Plasma concentrations of 13,14-dihydro-15-keto prostaglandin F2-alpha (PGFM), progesterone and estradiol in pregnant and nonpregnant diestrus cross-bred bitches

The canine corpus luteum (CL) typically sustains elevated plasma progesterone concentrations for 2 months or more, with a peak approximately 15-25 days after ovulation, followed by a slow decline. The processes involved in the slow, protracted regression of the CL over the remaining 1.5-2-month period in nonpregnant bitches and until shortly prepartum in pregnant bitches are not well characterized. The rapid luteolysis that occurs immediately prepartum appears to be a result of a prepartum rise in peripheral PGF. The potential role of PGF in the slow regression process in the several weeks preceding parturition and in nonpregnant bitches after 15-25 days after ovulation is not known. Therefore, plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F2-alpha (PGFM), progesterone (P4) and estradiol (E2) were determined and compared in bitches during nonpregnant diestrus (n = 9) or pregnancy (n = 8). During the gradual decrease in plasma concentrations of progesterone in both groups, the P4 pattern appeared unrelated to changes in either E2 or PGFM concentrations. The PGFM pattern was different between diestrus and pregnant bitches (P > 0.01); there was an apparent progressive but slow increase in PGFM in pregnant bitches from Days 30 to 60, followed by a large increase prior to parturition; concentrations declined immediately postpartum. However, there were no increases in PGFM during the same interval in nonpregnant bitches. Mean estradiol concentrations were sporadically elevated during the last third of pregnancy and less so in nonpregnant diestrus; there was no acute prepartum increase in estradiol associated with the PGFM increase. In summary, although there were no apparent changes in peripheral PGF2alpha concentration involved in regulating the slow protracted phase of luteal regression in nonpregnant bitches, modest increases in PGFM may play a role in ovarian function after mid-gestation in pregnant bitches. Furthermore, the acute prepartum rise in PGFM was not dependent on any concomitant increase in estradiol concentrations.     

Role of luteinizing hormone in changes in concentrations of progesterone and luteal blood flow during the hours of a simulated pulse of 13,14-dihydro-15-keto-prostaglandin F(2alpha) (PGFM) in heifers

A bolus treatment (e.g., 25 mg) of prostaglandin F(2alpha) (PGF) in the study of luteolysis in cattle results in dubious interpretations. Therefore, in experiment 1 of the present study, a 13,14-dihydro-15-keto-PGF (PGFM) pulse was simulated by incremental intrauterine (IU) infusion of PGF for 2.7 h on Day 14 postovulation. Concentrations of PGFM during the first hour of infusion and at the maximum were not different between simulated (n = 7) and spontaneous (n = 7) pulses. In experiment 2, four groups (n = 6 per group) were treated at Minute 0 (beginning of infusion) as follows: saline (infused IU), PGF (infused IU), acyline/saline, and acyline/PGF. Two hours before Minute 0, each heifer was given flunixin meglumine to inhibit endogenous PGF secretion, and heifers in the acyline/saline and acyline/PGF groups were given acyline to inhibit luteinizing hormone (LH). Plasma progesterone concentrations were similar among groups during Minutes 0 to 60, with no indication of an initial transient progesterone increase in the two PGF groups. Progesterone began to decrease in the PGF groups at Minute 60 and to rebound at Minute 135 after the PGFM peak at Minute 120. The rebound was complete in association with an increase in LH in the PGF group, but it was not complete when LH was inhibited in the acyline/PGF group. Luteal blood flow increased during PGF infusion in the two PGF groups and remained elevated for approximately 2 h after the PGFM peak in the PGF group but not in the acyline/PGF group. Novel findings were that an initial transient increase in progesterone did not occur with the simulated PGFM pulse and that LH stimulated a progesterone rebound and maintained the elevated luteal blood flow after the PGFM peak.     

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.     

Temporal changes in serum prostaglandin F2alpha and oxytocin in dairy cows with short luteal phases after the first postpartum ovulation

Luteolysis in the cow depends upon an interaction between prostaglandin F(2alpha) (PGF(2alpha)) and oxytocin. The objectives of our study were 1) to determine oxytocin concentrations in postpartum dairy cows and 2) to identify the temporal relationship between oxytocin and PGF(2alpha) release patterns during luteolysis in normal and abbreviated estrous cycles in the postpartum period. Serum oxytocin and PGF(2alpha) metabolite (PGFM) concentrations from nine cows which had short estrous cycles (< 17 d) were compared with those of six cows which had normal estrous cycles. Serum basal oxytocin concentrations in short estrous cycle cows (23.7 to 31.1 pg/ml) were higher (P<0.05) than those of normal estrous cycle cows (14.6 to 19.8 pg/ml). Oxytocin concentrations increased to peak values in both short and normal cycle cows, during luteolysis. Basal PGFM concentrations (112.2 to 137.4 pg/ml) were higher in cows with short cycle (P<0.05) than in cows with normal cycles (62.9 to 87.5 pg/ml). The increase in PGFM concentrations during luteolysis was significant in both normal cycle and short cycle cows (P<0.05). Increases in serum PGFM concentrations were always associated with increases in serum oxytocin concentrations in normal cycle and short cycle cows and the levels decreased simultaneously before the subsequent estrus. Results support the idea of a positive relationship between PGF(2alpha) and oxytocin concentration during the estrous cycle as well as a possible synergistic action of these hormones in the induction of luteolysis in dairy cattle.     

Prevention of the luteolytic action of oxytocin in the goat by inhibition of prostaglandin synthesis

Oxytocin-induced luteolysis in goats was associated with significant increases in peripheral plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F(2alpha) (PGFM). Oral administration of the prostaglandin (PG) synthetase inhibitor meclofenamic acid (lg/day) prevented both the luteolytic action of oxytocin and the increase in PGFM concentrations. These results confirm that the luteolytic effect of oxytocin is mediated via the production and release of PGF(2alpha).     

Control of luteolysis in the one-humped camel (Camelus dromedarius)

Blood plasma concentrations of 13,14-dihydro-15-keto PGF2 alpha (PGFM) were measured in groups of mature non-pregnant and pregnant camels to study PGF2 alpha release patterns around the time of luteolysis and the timing of the signal for pregnancy recognition. Injection of each of four camels with 10 and 50 mg of PGF2 alpha showed clearly that five times the dose of exogenous hormone produced five times the amount of PGFM in peripheral plasma, thereby indicating that, as in other animal species, PGFM is the principal metabolite of PGF2 alpha in the camel. Serial sampling of three non-pregnant camels on each of days 8, 10 and 12, and three pregnant camels on day 10, after ovulation for 8 h showed a significant (P < 0.05) rise in mean plasma PGFM concentrations only on day 10 in the non-pregnant, but not the pregnant, animals. A single intravenous injection of 20, 50 or 100 iu oxytocin given to three groups of three non-pregnant camels on day 10 after ovulation did not increase their basal serum PGFM concentrations. However, daily treatment of six non-pregnant camels between days 6 and 15 (n = 3) or 20 (n = 3) after ovulation with 1-2 g of the prostaglandin synthetase inhibitor, meclofenamic acid, inhibited PGF2 alpha release and thereby resulted in continued progesterone secretion throughout the period of meclofenamic acid administration. These results showed that, as in other large domestic animal species, release of PGF2 alpha from, presumably, the endometrium controls luteolysis in the dromedary camel. Furthermore, reduction in the amount of PGF2 alpha released is associated with luteal maintenance and the embryonic signal for maternal recognition of pregnancy must be transmitted before day 10 after ovulation if luteostasis is to be achieved. However, the results also indicate that, in contrast to ruminants, the release of endometrial PGF2 alpha in the non-pregnant camel may not be controlled by the release of oxytocin.     

Effect of PGF2alpha and 13,14-dihydro-15-keto-PGF2alpha (PGFM) on corpora luteal function in nonpregnant mares

The objective of this study was to determine if the primary circulating metabolite of PGF2alpha, 13,14-dihydro-15-keto-PGF2alpha (PGFM), is biologically active and would induce luteolysis in nonpregnant mares. On Day 9 after ovulation, mares (n = 7/group) were randomly assigned to receive: 1) saline control, 2) 10 mg PGF2alpha or 3) 10 mg PGFM in 5 mL 0.9% sterile saline i.m. On Days 0 through 16, blood was collected for progesterone analysis. In addition, blood was collected immediately prior to treatment, hourly for 6 h, and then at 12 and 24 h after treatment for progesterone and PGFM analysis; PGFM was measured to verify that equivalent amounts of hormone were administered to PGF2alpha- and PGFM-treated mares. Mares were considered to have undergone luteolysis if progesterone decreased to < or = 1.0 ng/mL within 24 h following treatment. Luteolysis was induced in 0/7 control, 7/7 PGF2alpha-treated, and 0/7 PGFM-treated mares. There was no difference (P>0.1) in the occurrence of luteolysis in control and PGFM-treated mares. More (P<0.001) PGF2alpha-treated mares underwent luteolysis than control or PGFM-treated mares. There was no difference (P>0.1) in progesterone concentrations between control and PGFM-treated mares on Days 10 through 16. Progesterone concentrations were lower (P<0.01) on Days 10 through 14 in PGF2alpha-treated compared with control and PGFM-treated mares. There was no difference (P>0.05) in PGFM concentrations between PGF2alpha- and PGFM-treated mares; PGFM concentrations in both groups were higher (P<0.001) than in control mares. These results do not support the hypothesis that PGFM is biologically active in the mare, since there was no difference in corpora luteal function between PGFM-treated and control mares.     

The relationship between 13,14-dihydro-15-keto PGF2 alpha and LH secretion in bulls

Half-life (t1/2), volume of distribution (Vd) and total body clearance (TBC) of 13,14-dihydro-15-keto PGF2 alpha (PGFM) were measured in order to determine optimal sampling frequency for accurate measurement of PGFM. Three yearling Holstein bulls (349.2 +/- 6.7 kg) and 3 yearling Holstein steers (346.7 +/- 7.0 kg) were utilized in a 3 X 3 Latin square design. Animals were given 0, 25 or 50 micrograms PGF2 alpha I.V.; blood samples collected every 2 min and plasma PGFM determined. The t1/2, Vd and TBC of PGFM were 2.3 +/- .2 min, 43.3 +/- 3.3 liters and 13.7 +/- 1.9 liters/min, respectively and were similar for 25 and 50 micrograms doses. To determine the relationship between endogenous PGFM and LH secretion in bulls, blood samples were collected every 2 min for 12 h in 4 yearling Angus bulls (489.1 +/- 11.6 kg). All animals elicited at least one LH surge and PGFM concentrations were measured in samples coincident with the LH surge. Mean plasma PGFM concentrations were greater prior to the LH surge than during the LH surge. In addition, mean plasma PGFM concentration and frequency of PGFM peaks appeared to increase prior to the LH surge suggesting an association between PGFM and pulsatile LH secretion in the bull.     

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)     

Temporal interrelationships at 15-min intervals among oxytocin, LH, and progesterone during a pulse of a prostaglandin F2α metabolite in heifers

A pulse of a PGF2α metabolite (PGFM) was induced by treatment with 0.1 mg of estradiol-17β on Day 15 (Day 0=ovulation; n=9 heifers). Blood samples were taken every 15 min for 9h beginning at treatment (Hour 0). For PGFM and LH, an intraassay-CV method was used to detect fluctuations in the 15-min samples and pulses in the hourly samples. A mean of 6.9 ± 0.4 PGFM fluctuations/9 h were superimposed on the hourly PGFM concentrations, compared to 2.1 ± 0.5 LH fluctuations/9 h (P<0.02). An increase (P<0.02) in oxytocin began 15 min before the beginning nadir of the PGFM pulse. A transient increase in progesterone did not occur at the beginning nadir of the PGFM pulse. Progesterone decreased (P<0.02) during the ascending portion and increased (P<0.03) as a rebound during the descending portion of the PGFM pulse. The peak of an LH pulse occurred 1.5 ± 0.4 h (range, 0.25-2.75 h) after the peak of the PGFM pulse. The wide range in the interval from a PGFM peak to an LH peak obscured the contribution of increasing LH to the rebound. The results did not support the hypothesis that oxytocin and PGFM increase concurrently. Results supported the hypothesis that the immediate transient progesterone increase that has been demonstrated with exogenous PGF2α does not occur during the ascending portion of an endogenous PGFM pulse. The hypothesis that the progesterone rebound after the peak of a PGFM pulse is temporally related to an LH pulse was supported.     

Prostaglandin concentrations in intra-uterine tissues from late-pregnant sheep before and after labour

Prostaglandin E (PGE), prostaglandin F (PGF) and 13,14-dihydro-15-keto-prostaglandin F (PGFM) have been measured in cotyledons and myometrium from sheep before and after labour. Fetal cotyledons contained more PGE than maternal cotyledons which in turn contained more than myometriu. The maternal cotyledon contained the highest concentrations of PGF, but the fetal cotyledon was the only tissue exhibiting a statistically significant rise in the concentration of PGF following labour. Concentrations of PGFM were closely correlated with (although usually lower than) those of PGF.     

Uterine secretion of prostaglandin F2 alpha in response to oxytocin in ewes: changes during the estrous cycle and early pregnancy.

Experiment 1 was conducted to determine when the ovine uterus develops the ability to secrete prostaglandin F2 alpha (PGF2 alpha) in response to oxytocin and how development is affected by pregnancy. Pregnant and nonpregnant ewes received an injection of oxytocin (10 IU, i.v.) on Day 10, 13, or 16 postestrus. Jugular venous blood samples were collected for 2 h after injection for quantification of 13,14-dihydro-15-keto-PGF2 alpha (PGFM). In nonpregnant ewes, concentrations of PGFM increased following oxytocin on Day 16 but not on Day 10 or 13. Concentrations of PGFM did not increase following treatment on Day 10, 13, or 16 in pregnant ewes. Therefore, the ability of oxytocin to induce uterine secretion of PGF2 alpha develops after Day 13 in nonpregnant but not in pregnant ewes. Experiment 2 was conducted to precisely define when uterine secretory responsiveness to oxytocin develops. Pregnant and nonpregnant ewes received oxytocin on Day 12, 13, 14, or 15. In nonpregnant ewes, concentrations of PGFM increased following treatment on Days 14 and 15, but not earlier. Peripheral concentrations of progesterone showed that uterine secretory responsiveness to oxytocin developed prior to the onset of luteal regression. As in experiment 1, the increase in concentrations of PGFM following administration of oxytocin was much lower in pregnant than in nonpregnant ewes; however, some pregnant ewes did respond to oxytocin with an increase in PGFM. In experiment 3, pregnant ewes received an injection of oxytocin on Day 18, 24, or 30 postmating. Concentrations of PGFM increased following oxytocin on Days 18 and 24. The conceptus appears to delay and attenuate the development of uterine secretory responsiveness to oxytocin.     

Prostaglandin F2 alpha as the luteolysin in swine: VI. Hormonal regulation of the movement of exogenous PGF2 alpha from the uterine lumen into the vasculature

To test the endocrine-exocrine theory of maternal recognition of pregnancy in the pig 16 gilts were assigned randomly to a 2 X 2 factorial involving pretreatment with sesame oil (SO) or estradiol valerate (5 mg; EV) injected on Days 11 through 14 of the estrous cycle and an intrauterine injection of saline (5 ml; SA) or prostaglandin F2 alpha (50 micrograms; PGF) on Day 14. Peripheral blood samples were collected for 120 min postinjection and analyzed for 15-keto-13,14-dihydro-PGF2 alpha (PGFM). PGFM concentrations were lower in EV than SO gilts (438 vs. 844 pg/ml; p less than 0.05). There was heterogeneity of regression between EV and SO gilts (p less than 0.01), with EV gilts having a slower release of PGF from the uterine lumen into the vasculature. Prostaglandin F2 alpha did not increase mean PGFM concentrations (p greater than 0.10), but resulted in an altered temporal pattern of PGFM (p less than 0.05) compared to SA gilts. There was an interaction between the two treatments over time, with EV-PGF gilts demonstrating a slower, more gradual release of PGFM than SO-PGF gilts. To test whether prostaglandins of the E series were involved in this mechanism, gilts were assigned to two 4 X 4 latin squares balanced for residual effects and treated with saline or flunixen meglumine (Banamine). Each gilt was treated with four PGE:PGF infusion sequences (SEQ) in each uterine horn: phosphate-buffered saline (PBS; PBS-SEQ), PGE1 (50 micrograms), PGE2 (50 micrograms), and PGE1 (25 micrograms) + PGE2 (25 micrograms) (PGE-SEQ), with each infusion followed 15 min later by PGF (25 micrograms).(ABSTRACT TRUNCATED AT 250 WORDS)     

The end of the tour de force of the corpus luteum in mares

Recent findings on the luteolytic process in mares are reviewed and differences from other farm species are noted. It is well known that the luteolysin, PGF2α (PGF), is secreted from the endometrium in the absence of pregnancy in farm animal species. But PGF is a potent chemical and safeguards have evolved so that only the corpus luteum (CL) is affected. The safeguards include a short PGF half-life and secretion in two or three pulses per day. In mares, endogenous PGF travels from the uterus to the CL through the systemic circulation, but the luteal-cell membranes are highly efficient in capturing the PGF molecules. In ruminants, luteal affinity is lower, but an efficient pathway has evolved for local delivery of PGF from a uterine horn to the adjacent ovary. The beginning of transition from luteal control is manifested within 1 h in mares and heifers, as indicated by a dynamic change in systemic progesterone concentrations. In mares, the transition into luteolysis begins during a relatively small transitional pulse of PGFM (a PGF metabolite) and oxytocin increases with the PGFM pulse. During luteolysis, estradiol increases in stepwise fashion within the hours of each PGFM pulse, with a plateau between pulses. Progesterone decreases linearly within the hours of a PGFM pulse and continuing during the interval between pulses, whereas luteal blood flow decreases during the declining portion of the pulse. In contrast, in heifers, progesterone decreases and increases within the hours of a PGFM pulse, and luteal blood flow increases and decreases concomitantly with the pulse.     

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)     

Stimulatory effect of PGF2α on PRL based on experimental inhibition of each hormone in mares

During the luteolytic period in mares, the peak of 65% of pulses of a PGF2α metabolite (PGFM) and the peak of a pulse of PRL have been reported to occur at the same hour. It is unknown whether the synchrony reflects an effect of PGF2α on PRL or vice versa. Controls, a flunixin meglumine (FM)-treated group (to inhibit PGF2α), and a bromocriptine-treated group (to inhibit PRL), were used at 14 days postovulation in June and in September (n = 6 mares/group/mo). Blood samples were collected hourly from just before treatment (Hour 0) to Hour 10. Concentrations of PGFM in the FM group were lower (P < 0.05) at Hours 4 to 6 than in the controls in each month, but bromocriptine had no detected effects on PGFM. Concentrations of PGFM averaged over all groups and within each group did not differ between June and September. Compared to the controls, concentrations of PRL in June were lower (P < 0.05) in the FM group at Hours 4 to 8 and in the bromocriptine group at Hours 4 to 10. Concentration of PRL averaged over groups was lower (P < 0.0001) in September (0.9 ± 0.05 ng/mL, mean ± SEM) than in June (3.0 ± 0.3 ng/mL). Results supported the hypothesis that the positive association between PGFM and PRL concentrations in mares represents an effect of PGF2α on PRL rather than an effect of PRL on PGF2α.     

Attenuation of luteolytic response following fish meal supplementation in dairy buffaloes (Bubalus bubalis)

Luteolysis of corpus luteum, due to un-inhibited PGF(2α) secretion, has been reported to be a cause of early embryonic mortality in dairy animals. The objective of this study was to determine the effects of fish meal (FM) supplementation on the uterine secretion of PGF(2α) and hence establish its supplementation as an antiluteolytic strategy in dairy buffaloes. Five cycling Murrah buffaloes were supplemented with 250g FM daily for 55 days in addition to their routine feed and seven buffaloes were kept as non-supplemented control. After 30 days of FM supplementation, the oestrus was synchronized in all the buffaloes using Ovsynch protocol. On day 15 of synchronized cycle, animals were challenged with oxytocin (OT; 100IU) intravenously and blood samples were collected at 15min interval, 1h before to 4h after OT challenge. The PGF(2α) response was measured as the venous concentration of 13,14-dihydro-15-keto PGF(2α) (PGFM). The mean hourly concentration of PGFM in FM supplemented buffaloes was lower than in the control buffaloes at all the occasions. During peak response (1h post-OT challenge), PGFM concentration was significantly lower (P<0.05) in FM supplemented buffaloes than in the control (197.4±41.7pg/ml versus 326.3±33.5pg/ml, respectively). Also the percent rise in PGFM after OT-challenge in FM supplemented buffaloes was less than the control (11.73% versus 22.47%). The dietary supplementation did not affect the size of corpus luteum (CL) and plasma progesterone concentration. Plasma glucose and total protein concentrations remained within the normal physiological limits during FM supplementation. The present study indicated that supplementing FM decreased the concentrations of PGF(2α) without alterations in the size of CL and plasma progesterone concentrations in dairy buffaloes.     

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)     

Prostaglandins in fetal tracheal and amniotic fluid from late pregnant sheep

Concentrations of prostaglandin E (PGE), prostaglandin F (PGF) and 13,14-dihydro-15-keto-prostaglandin F (PGFM) have been measured in fetal tracheal and amniotic fluid from chronically catheterized sheep during late pregnancy. Amniotic fluid contained significantly greater concentrations of these prostaglandins than tracheal fluid (p less than 0.01); there was no correlation between the level of prostaglandins found in each fluid. In tracheal fluid concentrations of PGE and PGFM exceeded those of PGF (P less than 0.01) whereas no significant differences were found in amniotic fluid. The levels of prostaglandins in these fluids were similar in ewes bearing hypophysectomized fetuses.     

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)