Day (GD) 18. This peak coincided with the final descent in plasma progesterone and birth on GD 19.3 +/- 0.2. Implantation of a progesterone-releasing pellet in intact pregnant dams on GD 16 delayed birth at term until GD 20.9 +/- 0.4 and inhibited the GD 18 increase in placental PGF(2alpha) levels in conjunction with a delayed fall in plasma progesterone that reached its lowest level 1 day after term birth. The mRNA levels of uterine activation proteins, connexin-43 (CX-43), oxytocin receptor, PGF(2alpha) receptor (FP), and PGHS-2, and the concentration of uterine PGF(2alpha) all increased at normal term birth. At progesterone-delayed term birth on GD 19.3, even though tissue PGF(2alpha) concentrations were at the same high levels observed at normal term birth, CX-43 and FP mRNA levels were lower than those at normal term birth, thereby possibly contributing to the delay of birth. These data are consistent with the hypotheses that fetal placental PGs affect the timing of birth by hastening luteolysis, that uterine activation initiates labor, and that birth may be delayed by blocking or decreasing the expression of two of the uterine activation proteins.     

The effect of indomethacin on ovarian prostaglandin release in hens

Indomethacin, an inhibitor of prostaglandin (PG) synthetase, will block uterine muscle electromyographic activity (EMG activity) and oviposition at a midsequence oviposition and ovulation in domestic hens, but does not block the increase in EMG activity associated with the first ovulation of a sequence. To assess the potential relationship between prostaglandin release from the ovarian follicles and EMG activity in egg-laying hens, we determined the concentrations of PGF2 alpha, 13,14-dihydro-15-keto-PGF2 alpha (PGFM), and PGE2 in brachial, ovarian follicular and uterine venous plasma and tissues in relation to uterine muscle EMG activity at the first ovulation and at a midsequence oviposition. The concentrations were measured after an i.m. injection (25 mg/hen) of indomethacin. In control hens sampled hourly, beginning 4 h before the peak of EMG activity at the first ovulation of a sequence, there was a sharp increase (p less than 0.05) in concentrations of PGF2 alpha and PGFM in brachial vein plasma coincident with the increase (p less than 0.05) in uterine EMG activity. Hens pretreated with indomethacin also had increased plasma PGF2 alpha and PGFM levels (p less than 0.05) in brachial vein plasma and increased uterine EMG activity (p less than 0.05) at this time. Indomethacin treatment lowered but did not eliminate mean levels of PGF2 alpha in the venous effluent from the largest preovulatory follicle at the first ovulation (36.0 +/- 9.9 ng/ml vs. 14.4 +/- 1.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of beta-adrenergic agonist infusions on myometrial activity and plasma prostaglandin levels in the nonpregnant sheep

Recent studies have reported that beta-adrenergic agonists stimulate the production of stimulatory prostaglandins (PGs) by intrauterine tissues in vitro. These drugs are used clinically to inhibit uterine contractions; consequently an increase in stimulatory PGs in vivo might have potentially adverse effects. We have, therefore, investigated whether beta-adrenergic agonists increase plasma PG concentrations in vivo. Samples of peripheral (aorta) and uterine venous enriched (vena cava) blood from nonpregnant sheep were collected at 15-min intervals for 1 h before, 3 h during, and 1 h postinfusion of either (a) the beta-adrenergic agonist isoproterenol (Isop) at a dose of 0.16 microgram.kg-1.min-1; (b) Isop at a dose of 0.08 microgram.kg-1.min-1; or (c) saline, 1 mL/h via a jugular vein catheter. The sheep were also equipped with intrauterine recording balloons to record intrauterine pressure and myometrial electromyographic (EMG) electrodes to measure EMG activity. Infusion of Isop at 0.16 microgram.kg-1.min-1 produced a significant initial inhibition of uterine activity, although contractions returned (within 60 min) despite continued administration of Isop. Plasma PGE2 (but not PGF2 alpha or 13,14-dihydro-15-keto-PGF2 alpha (PGFM] concentrations were significantly elevated during the Isop infusion. Administration of Isop at 0.08 microgram.kg-1.min-1 produced no effects on uterine contractile activity but was associated with a significant elevation in plasma PGE2 (but not PGF2 alpha or PGFM) concentrations. No changes in plasma PGE2, PGF2 alpha, or PGFM occurred during saline infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inhibition of uterine prostaglandin-F2 alpha production by bovine conceptus secretory proteins

The effect of bovine conceptus secretory proteins (CSP) on uterine prostaglandin (PG)-F2 alpha production was evaluated in dairy cattle following injection of estradiol-17 beta. 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 PGF2 alpha production. Plasma concentrations of progesterone (P4) and 15-keto-13,14-dihydro-PGF2 alpha (PGFM) were determined by RIA. The PGFM responses following E2 challenge were decreased (p less than 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 PGF2 alpha production during pregnancy recognition in the cow.     

Production of prostaglandin f2alpha and its metabolite by endometrium and yolk sac placenta in late gestation in the tammar wallaby, Macropus Eugenii

In this study, we investigated production of prostaglandin (PG) F2alpha and its metabolite, PGFM, by uterine tissues from tammar wallabies in late pregnancy. Endometrial explants were prepared from gravid and nongravid uteri of tammars between Day 18 of gestation (primitive streak) and Day 26.5 (term) and were incubated in Ham's F-10 medium supplemented with glutamine and antibiotics for 20 h. PGF2alpha and PGFM in the medium were assayed by specific, validated RIAs. Control tissues (leg muscle) did not produce detectable amounts of either PG. Both gravid and nongravid endometria secreted PGF2alpha, and production increased significantly in both gravid and nongravid uteri towards term. PGFM was produced in small amounts by both gravid and nongravid uteri, and the rate of production did not increase. Neither oxytocin nor dexamethasone stimulated PG production in vitro in any tissue at any stage. Thus, the surge in peripheral plasma PGFM levels seen at parturition may arise from increased uterine PG production, but further study is needed to define what triggers this release.     

Fetal-maternal secretion of prostaglandins in the cow

A study was conducted to measure the blood plasma concentrations of prostaglandin F2 alpha (PGF2 alpha), 13,14-dihydro-15-keto-prostaglandin F (PGFM), 6-keto-prostaglandin F1 alpha (6-keto), prostaglandin uterine artery, uterine vein, umbilical artery and umbilical vein in 24 cows from days 80 to 260 of pregnancy. Blood was collected during surgery and all prostaglandins were measured using specific radioimmunoassay procedures. Results indicate that PGF2 alpha blood levels are higher in the umbilical vessels and uterine vein than in the ovarian vein and uterine artery. PGFM and PGE2 showed a trend towards higher values in the umbilical than in the maternal vessels, but the levels of 6-keto and TBX2 were not different among the vessels studied. No differences across time could be observed in any of the prostaglandins measured, partly due to the great variability in blood levels among animals during the same stage of pregnancy.     

Effect of exogenous progesterone on prostaglandin F2 alpha release and the interestrous interval in the bovine

The present study was developed to determine if administration of progesterone, early in the estrous cycle of the cow, stimulated an advanced pulsatile release of PGF2 alpha from the uterine endometrium resulting in a decreased interestrous interval. Twenty-three cyclic beef cows were randomly assigned to receive either sesame oil or progesterone (100 mg) on Day 1, 2, 3 and 4 of the estrous cycle. Peripheral plasma concentrations of progesterone and the metabolite of prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha (PGFM) were measured by radioimmunoassay. Administration of exogenous progesterone increased peripheral plasma concentration of progesterone in treated (3.67 ng/ml) compared to control (1.28 ng/ml) cows from Day 2 through 5 of the estrous cycle. Progesterone administration shortened the interestrous interval (16.7 d) compared to controls (21.6 d). The shortened interestrous intervals in treated cows resulted from an earlier decline in peripheral plasma progesterone. Decline of peripheral plasma progesterone concentrations is coincident with an increased pulsatile release of PGFM in both progesterone treated and control cows. Results indicate that administration of exogenous progesterone stimulates an earlier maturation of endometrial development, causing an advanced release of PGF2 alpha which shortens the interestrous interval of the cow.     

Increases in the oxytocin-induced prostaglandin F2 alpha response and reduction in the concentrations of endometrial oxytocin receptors in ewes in response to progesterone.

Ovariectomized ewes were given progesterone and oestrogen priming as steroid pretreatment and subsequently treated with progesterone, prostaglandin F2 alpha (PGF2 alpha), or both. In Expt 1, plasma concentrations of the metabolite 13,14-dihydro-15-keto-PGF2 alpha (PGFM) were measured after an i.v. injection of oxytocin. There was little PGFM response in the untreated control ewes or in the pretreated ewes. Treatment with PGF2 alpha alone had no effect (P greater than 0.05), whereas treatment with progesterone either alone or with PGF2 alpha significantly (P less than 0.05) increased the uterine PGFM response to oxytocin. In Expt 2, chronically ovariectomized ewes had high concentrations of endometrial oxytocin receptors. Treatment with PGF2 alpha alone did not alter the concentrations of the receptors. Treatment with progesterone either alone or with PGF2 alpha significantly (P less than 0.05) reduced the concentrations of the receptors. It is concluded that progesterone promotes the PGFM response to oxytocin, but simultaneously suppresses the concentrations of endometrial oxytocin receptors.     

Prostaglandins in maternal and fetal plasma and in allantoic fluid during the second half of gestation in the mare.

The concentrations of the primary prostaglandins (PG) F-2alpha and E-2 and the metabolite 13,14-dihydro-15-oxo-prostaglandin (PGFM) in maternal and fetal plasma and in allantoic fluid were measured in chronically catheterized mares and fetuses. A gradual rise in all 3 PGs occurred with increasing gestational age. PGE-2 and PGF-2 alpha levels were highest in the allantoic fluid and lowest in the maternal plasma, whereas PGFM concentrations were greatest in maternal plasma. Significant venous-arterial plasma differences in PGFM concentration were detected across the uterine circulation between 180 and 280 days gestation. The 3--5-fold rise in maternal PGFM associated with fasting or intrauterine surgery was virtually abolished by meclofenamic acid, a prostaglandin synthetase inhibitor. Increases in PGE-2 and PGF-2 alpha in the fetal fluids preceded premature delivery of the foal, while PG changes in maternal plasma were minimal even 10--20 h before delivery.     

Trypanosome-induced increase in prostaglandin F(2alpha) and its relationship with corpus luteum function in the goat

Plasma progesterone and 13,14-dihydro-15-keto Prostaglandin F(2alpha) (PGFM) were measured in normal (uninfected) and Trypanosoma congolense -infected adult goats for a period of 121 d, from May to August, during the breeding season in Kenya. Chronic trypanosomiasis rapidly increased the baseline plasma PGFM levels and the occurrence of irregular PGFM peaks in several infected goats. Progesterone luteal levels declined rapidly from the second and subsequent cycles post patency. Estrous cycles also became irregular but predominately shorter (8 to 19 d) before cessation from the second to fourth cycle following infection. The PGFM levels were still high during the acyclic period in all goats when progesterone levels were very low (1.4 to 2.4 nmol/l). The reciprocal increase in peripheral PGFM and decline in progesterone in these goats would suggest, in part, a trypanosome-induced PGF(2alpha) mediated luteolysis, and the possible involvement of prostaglandins in trypanosome-induced infertility in female goats.     

Exogenous progesterone reduces follicular prostaglandin E and 6-keto prostaglandin F-1 alpha in the cyclic hamster

In cyclic hamsters, exogenous progesterone (100 micrograms) administered s.c. at 09:00 h on the day of dioestrus II reduced prostaglandin (PG) E and 6-keto PGF-1 alpha but not PGF concentrations in preovulatory follicles measured at 09:00 h of pro-oestrus. The injection of 10 micrograms ovine LH (NIADDK-oLH-25) concurrently with 100 micrograms progesterone on dioestrus II prevented the decline in follicular PGE and 6-keto PGF-1 alpha values. Administration of LH alone did not significantly alter follicular PG concentrations. Inhibition of follicular PGE accumulation by progesterone was due to a decline in granulosa PGE concentration and not thecal PGE. Progesterone administration also reduced follicular oestradiol concentrations. Administration of oestradiol-17-cyclopentanepropionate (ECP) (10 micrograms) with progesterone did not prevent the decline in follicular PGE and 6-keto PGF-1 alpha but did increase follicular PGF concentrations. However, ECP given alone on dioestrus II reduced follicular PGE and increased PGF concentrations in preovulatory follicles on pro-oestrus. It is concluded that exogenous progesterone administered on dioestrus II inhibits granulosa PGE and 6-keto PGF-1 alpha accumulation in preovulatory follicles, probably by reducing serum LH concentrations, and that the granulosa cells, which are LH-dependent, are a major source of follicular PGE.     

Effects of PGF2alpha and PGF2alpha, 1-15 lactone on the corpus luteum and on early pregnancy in the rhesus monkey.

The effects of prostaglandin (PG)F2alpha and PGF2alpha, 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 PGF2alpha, 1-15 lactone were significantly (P less than 0.02) shorter than those in vehicle treated animals. In the absence of hCG pretreatment, plasma progesterone concentrations were significantly (P less than 0.008) lower by the second day after the initial treatment with either PGF2alpha or PGF2alpha, 1-15 lactone than in vehicle treated monkeys. Menstrual cycle lengths in monkeys treated with either PG were significantly (P less than 0.04) shorter than those in animals treated with vehicle. There were no changes in plasma progesterone concentrations in early pregnant monkeys treated with PGF2alpha, and pregnancy was not interrupted. In contrast, plasma progesterone declined and pregnancy was terminated in 5 of 6 early pregnant monkeys treated with PGF2alpha, 1-15 lactone. These data indicate that PGF2alpha, 1-15 lactone decreases menstrual cycle lengths in non-pregnant rhesus monkeys. More importantly, PGF2alpha, 1-15 lactone terminates early pregnancy in the monkey at a dose which is less than an ineffective dose of PGF2alpha.     

Prostaglandin production in the umbilical and uterine circulations in pregnant sheep at 129-136 days gestation.

Prostaglandins circulating in the maternal and foetal blood have been implicated in important physiological systems. These functions include foetal adrenal function, maintenance of patency of the ductus arteriosus, regulation of uterine and umbilical circulations, and labor and delivery type myometrial contractions. The placenta is a major site of prostaglandin production in pregnancy. Limited data are available which combine measurements of veno-arterial differences across the uterine and umbilical circulations with blood flow in these circulations to enable calculation of umbilical-placental and utero-placental production rates for the prostaglandins. In chronically instrumented pregnant ewes, between 129 and 136 days of gestation, prostaglandin F2 alpha(PGF2 alpha), 13, 14 dihydro-15-keto prostaglandin F2 alpha (PGFM), prostaglandin E2 (PGE2) were measured in the maternal carotid artery and uterine vein. Foetal PGE2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (the major metabolite of prostacyclin) were measured in umbilical venous and foetal descending aorta arterial plasma. Umbilical and uterine blood flow were measured using the diffusion-equilibrium technique. Uterine blood flow was 1693 +/- 137 ml.min-1 (mean +/- SEM); uterine production rates were 480 +/- 88 ng.min-1 for PGF2 alpha, 517 +/- 144 ng.min-1 for PGFM, and 165 +/- 27 ng.min-1 for PGE2. Umbilical blood flow was 147 +/- 17 ml.min-1.kg-1 foetal body weight. Umbilical production rates into the foetal circulation were 11 +/- 2 ng.min-1.kg-1 for PGE2 and 6 +/- 2 ng. ng.min-1.kg-1 foetal body weight for PGI2.     

Effects of the fetal-placental unit on uterine prostaglandin levels at term in the pregnant rat

Uterine prostaglandins (PGs) increase markedly at term in the pregnant rat. To assess the contribution of the fetal-placental unit (FPU) on uterine tissue and uterine venous blood PG concentrations, each uterine horn of 14 unilaterally pregnant rats at day 21 of pregnancy were compared. In addition, 7 bilaterally pregnant rats were studied. Uterine tissue and uterine venous plasma PGF, PGE, 6-Keto-PGF1 (6KF) and thromboxane B2 (TxB2) and systemic plasma progesterone, estradiol and estrone were determined by radioimmunoassay. Uterine concentrations of PGs (ng/mg DNA) were always greater on the pregnant side of unilaterally pregnant rats (p less than .05) although the PGF levels were elevated to a lesser extent than were PGE, TxB2 or 6KF. However, no differences were detected between uterine tissue from the pregnant side of unilaterally pregnant compared to bilaterally pregnant rats. In addition, no differences were found in uterine venous plasma PGs adjacent or opposite the pregnant uterine horn and in systemic plasma progesterone, estradiol and estrone levels in unilaterally vs bilaterally pregnant rats. These data suggest that the presence of the FPU is associated with an increased capacity of uterine tissue to produce PGE, TxB2 and 6KF, and to a lesser degree PGF, and thus may contribute to the increase in uterine PGs periparturition.     

The effects of Arcanobacterium pyogenes on endometrial function in vitro, and on uterine and ovarian function in vivo

Uterine bacterial infection after parturition causes endometritis, perturbs ovarian function and leads to infertility in cattle. Although endometritis is caused by mixed infections, endometrial pathology is associated with the presence of Arcanobacterium pyogenes. The aims of the present study were to determine the effects of A. pyogenes on endometrial function in vitro, and on uterine and ovarian function in vivo. Heat-killed A. pyogenes did not affect the production of prostaglandin F2alpha (PGF) or prostaglandin E(2) (PGE) from endometrial explants, or purified populations of endometrial epithelial or stromal cells. However, the explants produced more PGF and PGE than controls when treated with a bacteria-free filtrate (BFF) cultured from A. pyogenes. Similarly, BFF stimulated PGF and PGE production by epithelial and stromal cells, respectively. So, BFF or control PBS was infused into the uterus of heifers (n=7 per group) for 8 days, starting the day after estrus. Emergence of the follicle wave, dominant follicle or corpus luteum diameter, and peripheral plasma FSH, LH, estradiol, progesterone, PGFM, or acute phase protein concentrations were unaffected by the BFF infusion. In the live animal it is likely that the intact uterine mucosa limits the exposure of the endometrial cells to the exotoxin of A. pyogenes, whereas the cells are readily exposed to the toxin in vitro.     

Effects of the fetal-placental unit on uterine prostaglandin levels at term in the pregnant rat

Uterine prostaglandins (PGs) increase markedly at term in the pregnant rat. To assess the contribution of the fetal-placental unit (FUP) on uterine tissue and uterine venous blood PG concentrations, each uterine horn of 14 unilaterally pregnant rats at day 21 of pregnancy were compared. In addition, 7 bilaterally pregnant rats were studied. Uterine tissue and uterine venous plasma PGF, PGE, 6-Keto-PGF₁ (6KF) and thromboxane B₂ (TxB₂) and systematic plasma progesterone, estradiol and estrone were determined by radioimmunoassay. Uterine concentrations of PGs (ng/mg DNA) were always greater on the pregnant side of unilaterally pregnant rats (p<.05) although the PGF levels were elevated to a lesser extent than were PGE, TxB₂ or 6KF. However, no differences were detected between uterine tissue from the pregnant side of unilaterally pregnant compared to bilaterally pregnant rats. In addition, no differences were found in uterine venous plasma PGs adjacent or opposite the pregnant uterine horn and in systematic plasma progesterone, estradiol and estrone levels in unilaterally vs bilaterally pregnant rats. These data suggest that the presence of the FPU is associated with an increased capacity of uterine tissue to produce PGE, TxB₂ and 6KF, and to a lesser degree PGF, and thus may contribute to the increase in uterine PGs periparturition.