Luteal function in sheep with ovarian autotransplants given concurrent infusions of prolactin and prostaglandin F2α into the ovarian artery

Four experimental sheep with ovarian autotransplants were infused with prolactin (10 or 100 μg/h), into the ovarian artery, for 6 hours and then prolactin together with prostaglandin F_2α (PGF_2α) (5 μg/h) for a further 6 hours. A control sheep received PGF_2α alone, for 6 hours on two separate occasions. Prolactin failed to overcome the luteolytic action of PGF_2α in 3 of the 4 experimental sheep.     

Cyclic AMP formation of isolated human corpora lutea in response to HCG — Interference by PGF2α

Human corpora lutea of defined ages were excise at operation cut into pieces and incubated in the presence of HCG, PGF_2α and PGE₂ alone or in combination. Following incubation cAMP formation in tissue and medium was determined. HCG-stimulated tissue cAMP content was most pronounced at a corpus luteum age of 7–10 days after ovulation. This stimulation was antagonized by PGF_2α in corpora lutea older than 6 days. PGE₂ stimulated cAMP formation $\text{per se}$ and this effect was more pronounced when HCG and PGE₂ were combined. A possible role for PGF_2α as a luteolytic substance in the human is suggested.     

Reduction by human chorionic gonadotropin of the luteolytic effect of prostaglandin F2 in ewes

The ability of human chorionic gonadotropin (HCG) to reduce the luteolytic effect of prostaglandin (PGF_2^α) was demonstrated in cycling ewes. As expected, treatment with 10 mg of PGF_2^α alone on Day 10 of the estrous cycle exerted a potent negative effect on the function and structure of corpus luteum (CL) as indicated by reduced plasma progesterone, CL progesterone, and CL weight. However, the identical PGF_2^α treatment failed to significantly reduce either luteal function or luteal weight when administered to ewes that were also treated with HCG on Days 9 and 10 of the estrous cycle. Treatment with HCG alone had a positive effect on CL as indicated by increased plasma progesterone, CL progesterone, and CL weight. Treatment with HCG did not render the CL totally insensitive to the negative effects of PGF_2^α because plasma progesterone was reduced when the dose of PGF_2^α was doubled. Whether CL regressed or continued to function after treatment with both HCG and PGF_2^α appeared to depend upon a balance between the positive and negative effects of the two hormones.     

The possible mode of action of prostaglandins. XII. Differential effects of prostaglandin F2a in inducing premature evacuation of conceptus in the intact and castrated pregnant rat

A single injection of 2.0 mg/kg prostaglandin F₂a (PGF₂a) on day 18 of pregnancy was consistent in inducing premature labor by 72 h following the injection. Conversely, castration before PGF₂a on day 18 of pregnancy made the animals almost inert to PGF₂a and only 20% of the treated animals showed premature evacuation of the conceptus. Injection of 10 μg of estradiol cyclopentylpropionate (ECP) on day 18 was, however, found to be effective in emptying the gravid uteri of 100% castrated pregnants by 72 h. Indomethacin, a consistent inhibitor of prostaglandin biosynthesis and release, along with ECP in an identical experimental situation was found to be ineffective in reversing the ECP-induced premature parturition in castrated pregnants. The importance of intact ovary for the action of PGF₂a concerning premature labor in rats has been discussed.     

The concentrations of urinary prostaglandins E and plasma prostaglandins F2α and E during induction of ovulation with human gonadotropins

Plasma prostaglandins F₂α and E (PGF₂α, PGE) and urinary PGE were measured in 10 women treated with human gonadotropins (HMG) and subsequently with human chorionic gonadotropins (HCG). Five women became pregnant (6 pregnancies). There was no correlation between concentrations of plasma PGF₂α or PGE and plasma estradiol or progesterone. Urinary PGE concentrations showed a positive correlation with estradiol before HCG and a negative correlation with progesterone after HCG, only in women who subsequently became pregnant.Higher urinary PGE concentrations before HCG suggest that either HMG or rising estradiol levels stimulate PGE renal production. The significant negative correlation.between urinary PGE and progesterone concentrations, after HCG, in those patients who became pregnant suggests that ovarian production of progesterone may decrease renal production of PGE.     

Comparison of PGF2α-induced luteolysis in early pregnant and estrogen-treated ‘pseudopregnant’ gilts

Conceptus estrogen clearly plays a major role in luteal maintenance in the pig; however, other conceptus-derived substances or conceptus-induced uterine secretory products appear to have a local luteotrophic/anti-luteolytic effect on the corpora lutea (CL) and likely may play a key role in maternal recognition of pregnancy in the pig. The objective of these studies was to compare PGF₂α-induced luteolysis in estrogen-treated ‘pseudopregnant’ gilts versus pregnant gilts during the period of maternal recognition of pregnancy. In Experiment 1, doses of PGF₂α ranging from 1 to 100 μg were administered via intraluteal silastic implants to pseudopregnant gilts to determine the dose necessary to cause functional (progesterone) and structural (weight) luteal regression similar to that observed during the natural estrous cycle. Luteal sensitivity to this minimally effective luteolytic dose of PGF₂α was then determined for both pseudopregnant and pregnant gilts in Experiment 2. Experiment 3 investigated whether Day 13 porcine conceptus tissue could directly prevent PGF₂α-induced luteolysis at the level of the CL. The minimally effective luteolytic dose of PGF₂α (100 μg) determined in the pseudopregnant pig caused a similar decline in progesterone concentration and weight of CL in pregnant gilts, suggesting that the susceptibility of CL of pregnant and pseudopregnant pigs to PGF₂α is similar. However, luteal weight was greater (P<0.05) for the pregnant gilts than for pseudopregnant gilts, suggesting that estrogen treatment alone cannot mimic the conceptus effects on CL growth and development. Experiment 3 demonstrated that lyophilized Day 13 conceptus tissue implanted directly into individual CL could partially inhibit PGF₂α-induced luteolysis, providing for the first time direct evidence that porcine conceptuses as early as Day 13 contain factors which can directly (i. e. at the level of the CL) prevent luteal regression.     

Prostaglandin F2α induced luteolysis,hypothermia, and abortions in beagle bitches

Luteal phase plasma progesterone was radioimmunoassayed in samples collected before, during, and after a 72 hr treatment period during which Beagle bitches received repeated i.m. injections of prostaglandin F₂α (n=17) or saline (n=3). PGF₂α (20 ug/kg every 8 hr or 30 ug/kg every 12 hr) was administered to 7 pregnant and 8 nonpregnant bitches during the mid or late luteal phase of the cycle (Day 25–58) and to 2 nonpregnant bitches during the early luteal phase (Days 5 and 20). Progesterone was depressed from pretreatment levels (3 – 40 ng/ml) in each of the 15 bitches given PGF₂α after Day 25 of the cycle. Mean progesterone (ng/ml plasma) at ?24, 0, 12, 24, 36, 48, 60, 72 and 96 hr from the initial PGF₂α injection were 16.6, 15.6, 9.3, 5.1, 2.1, 1.5, 1.4, 1.1 and 1.1 (±0.9, n=15). Thereafter, progesterone was nondetectable in the 8 nonpregnant bitches and in 4 pregnant bitches that aborted. Abortions occurred when progesterone was depressed to 0.6 – 1.4 ng/ml, 56–80 hr after starting PGF₂α treatment on Days 33–53 of the cycle. Three pregnant bitches did not abort when progesterone was depressed to a mean low value of 2.1 ng/ml during PGF₂α treatments begun on Day 31 – 40 of pregnancy. Progesterone in these bitches recovered to 5 – 10 ng/ml and was maintained until the normal prepartum decline. Since PGF₂α can induce complete luteolysis it may be of use as an abortifacient in the bitch.A transient fall in rectal temperature occurred in each of 12 luteal phase bitches injected with PGF₂α (20 ug/kg, i.m.). The hypothermia was detectable within 15 min, maximal at 45 – 60 min, and averaged 1.39° C. No temperature changes were noted in eight ovariectomized bitches similarly treated. In six luteal phase bitches, plasma progesterone fell 20–45% within the 15 min required to observe a consistent decline in rectal temperature following PGF₂α administration. The transient hypothermia following PGF₂α appears to be secondary to the luteolytic effect and dependent on a fall in progesterone.     

Effect of prostaglandin F2α on ovarian and pituitary function in the mid-luteal phase

The effects of PGF_2α infusion in a dose of 25 μg/min for 5 hours on serum levels of estradiol-17β, 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 PGF_2α 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 PGF_2α administration. These results confirm that PGF_2α is not luteolytic in humans and no apparent relationship between PGF_2α and pituitary hormone secretion exists.     

Induction of 20α-hydroxysteroid dehydrogenase in rat corpora lutea of pregnancy by prostaglandin F2α

20α-OH-SDH is a marker of luteolysis in rat corpora lutea and appearance of this enzyme is inhibited by prolactin but stimulated by LH or hCG. PGF₂α induced 20 α-OH-SDH activity in corpora lutea of pregnant rats and a significant fall in peripheral plasma progesterone concentrations when administered i.m. for two consecutive days. Rats treated with PGF₂ α on days 8 and 9 of pregnancy were resorbing implants by day 10. Exogenous progesterone, but not estrogen, prevented implant resorption, yet 20 α-OH-SDH appeared in the corpora marking luteolysis. HCG, LH and prolactin, but not FSH, prevented pregnancy termination and inhibited induction of 20 α-OH-SDH in rats treated with PGF₂ α in early pregnancy. PGF₂α also induced 20α-OH-SDH in luteal tissue of intact and hypophysectomized rats treated on days 14 and 15 of pregnancy, but neither exogenous steroids or gonadotrophins blocked the induction of the enzyme in rats treated at this time. The increase in lutein 20α-OH-SDH activity during the peripartal period was partially blocked by administration of the prostaglandin biosynthesis inhibitor, indomethacin, suggesting a role for endogenous prostaglandins in the induction of 20α-OH-SDH at term. It appears that PGF₂α acts directly on the ovary to induce 20α-OH-SDH activity by preventing the luteotrophic action of prolactin. Other luteal NADPH-dependent dehydrogenase activities are not markedly stimulated following PGF₂α administration.     

Effects of PGF2α-induced luteolysis and progesterone on follicular growth in pregnant mice

The effects of a luteolytic dose of prostaglandin F_2α on follicular development within the ovary of pregnant mice were studied and vitro. The results showed that 1) PGF_2α reduced the number of growing primary follicles both and , 2) , progesterone and LH/FSH override this effect of PGF_2α and 3) progesterone suppresses the rate at which primary and preantral follicles grow. It is concluded that in the ovary of the pregnant mouse, progesterone regulates the number of primary follicles which start to grow; while gonadotropins and intraovarian progesterone levels control the rate at which primary and preantral follicles develop.     

Midterm abortion in hamsters induced by Silastic-PVP-PGE2 tubes

Intrauterine insertion of a 0.5 cm long Silastic-PVP tube containing 750 μg PGE₂ (lyophilized sodium salt) caused midterm abortion in hamsters within 48 hours. An earlier study using a similar Silastic-PVP tube delivery system showed that 200 μg of PGF_2α (Tham) was sufficient to induce abortion in 100% of pregnant hamsters (18). Prostaglandin E₂ is, therefore, about 3.5–4 times less potent than PGF_2α as an abortifacient in the hamster. The release of ³H-PGE₂ from Silastic-PVP tube and is also described. It is suggested that an increase in LH release might be one of the factors leading to luteolysis; and that either PGE₂ exerts a direct luteolytic effect or this effect is manifested after its being converted to PGF_2α.     

Corpus luteum regression induced by ultra-low pulses of prostaglandin F2α

In view of the pulsatile nature of PGF_2α secretion from the ovine uterus at the time of luteolysis, experiments were designed to examine the effect of pulsed infusions of PGF_2α on luteal function and to re-examine the minimal effective levels of PGF_2α required to induce luteolysis. To mimic physiological conditions, hour-long infusions of PGF_2α in increasing concentrations were given either 4 times in 19 h or 5 times in 25 h into the arterial supply of the autotransplanted ovary in conscious sheep on day 12 of an induced cycle. Blood flow and progesterone secretion rate from the ovary were used to monitor directly the luteolytic effect of administered PGF_2α. The concentration of LH in peripheral plasma was measured throughout each infusion experiment and the presence of a preovulatory peak of LH was used as an indicator of the permanence of luteal regression. Four pulses of PGF_2α in 19 h caused complete corpus luteum regression in only 1 of 4 animals whereas the addition of a fifth pulse (5 pulses in 25 h) caused permanent regression in 4 out of 4 animals. Infusion of 5 hour-long pulses of saline or PGF_2α at a rate of <0.04 μg/h did not induce permanent suppression of progesterone secretion. The average total effective dose of PGF_2α required to induced luteal regression when given as 5 pulses was 1/40th of the amount currently regarded as the minimal effective one when given by constant infusion into the ovarian artery. In another series of experiments the luteolytic effect of a single hour-long pulse of 0.1 μg/h PGF_2α given daily for either 3 or 4 days was investigated. A significant fall (ANOVA, F_0.01) in progesterone secretion rate, which reached a nadir at $\text{5.3 ± 2.2}\text{h (}\text{x}\text{±}\text{S.D.}\text{, n=15)}$, was followed by a recovery of progesterone secretion rate. Permanent luteal regression did not occur with this protracted regimen, suggesting that a relatively short pulse frequency of PGF_2α over a minimal period of 24 h is a necessary condition for physiological regression of the corpus luteum in sheep.     

Effects of PGF2α and PGF2α, 1–15 lactone on the corpus luteum and on early pregnancy in the rhesus monkey

The effects of prostaglandin (PG)F_2α and PGF_2α, 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_2α, 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_2α or PGF_2α, 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_2α, and pregnancy was not interrupted. In contrast, plasma progesterone declined and pregnancy was terminated in 5 of 6 early pregnant monkeys treated with PGF_2α, 1–15 lactone. These data indicate that PGF_2α, 1–15 lactone decreases menstrual cycle lengths in non-pregnant rhesus monkeys. More importantly, PGF_2α, 1–15 lactone terminates early pregnancy in the monkey at a dose which is less than an ineffective dose of PGF_2α.     

Corpus luteum susceptibility to prostaglandin F2α (PGF2α) luteolysis in hysterectomized prepuberal and mature gilts

The susceptibility of induced corpora lutea (CL) of prepuberal gilts and spontaneously formed CL of mature gilts to prostaglandin F_2α (PGF_2α) 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_2α or 5.0 mg PGF_2α. An additional group of prepuberal gilts was injected with 1.25 mg PGF_2α, a dose of PGF_2α equivalent, on a per kilogram body weight basis, to the 2.5 mg PGF_2α 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_2α and 5.0 mg PGF_2α 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_2α was 75.1. These results indicate that induced CL of the prepuberal gilt were more susceptible to PGF_2α 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.     

Corpus luteum function in the guinea pig: effect of pgf2 alpha and inhibitors of prostaglandin and progesterone biosynthesis.

Exogenous PGF_2α failed to consistently alter estrous cycle length of the guinea pig. A wide range of dose levels were administered with varying frequency, at different stages of the estrous cycle, in different vehicles and by various routes. Massive doses of PGF_2α (5.0–10.0 mg) produced a significant (p<.05), although transient, lowering of plasma progesterone levels. Smaller doses were ineffectual. An i.p. injection of 25 mg of PGF_2α was toxic in four of five treated animals. It would appear that the intact guinea pig is extremely resistant to the luteolytic effects of parenterally administered PGF_2α.Estradiol-17β, administered s.c. on days 3 to 10 of the estrous cycle, significantly (p<.05) reduced corpus luteum diameter and plasma progesterone levels. Estrous cycle length was unaffected. Clomiphene, in the same experiment, caused premature vaginal opening in some treated animals, but corpus luteum size and plasma progesterone levels were unaffected and no ovulations occurred.The prolactin secretion inhibitor, CB-154, administered early in the estrous cycle, did not have any effect on estrous cycle length of the guinea pig alone or in combination with PGF_2α. The prostaglandin precursor, arachidonic acid, also failed to influence estrous cycle length when administered on days 8 and 9 of the cycle. Plasma progesterone levels remained unaltered.Oral administration of a prostaglandin synthetase inhibitor, (MK-715), caused a small, but non-significant (p>.05) prolongation of the estrous cycle. The progesterone biosynthesis inhibitors, aminoglutethimide and 6β-hydroxy-3α, 5α-cyclo-androstane-17-one did not effect estrous cycle length or plasma progesterone levels of the guinea pig.     

Changes in corpus luteum content of prostaglandin F2α and E in the adult pseudopregnant rat

Conflicting reports exist regarding the source of luteolytic PGF_2α in the rat ovary. To assess the quantities of different PGs, measurements of PGF_2α, PGE and PGB were performed by radioimmunoassay in the adult pseudopregnant rat ovary throughout the luteal lifespan. Ovaries of 84 rats were separated by dissection into two compartments, corpora lutea of pseudopregnancy and remainder of ovary. Tissue samples were homogenized and prostaglandins extracted and determined by radioimmunoassay. During the mid-luteal and late-luteal phases, levels of PGs were significantly higher in the corpora lutea of pseudopregnancy than in the remainder of ovary. An increase of PGF_2α-content in the corpus luteum was registered with peak-levels of 53.9 ± 8.5 (mean ± SEM, N=18) ng/g tissue wet weight at day 13 of pseudopregnancy. PGE-levels reached peak-values at day 11 of pseudopregnancy (271.6 ± 28.4 ng/g w w, mean ± SEM, N=12). PGB-levels were below detection limits in all compartments for all ages studied. The present study demonstrates increased availability of PGF_2α in the corpus luteum during the luteolytic period, and points toward either increased luteal synthesis or luteal binding of PGF_2α during the luteolytic period.     

Luteal function,largest follicle,and fertility in postpartum dairy cows treated with 14dCIDR-PGF2α versus 2xPGF2α-Ovsynch for timed AI

A method for timed artificial insemination (AI) that is used for beef cows, beef heifers, and dairy heifers employs progesterone-releasing inserts, such as the controlled internal drug release (CIDR; Zoetis, New York, NY, USA) that are left in place for 14 days. The 14-day CIDR treatment is a method of presynchronization that ensures that cattle are in the late luteal phase of the estrous cycle when PGF_2α is administered before timed AI. The objective of this study was to test the effectiveness of the 14dCIDR-PGF_2α program in postpartum dairy cows by comparing it with the traditional “Presynch-Ovsynch” (2xPGF_2α-Ovsynch) program. The 14dCIDR-PGF_2α cows (n = 132) were treated with a CIDR insert on Day 0 for 14 days. At 19 days after CIDR removal (Day 33), the cows were treated with a luteolytic dose of PGF_2α, 56 hours later were treated with an ovulatory dose of GnRH (Day 35), and 16 hours later were inseminated. The 2xPGF_2α-Ovsynch cows were treated with a luteolytic dose of PGF_2α on Day 0 and again on Day 14. At 12 days after the second PGF_2α treatment (Day 26), the cows were treated with GnRH. At 7 days after GnRH, the cows were treated with PGF_2α (Day 33), then 56 hours later treated with GnRH (Day 35), and then 16 hours later were inseminated. There was no effect of treatment or treatment by parity interaction on pregnancies per AI (P/AI) when pregnancy diagnosis was performed on Day 32 (115/263; 43.7%) or Days 60 to 90 (99/263; 37.6%) after insemination. There was an effect of parity (P < 0.05) on P/AI because primiparous cows had lesser P/AI (35/98; 35.7%) than multiparous cows (80/165; 48.5%) on Day 32. Cows observed in estrus after the presynchronization step (within 5 days after CIDR removal or within 5 days after the second PGF_2α treatment) had greater P/AI than those not observed in estrus (55/103; 53.4% vs. 60/160; 37.5%; observed vs. not observed; P < 0.01; d 32 pregnancy diagnosis). When progesterone data were examined in a subset of cows (n = 208), 55.3% of cows had a “prototypical” response to treatment (i.e., the cow had an estrous cycle that was synchronized by the presynchronization treatment and then the cow responded appropriately to the subsequent PGF_2α and GnRH treatments before timed AI). Collectively, cows with a prototypical response to either treatment had 52.2% P/AI that was greater (P < 0.001) than the P/AI for cows that had a nonprototypical response (19%) (P/AI determined at 60–90 days of pregnancy). In conclusion, we did not detect a difference in P/AI when postpartum dairy cows were treated with 14dCIDR-PGF_2α or 2xPGF2α-Ovsynch before timed AI. The primary limitation to the success of either program was the failure of the cow to respond appropriately to the sequence of treatments.     

Fertility in dairy cows following presynchronization and administering twice the luteolytic dose of prostaglandin F2α as one or two injections in the 5-day timed artificial insemination protocol

The objectives were to evaluate pregnancy per AI (P/AI) of dairy cows subjected to the 5-day timed AI protocol under various synchronization and luteolytic treatments. Cows were either presynchronized or received supplemental progesterone during the synchronization protocol, and received a double luteolytic dose of PGF_2α, either as one or two injections. In Experiment 1, dairy cows (n = 737; Holstein = 250, Jersey = 80, and crossbred = 407) in two seasonal grazing dairy farms were randomly assigned to one of four treatments in a 2 × 2 factorial arrangement. The day of AI was considered study Day 0. Half of the cows were presynchronized (G6G: PGF_2α on Day −16 and GnRH on Day −14) and received the 5-day timed AI protocol using 1 mg of cloprostenol, either as a single injection (G6G-S: GnRH on Day −8, PGF_2α on Day −3, and GnRH + AI on Day 0) or divided into two injections of 0.5 mg each (G6G-T: GnRH on Day −8, PGF_2α on Day −3 and −2, and GnRH + AI on Day 0). The remaining cows were not presynchronized and received a controlled internal drug-release (CIDR) insert containing progesterone from GnRH to the first PGF_2α injection of the 5-day timed AI protocol, and 1 mg of cloprostenol either as a single injection on Day -3 (CIDR-S) or divided into two injections of 0.5 mg each on Days -3 and -2 (CIDR-T). Ovaries were examined by ultrasonography on Days −8 and −3 and plasma progesterone concentrations were determined on Days −3 and 0. In Experiment 2, 655 high-producing Holstein cows had their estrous cycle presynchronized with PGF_2α at 46 ± 3 and 60 ± 3 days postpartum and were randomly assigned to receive 50 mg of dinoprost during the 5-day timed AI protocol, either as a single injection or divided into two injections of 25 mg each. Pregnancies per AI were determined on Days 35 and 64 after AI in both experiments. In Experiment 1, presynchronization with G6G increased the proportion of cows with a CL on Day −8 (80.6 vs. 58.8%), ovulation to the first GnRH of the protocol (64.2 vs. 50.2%), and the presence (95.6 vs. 88.4%) and number (1.79 vs. 1.30) of CL at PGF_2α compared with CIDR cows. Luteolysis was greater for two injections compared to a single PGF_2α injection (two PGF_2α = 95.9 vs. single PGF_2α = 72.2%), especially in presynchronized cows (G6G-T = 96.2 vs. G6G-S = 61.7%). For cows not presynchronized, two PGF_2α injections had no effect on P/AI (CIDR-S = 30.2 vs. CIDR-T = 34.3%), whereas for presynchronized cows, it improved P/AI (G6G-S = 28.7 vs. G6G-T = 45.4%). In Experiment 2, the two-PGF_2α injection increased P/AI on Days 35 (two PGF_2α = 44.5 vs. single PGF_2α = 36.4%) and 64 (two PGF_2α = 40.3% vs. single PGF_2α = 32.6%) after AI. Presynchronization and dividing the dose of PGF_2α (either cloprostenol or dinoprost) into two injections increased P/AI in lactating dairy cows subjected to the 5-day timed AI protocol.     

Prostaglandin E2: Midterm abortion in rats using Silastic-PVP tubes

The results of the present study establish that 1.5 mg PGE₂ (lyophilized sodium salt) incorporated in one cm long open-ended Silastic-polyvinylpyrrolidone (PVP) tube when inserted into 10 day pregnant rats induced abortion within 70–72 hours in all the treated rats. A combined treatment of PGE₂ and 17β-estradiol failed to increase the abortion inducing effect of a Silastic-PVP-PGE₂ tube. It is observed that PGE₂ is about 4 times less potent than PGF_2α in inducing midterm abortion in rats. It is suggested that either PGE₂ exerts luteolytic effect after being converted to PGF_2α, although how it occurs is not clear; or PGE₂ causes expulsion of the fetuses by its uterine stimulating property. 17β- estradiol increases the uterine synthesis of PGF_2α as described earlier but seems not affecting the production of PGE₂ by the uterus. The release rate of ³H-PGE₂ from Silastic-PVP tube and is also described.     

Elongation of oestrous cycle in the guinea-pig following active immunisation against prostaglandin F2α

Five guinea-pigs actively immunised against a PGF_2α-bovine serum albumin conjugate showed elongated cycles, whereas 5 control animals injected with a mixture of PGF_2α and bovine serum albumin showed no change in cycle length. These results are compatible with the hypothesis that the uterine luteolytic hormone in the guinea-pig is PGF_2α.