Evaluation of pituitary responsiveness to LHRH as a pregnancy test in ewes

Pregnant and nonpregnant ewes were injected with luteinizing hormone-releasing hormone (LHRH). Pituitary responsiveness, based on serum luteinizing hormone (LH), and follicle stimulating hormone (FSH) concentration, 2 hr after injection was then determined for each ewe, by radioimmunoassay (RIA) and correlated with the physiological reproductive state of each ewe. The serum LH release in pregnant ewes was significantly lower than that in nonpregnant ewes. Serum LH concentrations of pregnant ewes were further categorized according to whether the ewes were multiple (ML) or single lambing (SL). The responses by ML ewes were lower for LH than the SL responses. Follicle stimulating hormone responses were not different between pregnant or nonpregnant groups. Luteinizing hormone responses between pregnant ewes which were grouped according to 3 stages of pregnancy (1 to 5, 5 to 10 and 10 to 15 weeks pregnant) were not different from each other. Pregnancy diagnoses were made based on a fixed cut-off value, to which the LH response of each ewe to 5 mug LHRH was compared. Ewes whose response fell below this cut-off were diagnosed as pregnant. Accuracy of the diagnoses were determined by known lambing data. Diagnostic accuracy ranged from a low of 60% for nonpregnant, to a high of 95% for ML ewes. Accuracy for SL ewes (64%) was lower than for the overall pregnant group (79%), as well as that for ML ewes. Doses of LHRH, higher than 5 mug per ewe, generally produced LH release in pregnant ewes which was not significantly suppressed relative to responses of nonpregnant ewes. These results lead to the conclusion that gonadotropin response to exogenous LHRH injection is not an effective tool for pregnancy diagnosis.     

The effects of progesterone on follicular growth in the rabbit ovary

Studies were undertaken to measure the growth of follicles in the rabbit ovary during periods of elevated blood levels of progesterone. The progestin was increased in the blood by pregnancy or by implantation of progesterone pellets, which raised blood progesterone to near the levels measured during pregnancy. After 1, 2, 3, or 4 weeks of pregnancy or progesterone-pellet treatment, follicles of 1.0 mm external diameter or greater were dissected out of the ovaries and their external diameters were measured; then, each follicle was extracted for measurement of estradiol content. Blood levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in these animals as well. Follicles up to 2.5 mm in diameter were found in the ovaries of nonpregnant and untreated animals while 1.8 mm was the maximal size found during pregnancy or progesterone-pellet treatment. Furthermore, both in pregnant and in progesterone-treated rabbits, the follicular estradiol content and concentration were significantly suppressed compared to follicles from untreated rabbits. The progesterone pellets had no major effect on the levels of LH and FSH in the blood; the concentration of these gonadotropins in the progesterone-treated rabbits was virtually identical to levels previously measured in the blood of pregnant animals. The results of these studies indicate that progesterone exerts an inhibitory action on follicular development and steroidogenic function in the rabbit ovary. The progesterone action appears to be exerted directly on the ovary and is not indirect, by way of an inhibition of gonadotropin secretion.     

Ovulation and fertilization in the vole, Pitymys subterraneus

The females of Pitymys subterraneus bred in laboratory conditions have an irregular sexual cycle and induced ovulation. The first freshly ovulated eggs, surrounded by dense cumulus cells, appear in oviducts 10 h after copulation. Administering exogenous gonadotropins: pregnant mare's serum (PMS), human chorionic gonadotropin (hCG) or luteinizing hormone releasing hormone (LHRH), also induces ovulation in mature females of Pitymys subterraneus. In these experimental conditions females ovulate a similar number of eggs as after copulation. Dual stimulation (PMS and hCG plus copulation) does not result in the ovulation of a large number of normal ova, however, it does cause a release of degenerated oocytes.     

Pituitary and ovarian responses to luteinizing-hormone-releasing hormone during pregnancy and after parturition in brown hares (Lepus europaeus)

Female hares were given an i.v. injection of 5 micrograms luteinizing-hormone-releasing hormone (LHRH) between Days 7 and 19 (n = 21), 20 and 33 (n = 17) and 34 and 41 (n = 17) of pregnancy, and in the 3 days after parturition (n = 16). Whatever the stage of pregnancy, the LHRH injection induced a release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and an acute secretion of progesterone; these hormonal responses increased significantly during pregnancy, to reach values similar to those observed in nonpregnant, nonpseudopregnant females during the breeding season in the 3 days after parturition. However, the release of LH remained monophasic in pregnant and post-partum females, in contrast to the unmated females during the reproductive season, in which there was a biphasic profile. The proportion of ovulating females after LHRH treatment was approximately 60% at the beginning and end of pregnancy; and, after parturition, fell to 23% between Days 20 and 33. After Day 33, the pituitary response to LHRH was significantly higher in ovulating than in nonovulating females. At the beginning of pregnancy, 67% of females aborted after LHRH injection; after Day 20, the incidence of abortion decreased significantly and was 0% from Day 34. The amplitude and duration of progesterone secretion by the new corpora lutea resulting from ovulation after LHRH injection were similar to those of corpora lutea induced in nonpregnant females during the breeding season.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of porcine follicular fluid inhibin on gonadotropin secretion in the rabbit

Porcine follicular fluid (pff), treated with charcoal to remove steroids, was used to determine whether inhibin is active in the laboratory rabbit. When pff (5 ml/4 kg body weight) was injected (ip) into does that had been castrated 2 weeks earlier, there was a significant decline in blood follicle-stimulating hormone (FSH) levels; the decline lasted for 8-12 h. Blood levels of luteinizing hormone (LH) were suppressed, but only briefly at 3 h after injection. In other experiments, intact does which had been injected with pff 9 h and 10 min before receiving a single, i.v. injection of luteinizing hormone-releasing hormone (LHRH) (10 micrograms/kg body weight) showed a sharp reduction in the concentration of LH in the blood samples collected 15, 30 and 60 min after LHRH administration. Secretion of FSH responded poorly to LHRH stimulation, and pff had little suppressive action on blood levels. Having established that the pff preparation had inhibin activity, its action on the postovulatory surge of FSH secretion was next examined. This release of FSH, which occurs 6 to 36 h after ovulation, has been hypothesized to be required for the establishment of pregnancy by stimulating the growth of the ovarian follicles supplying the luteotropic estradiol. To test this hypothesis, pff was injected into rabbits every 8 h for the first 5 days of pregnancy and found to block the postovulatory FSH surge. The patterns of secretion of LH and progesterone in the same pff-injected animals were, however, not altered from normal pregnancy patterns by pff.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased LH and FSH release from the anterior pituitary of ovariectomized rat, in vivo, by copper-, nickel-, and zinc-LHRH complexes.

The effect of Cu2+, Ni2+, Zn2+ and their complexes with LHRH on the release of luteinizing hormone (LH) and follicle stimulating hormone (FSH) was estimated in in vivo experiments with the use of the method proposed by Ramirez and McCann. Ovariectomized, estradiol, and progesterone pretreated rats were injected intravenously either with LHRH alone, a metal ion alone, a mixture of metal and hormone, or a metal-LHRH complex. A metal alone or a mixture of it with LHRH did not affect gonadotropin release at all or no more than LHRH alone. However, the complex of Cu2+ with LHRH brought about a high release of LH and even higher release of FSH. This indicates that copper complex is more effective than metal-free LHRH. The nickel complex showed a similar although lesser effect. The zinc complex had similar potency to free LHRH though higher FSH-releasing ability was noticed. We conclude that copper-, nickel-, and zinc-LHRH complexes were more potent than the peptide hormone itself and promoted the FSH release in the ovariectomized, estradiol, and progesterone pretreated rats.     

A new male hypogonadism mutant rat (hgn/hgn): concentrations of testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in the serum and the responsiveness of accessory sex organs to exogenous T, FSH, human chorionic gonadotropin, and luteinizing hormone-releasing hormone

To determine the etiology of male hypogonadism in a newly found mutant rat (hgn/hgn, with a single autosomal recessive trait), concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were measured, and the responsiveness of the urogenital organs, hypothalamus, and pituitary gland to testosterone (1 mg/kg s.c. for 7 days), FSH (0.3 AU/kg s.c. for 7 days), human chorionic gonadotropin (hCG) (40 IU/kg s.c. for 7 days), and luteinizing hormone-releasing hormone (LHRH) (0.5 or 5.0 micrograms/kg s.c. for 7 days) were tested. Treatment with testosterone only increased the weights of all of the accessory sex organs, whereas treatment with FSH, hCG, or LHRH did not. Levels of serum FSH and LH were extremely higher and testosterone was lower in hgn/hgn males than in normal males. Serum FSH and LH decreased to levels found in intact animals after treatment with testosterone, suggesting that hypothalamic responsiveness to exogenous testosterone is present in the hgn/hgn males. Thus, the status of the hgn/hgn males was indicated to be due to primary Leydig cell dysfunction.     

Human chorionic gonadotropin and luteinizing hormone-releasing hormone reverse the blockade of ovulation in pregnant mare's serum gonadotropin-primed immature rats by the anti-androgenic drug, hydroxyflutamide

The present study was designed to examine mechanism(s) of the anti-ovulatory action of the anti-androgen, hydroxyflutamide (OH-F). Prepubertal rats were treated with 4 IU pregnant mare's serum gonadotropin (PMSG) (day -2) to induce first estrus and ovulation. They received OH-F in sesame oil or oil alone at 08:00 and 20:00 h on day 0 (the day of proestrus) and ovulations were assessed on the morning of day 1. Eighty-three percent of control animals ovulated with a mean of 7.7 +/- 1.1 corpora lutea per rat. Hydroxyflutamide blocked ovulation in all but 2 of the 12 rats receiving this drug alone. All of OH-F treated rats that received 5 and 25 IU human chorionic gonadotropin (hCG) ovulated with means +/- SEM of 9.1 +/- 0.1 and 7.3 +/- 1.4 corpora lutea per rat, respectively. The dose of 0.2 IU hCG was essentially ineffective, while the effect of 1.0 IU hCG was intermediate. At the dose of 20 ng and above (100 and 500 ng) luteining hormone-releasing hormone (LHRH) completely overcame the ovulation blockade in the OH-F treated animals, while a 4-ng dose was ineffective. At 18:00 h on the day of proestrus, serum LH levels in control animals were 17.56 +/- 2.60 ng/mL, which were 920% above basal levels (1.90 +/- 0.13) indicating a spontaneous LH surge. This surge was suppressed in OH-F treated rats. Injection of LHRH, at the dose of 20 ng and above, reinstated the LH release in OH-F treated animals. Thus, the anti-androgen, OH-F, inhibits ovulation in PMSG-treated immature rats through its interference with the preovulatory LH surge; the inhibition can be reversed by hCG or LHRH. Hydroxyflutamide does not appear to interfere at the level of the pituitary, but may have direct action at the hypothalamic and (or) extrahypothalamic sites involved in the generation of positive feedback signals that control LH release.     

Cocaine inhibits mating-induced, but not human chorionic gonadotropin-stimulated, ovulation in the rabbit.

The effects of cocaine on ovulation and corpus luteum function were investigated in New Zealand White rabbits. Forty females were randomly assigned to control and cocaine-treated groups. Controls were given vehicle s.c. daily for 5 days and cocaine-treated rabbits received 40 mg/kg cocaine hydrochloride s.c. daily for 5 days. One hour after the last cocaine dose, half the control and half of the cocaine-treated groups were mated with fertile males and the other half of each group received hCG i.v. Serial blood samples were obtained over 4 h on the day of mating or hCG treatment (Day 0), and then at intervals from Days 1-18. No mated, cocaine-treated rabbits ovulated, vs. 6 of 10 controls (chi-square: p = 0.01). In contrast, all animals given hCG had comparable numbers of corpora lutea (control: 7.1 +/- 0.8; cocaine: 5.7 +/- 0.8). Peak levels of benzoylecgonine (the major cocaine metabolite) occurred between 180 and 240 min after cocaine administration. In cocaine-treated animals that were mated, Day 0 serum LH (repeated measures MANOVA, p less than 0.01) and FSH (p less than 0.03) concentrations were lower than those in pregnant controls. Serum LH and FSH levels for all hCG recipients (cocaine-treated and control) did not differ. Serum prolactin concentrations in mated, pregnant rabbits were higher than in all other groups; cocaine treatment did not affect this hormone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transfemoral catheterization of the cavernous sinus outflow with comparison of “central” and “peripheral” gonadotropin patterns in bonnet monkeys

Concentrations of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in central (C) samples obtained by transfemorally catheterizing the inferior petrosal sinus of female bonnet monkeys were compared with those in peripheral (P) samples obtained simultaneously from the saphenous veins of two intact and two oophorectomized bonnet monkeys, before, during, and after luteinizing hormone releasing hormone (LHRH) stimulation. Significant differences between central and peripheral gonadotropin concentrations were detected intermittently in the resting state, and tended to be magnified by LHRH administration. In one animal in which LHRH was fortuitously administered during the course of a spontaneous LH surge, a C/P ratio for LH of 12.71, the maximum observed, was obtained. Spectral analysis exhibited periodicity for LH and, to a lesser extent, for FSH in the oophorectomized, but not in the intact, animals.     

Fecal steroid hormone analysis as an indicator of reproductive function in the cheetah

Techniques were developed and validated to measure fecal estrogen and progesterone concentrations of the female cheetah. Fecal samples were collected from seven mature females. Cheetahs were monitored before mating and continued until parturition. Four females had normal pregnancies, one conceived but the pregnancy resulted in spontaneous abortion, one was mated but apparently did not conceive and one was treated with gonadotropin-releasing hormone (GnRH) and human chorionic gonadotropin (hCG) to induce follicular growth and ovulation. Vaginal superficial cells increased with increasing estrogen concentrations. Peak estrogen occurred one day postcopulation. Increases in fecal progesterone concentrations, indicative of ovulation, occurred after copulation and hormonally induced ovulation. For the first time reproductive function can be monitored in the cheetah using noninvasive sample collection. © 1994 Wiley-Liss, Inc.     

Correlation between follicular fluid content and the results of in vitro fertilization and embryo transfer. III. Proteoglycans

Using a specific proteoglycan (PG) radioimmunoassay (RIA) in which human cartilage antiserum was directed against the PG protein core, the PG content of follicular fluid (FF) obtained from 42 women undergoing in vitro fertilization (IVF) and embryo transfer (ET) was studied as a function of IVF-ET outcome. Inhibition curves of purified PG cartilage preparations were parallel to those of large and small nonstimulated follicles and follicles that had been stimulated by a luteinizing hormone-releasing hormone (LHRH) agonist, d-tryptophan-6 (Decapeptyl: D-Trp6 analogue, Beaufour Laboratories, IPSEN Biotech, Paris, France), and human menopausal gonadotropin (hMG). While FF levels of immunoreactive PG-like material (Ir-PG) did not differ according to IVF-ET outcome, highly significant negative correlations were obtained between FF 17 beta-estradiol levels and FF Ir-PG levels in oocyte groups where pregnancy was obtained, i.e., oocytes were fertilized and cleaved, and pregnancy followed either for each ET or for one of two embryos reimplanted. The correlation persisted but weakened when all groups were pooled together. No correlation was observed between FF Ir-PG and progesterone. RIA or bioassay showed a positive correlation between FF inhibin and Ir-PG for the group in which each ET led to a pregnancy. Ir-PG concentrations were significantly greater in smaller than in larger follicles collected from untreated women. Upon induction of ovulation with either pure follicle-stimulating hormone (FSH), FSH + human chorionic gonadotropin (hCG), or D-Trp6/hMG + hCG, this difference no longer appeared. These results indicate that the reduction of Ir-PG concentrations constitutes an index of follicular maturation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pituitary and ovarian hormone secretion and ovulation in gilts injected with gonadotropins during and after oral administration of progesterone agonist (Altrenogest)

We determined changes in plasma hormone concentrations in gilts after treatment with a progesterone agonist, Altrenogest (AT), and determined the effect of exogenous gonadotropins on ovulation and plasma hormone concentrations during AT treatment. Twenty-nine cyclic gilts were fed 20 mg of AT/(day X gilt) once daily for 15 days starting on Days 10 to 14 of their estrous cycle. The 16th day after starting AT was designated Day 1. In Experiment 1, the preovulatory luteinizing hormone (LH) surge occurred 5.6 days after cessation of AT feeding. Plasma follicle-stimulating hormone (FSH) increased simultaneously with the LH surge and then increased further to a maximum 2 to 3 days later. In Experiment 2, each of 23 gilts was assigned to one of the following treatment groups: 1) no additional AT or injections, n = 4; 2) no additional AT, 1200 IU of pregnant mare's serum gonadotropin (PMSG) on Day 1, n = 4); 3) AT continued through Day 10 and PMSG on Day 1, n = 5, 4) AT continued through Day 10, PMSG on Day 1, and 500 IU of human chorionic gonadotropin (hCG) on Day 5, n = 5; or 5) AT continued through Day 10 and no injections, n = 5. Gilts were bled once daily on Days 1-3 and 9-11, bled twice daily on Days 4-8, and killed on Day 11 to recover ovaries. Termination of AT feeding or injection of PMSG increased plasma estrogen and decreased plasma FSH between Day 1 and Day 4; plasma estrogen profiles did not differ significantly among groups after injection of PMSG (Groups 2-4). Feeding AT blocked estrus, the LH surge, and ovulation after injection of PMSG (Group 3); hCG on Day 5 following PMSG on Day 1 caused ovulation (Group 4). Although AT did not block the action of PMSG and hCG at the ovary, AT did block the mechanisms by which estrogen triggers the preovulatory LH surge and estrus.     

Effects of the antiandrogen hydroxyflutamide on progesterone secretion by preovulatory rat follicles in vivo and in vitro.

Serum and ovarian progesterone levels and in vitro production of progesterone by preovulatory follicles were measured on proestrus in pregnant mare's serum gonadotropin (PMSG) primed immature rats in which the luteinizing hormone (LH) surge and ovulation were blocked by administration of the antiandrogen hydroxyflutamide. Serum progesterone levels observed at 12:00 on proestrus were significantly elevated, twofold above those observed in vehicle-treated controls, by in vivo administration of 5 mg hydroxyflutamide 4 h earlier. In control rats, proestrous progesterone did not increase until 16:00, in parallel with rising LH levels of the LH surge. No LH surge occurred in the hydroxyflutamide-treated rats, ovulation was blocked, and serum progesterone declined throughout the afternoon of proestrus, from the elevated levels present at 12:00. Administration of human chorionic gonadotropin (hCG) at 11:00 advanced the elevation of serum progesterone by 2 h in vehicle-treated controls and prevented the decline in progesterone levels in hydroxyflutamide-treated rats. The patterns of change in ovarian tissue concentrations with time and treatment were essentially similar to those observed for serum progesterone. In in vitro experiments, progesterone secretion during 24 h culture of preovulatory follicles obtained on PMSG-induced proestrus was significantly increased, sixfold, by addition to the culture media of 370 microM but not of 37 microM hydroxyflutamide. Testosterone (50 nM) and hCG (20 mIU/mL) caused 26- and 14-fold increases, respectively, in progesterone secretion by cultured follicles. Hydroxyflutamide significantly reduced the stimulatory effect of testosterone but not of hCG on progesterone secretion in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)     

Multiple causes of pregnancy failure in hamsters precociously ovulated by human chorionic gonadotropin

Cycling adult female hamsters can be induced to mate and ovulate 24 h early by the injection of 20 IU human chorionic gonadotropin (hCG) at 1500 h on Day 3 (day before proestrus), but pregnancy is not established. Although there is evidence of decreased sperm transport in precociously ovulated females, this does not appear to be the primary cause of infertility. Reduced size and vascularity of corpora lutea (CL) in treated females suggests incomplete or failed CL activation. Control and hCG-treated females were killed by exsanguination under ether anesthesia at intervals for the first 5 days after mating. Serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, estradiol, and progesterone were measured by radioimmunoassay. Luteinizing hormone in treated animals was very high at 2200 h on Day 1 after mating (31 h after the hCG injection), due to endogenous release, and dropped below control levels thereafter. Follicle-stimulating hormone, by contrast, was significantly lower than controls at 2200 h on Day 1 and remained low until 2200 h on Day 3 after mating. Prolactin in treated animals was not different from that in controls, except for 1000 h on Day 4, when it showed a significant dip. Estradiol in treated animals was significantly higher than in controls at 2200 h on Day 1 (when LH was also high and FSH was low), and remained high at 1000 h and 2200 h on Day 2, dropping thereafter to control levels. Progesterone was initially at control levels but had dropped significantly by 1000 h on Day 2 and remained low for the next 24 h. These results suggest that pregnancy failure is due to inadequate activation of corpora lutea. This may be due to: 1) immaturity of follicles at the time of ovulation; 2) inappropriate timing of preovulatory events; 3) the luteolytic effects of high levels of LH or estradiol or both; 4) the low level of FSH in the early stages of corpus luteum development; or 5) a combination of the above. Abnormalities of prolactin secretion were not investigated in detail but cannot be ruled out at this time.     

Stimulatory and inhibitory effects of progesterone on follicular development in the hypophysectomized follicle-stimulating hormone/luteinizing hormone-treated hamster

Cyclic hamsters hypophysectomized at estrus (Day 1 of the cycle) and injected with 5 micrograms follicle-stimulating hormone (FSH) on Day 1 and 20 micrograms luteinizing hormone (LH) in polyvinylpyrrolidone (PVP) from Days 1-4 ovulated 15.3 ova, in response to 30 IU human chorionic gonadotropin (hCG) administered at 1500 h on Day 4 (Kim and Greenwald, 1984). When 1 mg progesterone (P4) was administered daily from Days 1-4 concurrent with the above regimen, ovulation increased to 38 ova, a clearcut superovulatory response. However, daily injection of 1, 10, or 100 micrograms P4 plus FSH and LH reduced the number of antral follicles present on the afternoon of Day 4 to 3-4 per ovary, compared to 9 per ovary after FSH-LH alone, and the ovulation rate was drastically reduced with most animals being anovulatory. Substituting 1 mg 17 alpha-hydroxyprogesterone or estradiol cyclopentylpropionate for P4 on Days 1-4 did not alter the number of antral follicles on Day 4 from FSH-LH alone, whereas 1 mg androstenedione or 1 mg testosterone cyclopentylpropionate reduced the number of antral follicles to 3 or less. Hence, the stimulatory effects of 1 mg P4 are not attributable to its conversion to other P4 derivatives. After the concurrent injection of 1 mg P4 and FSH-LH, on the afternoon of Day 3, an average of only 1.8 large preantral follicles was present per ovary. By the morning of Day 4, however, the ovary contained 14 large preantral and early antral follicles in addition to 8 large antral follicles. Injection of hCG at this time resulted in the ovulation of 14.5 ova.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modification of the level of pituitary FSH in pregnant rats subjected to the luteinizing or ovulatory action of estradiol

In pregnant female rats injected on the 10th day of pregnancy with 10 mcg of estradiol, pituitary follicle stimulating hormone (FSH) is released on the 12th day, simultaneously with luteinizing hormone (LH) and a luteinizing or ovulatory effect. It is concluded that the test, which is described in detail, supports the hypothesis concerning the role played by FSH in determining the luteinizing action induced by estrogen in pregnant females, according to which the luteinizing effect is only produced when estradiol induces the simultaneous release of LH and FSH.     

Binding of high-density lipoproteins to luteal membranes: the role of prolactin, luteinizing hormone, and circulating lipoproteins

Ovarian and adrenal membranes from immature gonadotropin-primed rats, treated with 4-amino-pyrazolopyrimidine (4APP) to reduce endogenous lipoprotein levels, displayed higher binding of porcine high-density lipoprotein (HDL) when compared to control rats. Immature, hypophysectomized (HYPOX) rats bearing corpora lutea (CL) on Day 5 after ovulation had lower levels of serum progesterone and reduced capacity for HDL and human chorionic gonadotropin (hCG) binding to ovarian membranes when compared with intact animals. Hypophysectomy also reduced the number of HDL binding sites in adrenal membranes. Treatment of HYPOX animals with luteinizing hormone (LH) and prolactin (Prl) alone or in combination increased the HDL binding sites in the ovary relative to HYPOX-untreated rats. Neither hormone affected binding to adrenals, where only adrenocorticotropic hormone (ACTH) enhanced HDL binding. LH treatment reduced the serum progesterone levels and hCG binding to the ovaries, whereas Prl administration increased progesterone levels with no effect on hCG binding. We conclude from this study that HDL binding in the luteinized ovary is regulated by Prl and LH and circulating lipoproteins, whereas in adrenals it is regulated by ACTH and circulating levels of lipoproteins.     

The effect of mating on the afternoon of proestrus on serum LH (and FSH) and ovulation in the rat

Possible relationships between coitus and serum gonadotrophin levels and ovulation in the rat were investigated. Female rats were mated betw een 1700 and 1730 or between 1800 and 1830 hours. 1.3 ml of blood was withdrawn by cardiac puncture 30 minutes postcoitus for luteinizing hormone (LH) analysis. After autopsy on the morning of estrus, counts were made of tubal ova, and LH and follicle-stimulating hormone (FSH) were measured in terminal blood from all animals. Those mated at 1700-1730 with no cardiac puncture showed significantly more ova than those with cardiac puncture (p less than .05) and those which were neither mated nor received cardiac puncture (p les than .05). No differences were found between those mated at 1800-1830 hours because of the large variance in each group. Coitus during the time of normal mating did not increase LH levels 30 minutes postmating or terminal LH and FSH levels. Terminal LH levels were significantly increased in the no cardiac puncture-no mate animals (p less than .05) in comparison with the cardiac puncture-no mate animals.     

A 2 year follow-up of effects of biotechniques on reproduction in the domestic rabbit, Oryctolagus cuniculus

Routinely employed reproductive techniques such as gonadotropin treatment (0.3 mg follicle-stimulating hormone (FSH) subcutaneously twice daily for three consecutive days) followed by natural mating or artificial insemination as well as induction of ovulation by human chorionic gonadotropin (hCG) (75 i.u. hCG intravenously) were analysed in the rabbit after 2 years of consecutive experiments. 85% of gonadotropin-treated animals mated spontaneously. All 222 FSH-primed donor rabbits and 59 hCG-injected non-primed controls ovulated. The average number of ovulations per female was 30 (FSH and hCG) and 7.4 (hCG only). The fertilization rate was 88%, and 22.7 embryos were recovered per FSH-treated donor rabbit. With increasing time after mating the embryo recovery rate decreased (day 1 post coitum (p.c.), 36 embryos per rabbit; day 3 p.c., 26 embryos per rabbit; day 5 p.c., 16 embryos per rabbit) and a higher percentage of females had no embryos recovered. Embryo recovery was poor in donors with ovulation numbers greater than 40. Artificial insemination of nonreceptive females yielded smaller numbers of embryos compared with natural mating. Differences in fertility between the seasons of the year was revealed to be small. We conclude that gonadotropin treatment is efficient in increasing the number of embryos. Management of laboratory rabbits (dating, mating and expected number of embryos) is more predictable, and experiments can be performed successfully in all seasons of the year. However, the incidence of embryonic mortality seems to be increased when gonadotropin treatment is applied.