Units Of Human Chorionic Gonadotropin Research Articles

Live Delivery in a 46.5-Year-Old Woman in Overt Menopause by Restoring Follicular Sensitivity to Follicle Stimulating Hormone (FSH)

For almost 40 years, there have been several publications where ovulation induction has occurred by lowering elevated serum follicle stimulating hormone (FSH) to up-regulate down-regulated FSH receptors on granulosa theca cells thus restoring follicular sensitivity to endogenous gonadotropins resulting in live deliveries. The majority of case reports used ethinyl estradiol to lower FSH. The advantage of ethinyl estradiol is that it does not add to the serum estradiol and thus allows the physician to better determine follicular maturation. To date the oldest woman to have ovulation induction and live delivery despite menopause was aged 45. A 46.5-year-old woman with 9 months of amenorrhea with a serum estradiol <15 pg/mL and a serum FSH of 117 mIU/mL was given ethinyl estradiol 20 micrograms daily. She attained a mature follicle on day 44 and conceived with natural intercourse with vaginal progesterone supplementation in the luteal phase. She delivered a full-term healthy chromosomally normal baby. Interestingly, she also had a successful live delivery when we treated her with progesterone in the luteal phase at age 42 when her day 3 serum FSH was 47 mIU/mL. Besides a luteal phase defect, she failed to release the egg from the follicle first naturally then with 10,000 units of human chorionic gonadotropin (hCG) but finally did release and conceived with the novel use of granulocyte colony stimulating factor, which was used again at age 46.5. Live deliveries are uncommon in women aged 46 even with regular menses and normal egg reserve. Precedents are important in medicine. Thus, this case represents the oldest woman with documented menopause to conceive naturally.

106 Maternal recognition of pregnancy (MRP) and mares: Is the epithelial sodium channel (ENaC) involved?

Maternal recognition of pregnancy (MRP) describes the prevention of luteolysis via the early conceptus. By prolonging the presence of the corpus luteum (CL), the conceptus ensures an environment capable of supporting pregnancy. In mares, MRP is enigmatic; the horse is one of few domesticated species wherein the MRP signal has yet to be discovered. Equine conceptus mobility throughout the uterine horns, termed migration, is known to be essential for pregnancy establishment. However, while the MRP signal in several other species is conceptus-derived, such a signal has yet to be observed from the equine embryo. We hypothesize that the migration of the equine conceptus itself activates MRP, potentially through epithelial sodium channel (ENaC). ENaC has been previously detected in multiple equine organs, observed in the uteri of various mammalian species, and also found to be upregulated during preimplantation in mice. However, neither the presence of ENaC within the mare uterus nor its potential involvement with the equine pregnancy has been researched. The aim of this study was 1) to determine if ENaC was present within the endometrium of the mare uterus and 2) to describe the location of ENaC if observed. Estrus synchronization was completed in mares (n = 14) during peak breeding season. Mares were subsequently blocked by age and breed and then placed into one of 2 groups: control mares (C; n = 7) and treatment mares (T; n = 7). Transrectal ultrasonography (US) was completed in all mares daily when one or more ovarian follicles reached 25 mm. When a mare had a 35 mm or larger follicle present, she received 2,000 international units of human chorionic gonadotropin intramuscularly to induce ovulation (OV) and US continued daily. Additionally, T mares were artificially inseminated (AI) with fresh, extended semen every day until the day after OV and were subsequently checked for pregnancy 12 d post-OV. C mares had the cervix manually manipulated the day after OV to replicate physical stimulation that occurs to the cervix when AI; however, no semen was deposited in C mare reproductive tracts. Endometrial biopsies were collected from all mares before OV, after OV, and during early pregnancy (when applicable) and samples were then processed for ENaC immunohistochemistry analysis. ENaC protein was immunodetected in all C and T mare endometrial samples and was localized to both uterine luminal epithelium and uterine glands. While further analysis will be conducted to quantify endometrial ENaC expression in C versus T (open versus pregnant) mares, the present histological data confirms that ENaC is present within the equine uterus.

نتایج بارداری بهروش لقاح خارج رحمی در تحریک با آگونیست آزاد کننده گنادوتروپین، گنادوتروپین جفتی انسان و یا گنادوتروپین جفتی انسان به همراه آگونیست آزادکننده گنادوتروپین در زنان نابارور؛ کارآزمایی بالینی تصادفی

Introduction: Human chorionic gonadotropin for the final maturation of eggs in the In-vitro fertilization cycle was associated with the possibility of a negative effect on endometrial acceptance, fetal quality and ovarian hyper stimulation syndrome. Replacing it with a gonadotropin-releasing hormone agonist to trigger final ovulation is expected to reduce these effects. Therefore, this study was performed with aim to evaluate the outcome of triggering in in vitro fertilization with antagonist protocol by gonadotropin-releasing hormone agonist, human chorionic gonadotropin simultaneously with human gonadotropin-releasing hormone agonist and human chorionic gonadotropin. Methods: In this randomized clinical trial study conducted in 2015 and 2016, women were divided into three random groups after preparing the follicles for triggering and ovum retrieval. One group received 0.2 mg of dipherline, the second group received 10,000 units of human chorionic gonadotropin and the other group received 0.2 mg of dipherline along with 1500 units of human chorionic gonadotropin. The number and quality of eggs and embryos were the outcomes of the study. Data were analyzed by SPSS software (version 17) and Leven tests and one-way analysis of variance. P < 0.05 was considered statistically significant. Results: The number of retrieved oocytes in the group receiving gonadotropin-releasing agonist was significantly higher than the other groups (p = 0.001). More embryos were produced in the gonadotropin-releasing hormone agonist group compared to the other two groups (p = 0.009). However, the number of high quality embryos produced in the groups was similar. Conclusion: The onset of final oocyte maturation with gonadotropin-releasing hormone agonist significantly increases the number of retrieved oocytes and obtained embryos. However, dual stimulation using low-dose human chorionic gonadotropin (IU1500) and gonadotropin-releasing hormone agonist did not alter quality of embryo compared to the standard dose of human chorionic gonadotropin (IU10000).

Association between Anti-Mullerian Hormone and Ovarian Response and Pregnancy in Polycystic Ovary Syndrome Patients

Objectives: Polycystic ovary syndrome (PCOS) is considered as one of the causes of infertility. Anti-Mullerian hormone (AMH) is 2-3 times higher in patients with the PCOS compared to others. The present study aimed to survey the association between basal AMH levels and ovarian response in infertile PCOS patients. Materials and Methods: In this cross-sectional study, 70 infertile PCOS women were enrolled referring to Milad Infertility Center (Mashhad, Iran) from May 2011 to April 2012. The basal blood level of AMH was evaluated. The patients received 5 mg of letrozole from the fifth cycle day (for 5 days) and then received 150 units of gonal F in the form of the recombinant follicle-stimulating hormone (FSH) on the ninth day of the cycle. Five thousand units of human chorionic gonadotropin (hCG) were prescribed for the patients who had one follicle of ≥ 18mm. Then, they should have had intercourse 36 hours later. After ovulation induction (OI) on the 10th cycle day, the second serum sample of AMH was taken. Results: Changes of AMH did not have a significant relationship with the ovarian response, namely, it was lower in patients with positive ovarian response compared to those without any ovarian response. In addition, the basal level of AMH in patients with a positive response (3.91 ± 2.14) had no significant difference with the secondary AMH (3.27 ± 2.39) after the OI (P = 0.19). Conclusions: Generally, the AMH was not a predictor of ovarian response in PCOS patients and the amount of AMH reduced after the treatment. This effect was maybe related to letrozole and gonadotropin.

Oocyte retrieval versus conversion to intrauterine insemination in patients with poor response to gonadotropin therapy

We compared cycle characteristics and outcomes for planned in vitro fertilization cycles with five or fewer developing follicles that proceeded to retrieval (n = 170) with those that converted to intrauterine insemination (IUI) (n = 50). The risk of no embryo transfer was 24% in cycles that proceeded to retrieval. Live birth rate per cycle started was similar for IUI (6%) compared with retrieval (7%).

Airway Smooth Muscle Cells Synthesize Hyaluronan Cable Structures Independent of Inter-α-inhibitor Heavy Chain Attachment

The covalent association of inter-alpha-inhibitor-derived heavy chains (HCs) with hyaluronan was first described in synovial fluid from arthritic patients and later described as a structural and functional component of hyaluronan "cable" structures produced by many different cells and stimuli. HC transfer has been shown to be mediated by the protein product of TSG-6 (tumor necrosis factor-stimulated gene 6). Considering the accumulation of hyaluronan in airways following asthmatic attacks and the subsequent infiltration of leukocytes, we sought to characterize HC substitution of hyaluronan "cables" in primary mouse airway smooth muscle cells (MASM) and primary human airway smooth muscle cells (HASM). We found that cells derived from mice lacking TSG-6 had no defect in hyaluronan production or hyaluronan-mediated leukocyte adhesion when treated with the viral mimic poly(I,C). Functional hyaluronan cables were induced by cycloheximide in the confirmed absence of protein synthesis, with or without simultaneous treatment with poly(I,C). We characterized the species specificity of the antibody other investigators used to describe the HC-hyaluronan complex of hyaluronan cables and found minimal affinity to bovine-derived HCs in contrast to HCs from mouse and human sera. Thus, we cultured MASM and HASM cells in serum from these three sources and analyzed hyaluronan extracts for HCs and other hyaluronan-binding proteins, using parallel cumulus cell-oocyte complex (COC) extracts as positive controls. We conclude that, if hyaluronan cables derived from MASM and HASM cells are substituted with HCs, the amount of substitution is significantly below the limit of detection when compared with COC extracts of similar hyaluronan mass.

Aquaporin-4 deficiency induces subfertility in female mice

To investigate the effects of aquaporin-4 (AQP4) on female fertility. Prospective, randomized animal study. Medical university. AQP4(+/+) and AQP4(-/-) female mice. Eight- to 10-week-old virgin female AQP4(+/+) and AQP4(-/-) mice were subjected to a mating study. Superovulation was carried out on 4-week-old AQP4(+/+) and AQP4(-/-) mice. The protocol consisted of a single intraperitoneal (IP) injection with 5 units of pregnant mare serum gonadotropin (PMSG) for 48 hours, followed by 5 units of human chorionic gonadotropin (hCG) for an additional 14 or 48 hours. Pregnancy success, oocyte count, morphological changes in ovaries and uteri, and alterations of estrous cycle. AQP4-null mice displayed subfertility as evidenced by a lower rate of pregnancy and decreased litter size. Further studies revealed that in AQP4-null mice, there were fewer numbers of antral follicles and corpora lutea in the ovaries and that uteri presented as hyporeactive to gonadotropins. In addition, in AQP4-null mice, superovulation induced by hCG and PMSG yielded fewer numbers of antral follicles, atretic follicles, corpora lutea, and oocytes in ovaries, and uteri exhibited a decreased response to exogenous gonadotropins. AQP4 deficiency induces subfertility in female mice.

PGAP1 Knock-out Mice Show Otocephaly and Male Infertility

A palmitate linked to the inositol in glycosylphosphatidylinositol (GPI) is removed in the endoplasmic reticulum immediately after the conjugation of GPI with proteins in most cells. Previously, we identified PGAP1 (post GPI attachment to proteins 1) as a GPI inositoldeacylase that removes the palmitate from inositol. A defect in PGAP1 caused a delay in the transport of GPI-anchored proteins (GPI-APs) from the endoplasmic reticulum to the cell surface in Chinese hamster ovary cells, although the cell-surface expression of GPI-APs in the steady state was normal. Nevertheless, in most cells, GPI-APs undergo deacylation. To elucidate the biological significance of PGAP1 in vivo, we established PGAP1 knock-out mice. Most PGAP1 knock-out mice showed otocephaly, a developmental defect, and died right after birth. However, some survived with growth retardation. Male knock-out mice showed severely reduced fertility despite the capability of ejaculation. Their spermatozoa were normal in number, motility, and ability to ascend the uterus, but were unable to go into the oviduct. In vitro, PGAP1-deficient spermatozoa showed weak attachment to the zona pellucida and a severely diminished rate of fertilization. Therefore, an extra acyl chain in GPI anchors caused severe deleterious effects to development and sperm function.

P-995: Sperm wash by gradient column technique improves IUI success rate

P-995: Sperm wash by gradient column technique improves IUI success rate

A comparison of pregnancy rates following in vitro fertilization in poor responders according to two different low-dose regimens of using leuprolide acetate in conjunction with gonadotropins

Background: Leuprolide acetate has been found to inhibit to some degree the recruitment of oocytes following stimulation with gonadotropins. Objective: Compare the outcome of two low dose leuprolide acetate regimens. Materials and Methods: Regimen 1 (stop protocol) leuprolide 0.5mg s.c. is given on the 7th day of the rise of serum progesterone (P) for 10 days and stopped in the early follicular phase of the next cycle. Regimen 2— (microdose flare) leuprolide 0.02mg daily from day 2 until injection of 10,000 units of human chorionic gonadotropin (hCG). Both regimens used 450 IU gonadotropin daily. The study patients were women who were >40 years of age, or were previous poor responders to a longer luteal phase use of leuprolide, or had serum follicle stimulating hormone (FSH) >12 mIU/mL on day 3. The choice of regimen was random but not prospective. Results: Stop protocol—clinical pregnancy rates (PRs) and implantation rates per transfer were 39.6% (88/222) and 15.7% (119/758) vs 28.4% (103/363) and 11.5% (139/1206) for microdose flare (p < .05, p < .05). The average number of embryos transferred were 3.2 vs 3.3. The biggest difference in success was seen in the group using these regimens because of age. The total dosage of leuprolide used in the stop protocol was 25 fold higher then in the microdose flare regimen. Embryo morphology and serum P prior to hCG were similar. Conclusions: Both regimens allowed a reasonable number of embryos to be transferred in this group with potentially poor response. However, getting leuprolide out of the system at least 10 days or more before ET is associated with higher PRs and implantation rates despite the fact that the total dosage used in this regimen is 25 times higher then microdose flare.

Transient induction of polycystic ovary-like syndrome in immature hypothyroid rats.

Hypothyroidism in the human female is often associated with ovarian follicular cysts and hyperandrogenism, two cardinal signs of polycystic ovary syndrome. To explore the intraovarian changes that lead to follicular cyst formation in hypothyroidism, we have created a prepubertal hypothyroid rat model. These hypothyroid rats are hyperandrogenic and develop transient ovarian follicular cysts. Hypothyroidism in newborn rats was induced by providing the lactating dams with 0.04% propylthiouracil (PTU)-containing water. Subsequently, female rats were weaned and kept on PTU-containing water. On Day 25 of age, the rats were primed with 15 international units of pregnant mare's serum gonadotropin (PMSG) in 100 microl of phosphate buffered saline. Two days later, to initiate pseudopregnancy, they were injected with five international units of human chorionic gonadotropin (hCG). The animals were sacrificed at appropriate times, and blood and ovaries were collected for analyses. Control experiments were done with euthyroid rats. Two days after PMSG injection, well-developed antral follicles were observed in both the hypothyroid and euthyroid rats. Two days after hCG injection, while the euthyroid rat ovaries, as expected, contained numerous corpora lutea (CL), the hypothyroid rat ovaries still retained antral follicles. Some of these follicles with degenerating oocytes showed signs of luteinization. By 3-4 days post-hCG injection, the hypothyroid rat ovaries developed cystic follicles. By Day 6, however, the hypothyroid rat ovaries were indistinguishable from those of the euthyroid rats. Although serum testosterone concentrations were significantly elevated in the hypothyroid rats on Days 1-3, progesterone concentrations were not significantly different from the euthyroid animals. However, by Days 8-14, the hypothyroid rats had significantly higher serum progesterone concentrations. This model will be useful for investigating the intraovarian biochemical changes that lead to follicular cyst development in response to acute gonadotropin treatment.

Decreased Hypothalamic Gonadotropin-Releasing Hormone Secretion in Male Marathon Runners

Abstract Hypogonadotropic hypogonadism due to a deficiency in hypothalamic gonadotropin-releasing hormone is common in female athletes (hypothalamic amenorrhea). It is not known, however, whether a similar phenomenon occurs in male athletes. We investigated the integrity of the hypothalamic-pituitary-gonadal axis in six highly trained male marathon runners (who were running 125 to 200 km per week). The mean (±SEM) frequency of spontaneous luteinizing hormone pulses was diminished in the runners, as compared with healthy controls (2.2±0.48 vs. 3.6±0.24 pulses per eight hours, P<0.05). The amplitude of the pulses was also low in the runners (0.9±0.24 vs. 1.6±0.15 mIU per milliliter; P<0.05), and the responses of luteinizing hormone to gradually increasing doses of exogenous gonadotropin-releasing hormone were decreased. Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin. During short-term i...

Decreased hypothalamic gonadotropin-releasing hormone secretion in male marathon runners.

Hypogonadotropic hypogonadism due to a deficiency in hypothalamic gonadotropin-releasing hormone is common in female athletes ("hypothalamic amenorrhea"). It is not known, however, whether a similar phenomenon occurs in male athletes. We investigated the integrity of the hypothalamic-pituitary-gonadal axis in six highly trained male marathon runners (who were running 125 to 200 km per week). The mean (+/- SEM) frequency of spontaneous luteinizing hormone pulses was diminished in the runners, as compared with healthy controls (2.2 +/- 0.48 vs. 3.6 +/- 0.24 pulses per eight hours, P less than 0.05). The amplitude of the pulses was also low in the runners (0.9 +/- 0.24 vs. 1.6 +/- 0.15 mlU per milliliter; P less than 0.05), and the responses of luteinizing hormone to gradually increasing doses of exogenous gonadotropin-releasing hormone were decreased. Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin. During short-term intense physical exercise (a treadmill run at 72 percent of maximal oxygen consumption for two hours), the plasma gonadotropin levels in the athletes remained stable, but significant elevations in plasma levels of cortisol, prolactin, and testosterone occurred. We conclude that highly trained male athletes, like their female counterparts, may have a deficiency of hypothalamic gonadotropin-releasing hormone. This condition may be caused by the prolonged, repetitive elevations of gonadal steroids and other hormones known to suppress gonadotropin-releasing hormone secretion that are elicited by their daily exercise.

The significance of the ratio in follicle-stimulating hormone and luteinizing hormone in induction of multiple follicular growth

Among the patients enrolled in the Norfolk In Vitro Fertilization Program there were 32 who had been stimulated according to the basic stimulation protocol using two ampules of human menopausal gonadotropin (hMG) daily. Because of their inadequate response, 23 of these 32 patients were stimulated subsequently with a combination of two ampules of "pure" follicle-stimulating hormone (FSH) and two ampules of hMG on cycle days 3 and 4. The remaining nine patients received four ampules of "pure" FSH only on cycle days 3 and 4. Stimulation was continued with hMG in both FSH regimens. Ten thousand units of human chorionic gonadotropin was used for final maturation. Parallel with the increase in the ratio of exogenous FSH to luteinizing hormone, an increase in oocyte recovery was observed, as well as an improvement in transfer and pregnancy rates. It was concluded that FSH enrichment had a beneficial effect in these patients.

Structure and location of the O-glycosidic carbohydrate units of human chorionic gonadotropin.

Structure and location of the O-glycosidic carbohydrate units of human chorionic gonadotropin.

Continued Clinical Experience with an Increasing Dosage Regimen of Clomiphene Citrate Administrations

Between August 1, 1975, and July 31, 1977, 60 patients with infertility and ovulatory dysfunction were evaluated at the Naval Regional Medical Center, Oakland. Of these, 15 had incomplete work-ups or were lost to follow-up. Of the remaining 45 patients, 2 (4.5%) failed to ovulate at a maximal dose of 250 mg of clomiphene for 5 days with 10,000 units of human chorionic gonadotropin. Of the 43 (95.5%) who did ovulate, 33 conceived. Of these 33 patients, 9 (27%) required greater than 100 mg of clomiphene and/or longer than three ovulatory cycles to conceive. Of the 10 patients who did not become pregnant, additional infertility factors were present in 5. When these 5 were eliminated, the corrected pregnancy rate was 87% (33 of 38). The spontaneous abortion rate was 12.2% and there were no multiple gestations. These results would further emphasize that clomiphene can be used safely and effectively at doses greater than 100 mg or for longer than three ovulatory cycles.

LEYDIG-CELL FAILURE AND HYPOGONADISM IN A 21 YEAR OLD MALE

A 21 year old male, with normal stature and an XY karyotype, presented with sparse pubic hair, no axillary hair, microphallus and otherwise normal external genitalia. Leydig-cell dysplasia and tubular degeneration were found on testicular biopsy. The mean 24 hr. plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations were 50 and 8 mIU/ml respectively. LH levels were higher during sleep than during waking hours. There were no sleep-wake differences in FSH levels. Plasma LH rose to 115 mIU/ml in response to 25 μg of LH releasing factor (LH-RF). Plasma FSH responded poorly to LH-RF. The mean 24 hr. plasma concentrations of testosterone (T) and dihydrotestosterone (DHT) were 95 and 84 ng/dl respectively. Plasma T rose from 120 to 160 ng/dl in response to 20,000 units of human chorionic gonadotropin (HCG), given over a 4 day period. Following an additional 20,000 units of HCG, given in 4 equal weekly doses, the plasma T concentration was 120 ng/dl. These data show that this patient has an unusual form of testicular degeneration characterized by diminished T production and poor T response to HCG. Normal concentrations of FSH suggest sufficient Inhibin production. The concentrations of T and DHT in utero, must have been adequate to enable normal differentiation of the external genitalia. This patient's abnormality fits into a spectrum of anomalies with Leydig-cell agenesis at one end and premature Leydig-cell failure (early climacteric) at the other.

The control of time of oestrus and ovulation and the induction of superovulation in cattle: Moore, N. W.: Aust. J. Agric. Res., [formula omitted]:295–304, 1975. Department of Animal Husbandry, University of Sydney, University Farms, Camden, N.S.W. 2570, Australia

To investigate the effects of aquaporin-4 (AQP4) on female fertility.Prospective, randomized animal study.Medical university.AQP4+/+ and AQP4−/− female mice.Eight- to 10-week-old virgin female AQP4+/+ and AQP4−/− mice were subjected to a mating study. Superovulation was carried out on 4-week-old AQP4+/+ and AQP4−/− mice. The protocol consisted of a single intraperitoneal (IP) injection with 5 units of pregnant mare serum gonadotropin (PMSG) for 48 hours, followed by 5 units of human chorionic gonadotropin (hCG) for an additional 14 or 48 hours.Pregnancy success, oocyte count, morphological changes in ovaries and uteri, and alterations of estrous cycle.AQP4-null mice displayed subfertility as evidenced by a lower rate of pregnancy and decreased litter size. Further studies revealed that in AQP4-null mice, there were fewer numbers of antral follicles and corpora lutea in the ovaries and that uteri presented as hyporeactive to gonadotropins. In addition, in AQP4-null mice, superovulation induced by hCG and PMSG yielded fewer numbers of antral follicles, atretic follicles, corpora lutea, and oocytes in ovaries, and uteri exhibited a decreased response to exogenous gonadotropins.AQP4 deficiency induces subfertility in female mice.

A gonadotropin-responsive adrenocortical adenoma.

A 49-yr-old virilized woman had a peripheral plasma testosterone (T) concentration of 783–911 ng/100 ml with a normal plasma concentration of androstenedione (A) and normal urinary 17-ketosteroids (17-KS). Plasma LH was below normal and FSH was low normal. Plasma T was not changed by dexamethasone 2 mg/day and the 17-KS were not normally suppressible. The administration of 5,000 units of human chorionic gonadotropin (hCG) increased plasma T to 3,744 ng/100 ml and also increased A and the 17-KS. Based on these results an ovarian source of T was suspected and bilateral oophorectomy was performed. Bilateral ovarian cortical stromal hyperplasia was found. Removal of both ovaries did not correct the hypertestosteronemia. Because an adrenal lesion was suspected, an 8-hr ACTH infusion test was done. Plasma T was decreased 42% and LH 31% at the sixth hour of the ACTH infusion. Plasma T was again increased by hCG to 2,379 ng/100 ml after the ovaries were removed. Both adrenals were explored and a 4 cm × 3 cm × 2 cm brown adrenocortical adenoma weighing 21 g was removed from the right adrenal. Plasma T was 17 ng/100 ml after the removal of the tumor and was now not increased by hCG. This gonadotropin-responsive adrenal adenoma further emphasizes that the results of hormonal manipulative procedures may be misleading in determining the source of excess androgen production.

Luteinizing Hormone, Prolactin, and Interval to Ovulation After Melengestrol Acetate in Cattle

Nine Holstein heifers were fed 1 milligram melengestrol acetate daily for 18 days. After melengestrol acetate withdrawal, duration and magnitude of ovulatory surge of luteinizing hormone resembled that reported for control estrus, and serum prolactin was elevated the day before or on the day of luteinizing hormone surge. In another experiment 25 Holsteins lactating 60 to 90 days were fed 1 milligram melengestrol acetate daily for 14 days and injected with 2,500 international units of human chorionic gonadotropin on day 17. Based upon twice-a-day rectal palpations, 22 cows ovulated at an average of 36±3 hours after injection.