Luteinizing hormone receptor number and affinity in corpora lutea from prepuberal gilts induced to ovulate and spontaneous corpora lutea of mature gilts

This study was designed to determine if luteal cell receptors for luteinizing hormone/human chorionic gonadotropin (LH/hCG) contribute to the previously demonstrated abnormal function of induced corpora lutea (CL) in gilts. Twenty-five prepuberal (P) gilts, induced to ovulate with 1,500 IU pregnant mare serum gonadotropin followed 72 h later with 500 IU hCG (d 0 = day of hCG), and 22 mature (M) gilts that had displayed two or more estrous cycles were ovariectomized (OVX) on d 10, 14, 18, 22 or 26 after the onset of estrus. All gilts except those OVX on d 10 were hysterectomized between d 6 and 9 to ensure luteal maintenance. The CL were stored at -196 degrees C until determination of LH/hCG receptor number and dissociation constant (KD) by saturation analysis. Receptor number was greater for M than for P gilts on d 14 (P less than .07) and d 18 (P less than .01). The KD was greater in M than in P gilts on d 14 (P less than .01) and d 18 (P less than .0001). The LH/hCG receptor number and KD of P gilts remained the same throughout the days studied. The LH/hCG receptor number (fmol/mg protein) of M gilts was elevated on d 10, 14, and 18 (50.8, 50.4 and 51.4, respectively) and decreased on d 22 (26.5) and d 26 (25.4) to values similar to those of P gilts. In M gilts, KD increased on d 14, remained high on d 18 and decreased on d 22. We suggest that abnormal function of induced CL in P gilts may be due to an elevated LH receptor number.     

Comparison of induced corpora lutea from prepuberal gilts and spontaneous corpora lutea from mature gilts: hydroxysteroid dehydrogenase activity

The activity of hydroxysteroid dehydrogenases was histochemically quantified in corpora lutea (CL) from prepuberal gilts induced to ovulate and mature gilts. Prepuberal (P) gilts, 120 to 130 d of age were induced to ovulate with 1,500 IU pregnant mare serum gonadotropin (PMSG) followed 72 h later by 500 IU human chorionic gonadotropin (hCG). Three P gilts and three mature (M) gilts each were ovariectomized on d 10, 14, 18, 22 and 26 (d 0 = day of hCG for P gilts and onset of estrus for M gilts). Gilts ovariectomized on d 14, 18, 22 and 26 were hysterectomized on d 6 to ensure luteal maintenance. At the time of ovariectomy, CL were frozen in liquid nitrogen and then stored at -80 C until analysis. Cryostat sections (12 microns) were histochemically analyzed for delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta OHSD), 17 alpha-hydroxysteroid dehydrogenase (17 alpha OHSD) and 20 alpha-hydroxysteroid dehydrogenase (20 alpha OHSD). The intensity of staining (greater enzyme activity resulted in darker staining) was quantified using a Zeiss SF microscope integrated with a Zonax photometer, which measured the percentage of light transmitted through a given area (22,500 microns 2) of the tissue section. Data were subjected to analysis of variance using the general linear models procedure of Statistical Analysis System (SAS). The 3 beta OHSD activity did not change over days, but the mean activity (throughout all days) in the P gilts (32.6 +/- 1.8) tended (P less than .08) to be elevated above that of M gilts (27.9 +/- 1.7).(ABSTRACT TRUNCATED AT 250 WORDS)     

Regression of induced corpora lutea in mature cyclic gilts by human chorionic gonadotropin.

This study was conducted to determine whether chronic hCG treatment would cause regression of induced corpora lutea (CL) in mature cyclic gilts. Thirty-two mature gilts that had displayed one or more estrous cycles of 18 to 22 d were used. Sixteen gilts were hysterectomized (HYSTX) on d 6 to 9 (d 0 = onset of estrus) and their CL were marked with charcoal (spontaneous group). Sixteen gilts (induced group) were injected with 1,500 IU of pregnant mare's serum gonadotropin (PMSG) on d 6 and 500 IU of hCG on d 9 (day of hCG = d 0 of the induced cycle). Ovulation was assumed to occur on d 2 of the induced cycle. Induced gilts were HYSTX on d 8 to 9 (d 17 to 18 of the original spontaneous cycle) and their CL were marked with charcoal. Only gilts (n = 14) in which induced CL were present and in which the original CL had regressed were then subjected to treatment with saline or hCG. From d 10 to 29, gilts with spontaneous CL were injected daily with 500 IU of hCG (n = 8) or saline (n = 8). From d 10 to 29 of the induced cycle, induced gilts were injected daily with 500 IU of hCG (n = 6) or saline (n = 8). Jugular blood samples were collected every other day from all gilts beginning on the 1st d of daily hCG treatment and quantified for estradiol and progesterone by RIA. On the day after the last hCG injection, the number of charcoal-marked CL and charcoal-marked corpora albicantia (CA) were determined.(ABSTRACT TRUNCATED AT 250 WORDS)     

Observations on the influence of exogenous gonadotrophins and cloprostenol on ovulation in gilts

We studied the effects of gonadotrophins and prostaglandin (PG) F_2α on ovulation in gilts. Twenty-eight gilts were induced to ovulate using 750 IU pregnant mares serum gonadotrophin (PMSG) and 500 IU human chorionic gonadotrophin (hCG), administered 72 h apart. At 34 and 36 h after hCG, gilts received injections of either 500 μg or 175 μg PGF_2α (cloprostenol), or had no injections. Laparotomies were performed at 36 h (cloprostenol gilts) or 38 h (controls) after hCG injection. The ovaries were examined and the proportion of preovulatory follicles that had ovulated (ovulation percent) was determined at 30 min intervals for up to 6 h. The number of gilts in which ovulation was initiated and the ovulation percent increased (p<0.001) with time, but was not affected by treatment. Many medium sized follicles (≤6 mm) were also observed to ovulate, or to exhibit progressive luteinization without overt ovulation, during the surgical period. A discrepancy between numbers of preovulatory follicles and corpora lutea suggests that luteal counts may not be an accurate assessment of ovulation rate following gonadotrophic stimulation.     

Comparison of induced corpora lutea from prepuberal gilts and spontaneous corpora lutea from mature gilts: in vitro progesterone production

Prepuberal (P) gilts were induced to ovulate with pregnant mare serum gonadotropin followed 72 h later by human chorionic gonadotropin (hCG). Three P gilts and three mature (M) gilts each were ovariectomized on d 10, 14, 18, 22 and 26 (d 0 = day of hCG for P gilts and onset of estrus for M gilts). Gilts ovariectomized on d 14, 18, 22 and 26 were hysterectomized on d 6 to ensure maintenance of the corpora lutea (CL). Two to five grams of minced luteal tissue were dispersed using collagenase and hyaluronidase in HEPES buffered salt solution supplemented with glucose and bovine serum albumin. Dispersed cells were rinsed in Dulbecco's Modified Eagle Medium (DMEM), counted (ratio of large to total number of luteal cells determined) and then incubated for 1 h in DMEM. With aliquots standardized to 2.5 X 10(4) viable, large cells (greater than 25 micron diameter) were incubated in 1 ml DMEM for 2 h in the presence of either 10, 50, 100 or 1,000 ng luteinizing hormone (LH); .1, 1, 10 or 100 ng hCG; 10, 100 or 1,000 ng norepinephrine (NE) or either .75, or 1.5 mM dibutyrl cyclic adenosine monophosphate (dbcAMP). Progesterone (P4) in the medium was quantified by radioimmunoassay. Basal P4 production (no P4 stimulator added to the medium) on d 10, 14, 18, 22 and 26 for P gilts was 246 +/- 9, 66 +/- 4, 64 +/- 6, 41 +/- 3 and 69 +/- 6 ng/ml medium, respectively, and for M gilts was 281 +/- 12, 128 +/- 8, 53 +/- 4, 82 +/- 6, 101 +/- 5 ng/ml medium, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Induction of fertile estrus in prepuberal gilts by treatment with a combination of pregnant mare's serum gonadotropin and human chorionic gonadotropin

Ten trials involving 678 presumed prepuberal gilts (5.5 to 7.5 mo old) were conducted in North Carolina, Illinois and Missouri to evaluate the reproductive performance of gilts given a combination of 400 IU of pregnant mare's serum gonadotropin and 200 IU of human chorionic gonadotropin (P. G. 600). Gilts that were presumed to be prepuberal received P. G. 600 or no treatment (control) on the day of movement from finishing facilities to pens for breeding. Detection of estrus, with the aid of mature boars, was conducted daily for 28 d; gilts in estrus were mated naturally. Treatment with P. G. 600 increased the percentage in estrus within 7 (57.5 vs 40.9%) or 28 d (72.9 vs 59.5%); average interval to estrus was reduced (P less than .05) from 10.4 to 7.5 d. Farrowing rate (78.5 +/- 3.1%), number of pigs born alive (8.6 +/- .2) or dead (.26 +/- .06) and number of pigs weaned (8.0 +/- .2) were unaffected by treatment. Gilts that were heavier than the median for each farm were in heat sooner and more were detected in heat, but no other reproductive traits differed between heavy and light gilts. Overall, the results reveal that P. G. 600 was useful for induction of fertile estrus in prepuberal gilts.     

Appearance of the uterine specific proteins following induction of ovulation in prepubertal gilts.

The appearance of the uterine specific proteins following induction of ovulation in prepubertal gilts is described. 12 gilts each at 3, 4, and 5 months of age were allotted randomly to 1 of 2 treatment groups prior to induction of ovulation: 1) saline treated and 2) human chorionic gonadotropin (HCG) treated (400 IU daily from Days 12 through 16 of the induced cycle). Ovulation was induced with HCG following treatment with pregnant mare serum gonadotropin and the day of ovulation was designated as Day 1. All the gilts were laparotomized and uteri infused with phosphate-buffered saline on Day 16 to obtain uterine protein secretions. Plasma progesterone levels on Day 11 and observations made at laparotomy indicated that only 1 gilt 3 months of age failed to ovulate. The number of corpora lutea, plasma progesterone, total recoverable uterine protein, and uterine specific protein on Day 16 were markedly affected by the age of the gilt. These same characteristics, except uterine specific protein, were additionally affected by HCG treatment. Total recoverable uterine protein and uterine specific protein in saline and HCG-treated gilts at 3, 4, and 5 months of age were 6.3 and 1.5, 10.4 and 2.8; 38.8 and 15.2, 51.6 and 15.9; 20.4 and 7.7, 47.8 and 14.6 mg, respectively. Polyacrylamide slab gel electrophoresis showed that HCG-treated gilts at 3 months of age and both saline- and HCG-treated gilts at 4 and 5 months of age generally produced the purple basic protein and the complete profile of the low molecular weight acidic proteins during the induced cycle.     

Possibilities of ovulation synchronization in puberty-induced gilts

Puberty was induced in 39 clinically prepuberal gilts (two groups of three sub-groups each) by parallel but locally separated application of 500 IU PMSG ("Maretropin") and 250 IU HCG ("Gonadex"), with the view to testing ways to synchronise ovulation. Seventy-two hours were allowed to elapse, before 24 animals received another application of 500 IU HCG and 15 animals 250 IU HCG. The animals were slaughtered in consecutive groups of study ovulation and histolotically examined to disclose endometrial processes. Ovulations were found to be well synchronised in the recipients of a second injection of 500 IU HCG. Only sub-threshold effects with no synchronised ovulation were recorded from the animals that had received a second dose of 250 IU HCG. A second injection of 500 IU HCG should be given not until something between 78 and 82 hours after puberty induction for optimum follicle maturation and adequate proliferation of the endometrium.     

Technical note: use of slow-release estradiol and prostaglandin F2alpha to induce pseudopregnancy and control estrus in gilts

We determined whether a single injection of slow-release estradiol-17beta (SRE2) would induce pseudopregnancy in gilts and whether PGF2alpha would regress the corpora lutea (CL) of pseudopregnancy. Crossbred gilts (n = 40) were induced to ovulate by treatment with 400 IU of hCG + 200 IU of eCG (PG600, Intervet, Millsboro, DE) given at 180 d of age (d = 0). On d 14, gilts were injected i.m. with one of five doses (n = 8 gilts/dose) of SRE2 (0, 12.5, 25, 50, or 100 mg). Blood samples were collected before SRE2 and twice weekly until d 73 to monitor serum progesterone (P4) and estradiol (E2). On d 59, gilts received (i.m.) 10 mg of PGF2alpha (Lutalyse, Pharmacia Upjohn, Kalamazoo, MI) and were checked for estrus for 7 d. On d 62, mammary development was scored (0 = no development; 1 = some development; 2 = teat and gland development) by a neutral observer. Treatment with SRE2 increased (P < .05) peak E2 concentrations, duration of luteal function, and mammary gland score. There were no differences (chi-square, P > .05) among doses of SRE2 in the percentage of pseudopregnant gilts that showed luteolysis after PGF2alpha. We conclude that a single injection of SRE2 can induce pseudopregnancy and that the CL can be regressed with PGF2alpha, providing a simple method for controlling estrus in gilts.     

Follicle growth in hypophysial stalk-transected pigs given pulsatile GnRH and pregnant mare serum gonadotropin

In experiment 1, nine prepuberal crossbred gilts 145 +/- 2 days of age and 90.3 +/- 1.6 kg body weight (BW) were hypophysial stalk-transected (HST) or sham-HST. Starting at 0800 on Day 1 (35 +/- 2 days after surgery), three sham-HST and two HST gilts received 3.5% sodium citrate vehicle (V) while two HST gilts and two sham-HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 9 days via a jugular vein cannula. At 0800 on day 7, all gilts received 1,000 IU of pregnant mare serum gonadotropin (PMSG) im. Blood was sampled every 15 min from 0800 to 0845 on Days 1 through 6. On Day 10, ovarian morphology and ovarian and follicular fluid weights were recorded. In experiment 2, eight prepuberal crossbred gilts, 146 +/- 6 days of age and 79.5 +/- 1.5 kg BW, were HST or sham-HST. Starting at 0800 on Day 1 (7 +/- 4 days after surgery), two sham-HST and three HST gilts received V, while three HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 8 days. At 1200 on Day 5, all gilts, including three unoperated controls (UC), received 1,000 IU of PMSG im. Blood was sampled from all but UC gilts every 15 min from 0800 to 0845 on Days 1 through 5. Ovarian data were obtained on Day 9. The HST + V gilts failed to respond to PMSG, whereas growth of ovulatory follicles was stimulated in the other groups in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ovarian response to pregnant mare serum gonadotropin and porcine pituitary extract in gilts actively immunized against gonadotropin releasing hormone

Two experiments were conducted to determine the effect of exogenous gonadotropins on follicular development in gilts actively immunized against gonadotropin releasing hormone (GnRH). Four gilts, which had become acyclic after immunization against GnRH, and four control gilts were given 1,000 IU pregnant mare serum gonadotropin (PMSG), while four additional control gilts were given saline. Control animals were prepuberal crossbred gilts averaging 100 kg body weight. Control gilts given saline had ovaries containing antral follicles (4 to 6 mm in diameter). Control gilts given PMSG exhibited estrus and their ovaries contained corpora hemorrhagica and corpora lutea. PMSG failed to stimulate follicular growth in gilts immunized against GnRH, and ovaries contained regressed corpora albicantia and small antral follicles (less than 1 mm in diameter). Concentrations of luteinizing hormone (LH) and estradiol-17 beta (E2) were non-detectable in gilts immunized against GnRH and given PMSG. In the second experiment, five gilts actively immunized against GnRH were given increasing doses of PMSG every third day until unilateral ovariectomy on d 50. PMSG failed to stimulate follicular growth, and concentrations of follicle stimulating hormone (FSH), E2 and LH were not detectable. Six weeks later, gilts were given a booster immunization and then were given 112 micrograms LH and 15 micrograms FSH intravenously every 6 h for 9 d. The remaining ovary was removed on d 10. Although LH and FSH concentrations were elevated, administration of gonadotropins did not stimulate follicular growth or increase E2 concentrations. These results indicate that neither PMSG or exogenous LH and FSH can induce E2 synthesis or sustain follicular development in gilts actively immunized against GnRH.     

Uterine influences on the formation of subnormal corpora lutea in seasonally anestrous ewes

The hypothesis that subnormal luteal function after induced ovulation in anestrous ewes was the result of uterine influences exerted during the periovulatory period was tested. Crossbred ewes (n = 27) in seasonal anestrus were induced to ovulate by administration of 12 doses of 250 ng of LHRH at 2-h intervals, followed immediately by a bolus injection of LHRH (250 micrograms; d 0). Ewes were unilaterally hysterectomized on either d -3 (PRELHRH) or 2 (POSTLHRH). Daily blood samples were collected and assayed for progesterone (P4) and 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM). All ewes were slaughtered on d 10, and corpora lutea (CL) were collected, weighed, and assayed for concentration of P4. All ewes that ovulated exclusively in the ovary ipsilateral to the remaining uterine horn had a transient increase in plasma P4 of 2 to 3 d (short luteal phase). In ewes with at least one CL in the isolated ovary, elevated plasma P4 was maintained after hysterectomy but was consistently lower (P less than .05) in POSTLHRH ewes than in PRELHRH ewes. Concentrations of PGFM did not differ between treatments. The CL ipsilateral to the remaining uterine horn weighted less (P less than .01) and contained less P4 (P less than .01) than contralateral CL. These data confirm the hypothesis that premature regression of subnormal CL is uterine-dependent in a local fashion. Presence of the uterus during the follicular and(or) early luteal phase inhibited subsequent luteal function in seasonally anestrous ewes.     

Effects of gonadotropin treatment on ovarian follicle growth and granulosal cell aromatase activity in prepuberal gilts

This experiment was conducted to compare the ability of USDA porcine FSH-B-1 (pFSH), USDA porcine LH-B-1 (pLH), and pregnant mare's serum gonadotropin (PMSG) to grow large follicles and induce granulosal cell aromatase activity in prepuberal gilts. Twenty-four gilts (164 d old) received one of four treatments by i.m. injection: 1) saline once, n = 8; 2) pFSH (8 micrograms/kg BW, nine times at 8-h intervals), n = 5; 3) pLH (2 micrograms/kg BW, nine times at 8-h intervals), n = 6; or 4) PMSG (15 IU/kg BW, once), n = 5. At slaughter, 72 h after the first injection, the ovaries to saline-treated gilts contained an average of 104 surface antral follicles 1 to 3 mm in diameter. compared to treatment with saline, pFSH increased (P less than .05) the number of follicles 46%, whereas pLH or PMSG decreased (P less than .05) the number by 70 and 84%, respectively. Compared with saline, treatment with PMSG or pLH induced growth of large follicles (7 to 9 mm) (10.8 and 4.8 follicles/gilt, respectively), increased plasma estrogen, increased granulosal cell aromatase activity, and decreased plasma FSH by 51 and 69%; treatment with pFSH had no significant effect on these traits. Results indicate that injected pFSH did not cause growth of large follicles or induce granulosal cell aromatase activity in prepuberal gilts. In contrast, LH initiated growth and increased granulosal cell aromatase activity in a small number of follicles and accelerated atresia among the remaining follicles.     

Effect of age and physical or fence-line boar exposure on estrus and ovulation response in prepubertal gilts administered PG600

Boar exposure has been used for estrus induction of prepubertal gilts, but has limited effect on estrus synchronization within 7 d of introduction. In contrast, PG600 (400 IU of PMSG and 200 IU of hCG; Intervet, Millsboro, DE) is effective for induction of synchronized estrus, but the response is often variable. It is unknown whether boar exposure before PG600 administration might improve the efficiency of estrus induction of prepubertal gilts. In Exp. 1, physical or fence-line boar contact for 19 d was evaluated for inducing puberty in gilts before administration of i.m. PG600. Exp. 2 investigated whether 4-d boar exposure and gilt age influenced response to PG600. In Exp. 1, 150-d-old prepubertal gilts were randomly allotted to receive fence-line (n = 27, FBE) or physical (n = 29, PBE) boar exposure. Gilts were provided exposure to a mature boar for 30 min daily. All gilts received PG600 at 169 d of age. Estrous detection continued for 20 d after injection. In Exp. 2, prepubertal gilts were allotted by age group (160 or 180 d) to receive no boar exposure (NBE) or 4 d of fence-line boar exposure (BE) for 30 min daily before receiving PG600 either i.m. or s.c. Following PG600 administration, detection for estrus occurred twice-daily using fence-line boar exposure for 7 d. Results of Exp. 1 indicated no differences between FBE and PBE on estrus (77%), age at puberty (170 d), interval from PG600 to estrus (4 d), gilts ovulating (67%), or ovulation rate (12 corpora lutea, CL). Results from Exp. 2 indicated no effect of age group on estrus (55%) and days from PG600 to estrus (4 d). A greater (P < 0.05) proportion of BE gilts expressed estrus (65 vs. 47%), had a shorter (P < 0.05) interval from PG600 to estrus (3.6 vs. 4.3 d), and had decreased (P < 0.05) age at estrus (174 vs. 189 d) compared with NBE. Ovulation rate was greater (P < 0.05) in the BE group for the 180-d-old gilts (12.7 vs. 11.9 CL) compared with the NBE group. However, age group had no effect on ovulation (77%) or ovulation rate (12 CL). Collectively, these results indicate that physical boar contact may not be necessary when used in conjunction with PG600 to induce early puberty. The administration of PG600 to 180-d-old gilts in conjunction with 4 d prior fence-line boar exposure may improve induction of estrus, ovulation, and decrease age at puberty.     

Clinical study results of the embryonic development in gilts and brooding performance of gilts and sows after HCG treatment on the 11th day of pregnancy

Forty-four pregnant gilts were slaughtered on the 32nd and 33rd days of pregnancy, after 30 of them had received 100 or 400 IU of HCG on the eleventh day of pregnancy. Both doses had resulted in higher number of living embryos. Embryo survival rates of treated sows were up to 14.9 percent higher than those of untreated animals. Higher numbers of embryos had no adverse effect on their mass development. Fertility was measured of 77 HCG-treated and untreated gilts as well as of 54 adult sows. The number of non-pregnant sows which returned to oestrus was higher in the group of gilts and adult sows which had received treatment. The number of pregnant animals in the treated adult sow group was seven percent higher than that in the control group. Increased litter sizes were additionally recordable from those gilts and adult sows that had received HCG injections. Yet, those higher litter sizes were associated with lower weight of live-born piglets. In further studies more attention should be given to possible stimulation of LH secretion in early gravidity.     

Ovarian morphological conditions and the effect of injection of human chorionic gonadotropin on ovulation rates in prepuberal gilts with two morphologically different ovarian types

The purpose of this experiment was to determine the ovulation rate after treatment with human chorionic gonadotropin (hCG) in two groups of gilts characterized by different ovarian morphology: grape-type (GT; n = 11) and honeycomb-type (HT; n = 7). At 170 d of age (d 0), gilts were examined by laparoscopy and ovarian type was determined by the distribution of macroscopic follicles present on the ovarian surface. Five to ten minutes after surgery, each gilt received a single injection (i.m.) of 750 IU of hCG. At d 0, GT ovaries had a greater number of large follicles (greater than or equal to 6 mm) than HT ovaries (10.0 +/- .5 vs 2.6 +/- .3; P less than .05), whereas HT ovaries had more small follicles (1 to 3 mm; HT: 42.3 +/- .8 vs GT: 26.7 +/- .9; P less than .05) and total follicles (HT: 59.4 +/- 2.3 vs GT: 52.2 +/- 1.5; P less than .05), although numbers of medium follicles (4 to 5 mm) were similar (GT: 15.6 +/- .8 vs HT: 14.6 +/- 1.7; P greater than .10). Number of induced corpora lutea (CL) per ovary was greater (P less than .05) in gilts with GT ovaries (10.59 +/- 2.9 CL) than in gilts with HT ovaries (5.21 +/- .66 CL). Total weight of luteal tissue (LT) per ovary and serum progesterone concentrations 8 d after induction of ovulation were greater in GT gilts than in HT gilts (GT: 6.37 +/- 1.09 g vs HT: 3.31 +/- .49 g for LT, P less than .05; GT: 21.08 +/- 4.76 ng/ml vs HT: 13.40 +/- 2.05 ng/ml for progesterone, P less than .07).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of human chorionic gonadotropin on preovulatory luteinizing hormone surge and ovarian hormone secretion in gilts

The influence of varying doses of human chorionic gonadotropin (hCG) on the preovulatory luteinizing hormone (LH) surge, estradiol-17 beta (E2) and progesterone (P4) was studied in synchronized gilts. Altrenogest (AT) was fed (15 mg X head-1 X d-1) to 24 cyclic gilts for 14 d. Pregnant mares serum gonadotropin (PMSG; 750 IU) was given im on the last day of AT feeding. The gilts were then assigned to one of four groups (n = 6): saline (I), 500 IU hCG (II), 1,000 IU hCG (III) and 1,500 IU hCG (IV). Human chorionic gonadotropin or saline was injected im 72 h after PMSG. No differences in ovulation rate or time from last feeding of AT to occurrence of estrus were observed. All gilts in Groups I and II expressed a preovulatory LH surge compared with only four of six and three of six in Groups III and IV, respectively. All groups treated with hCG showed a rapid drop (P less than .01) in plasma levels of E2 11, 17, 23 h after hCG injection when compared with the control group (35 h). The hCG-treated gilts exhibited elevated P4 concentrations 12 h earlier than the control group (3.1 +/- .5, 3.4 +/- .72, 3.1 +/- .10 ng/ml in groups II, III and IV at 60 h post-hCG vs .9 +/- .08 ng/ml in group I; P less than .05). These studies demonstrate that injections of ovulatory doses of hCG (500 to 1,500 IU) had three distinct effects on events concomitant with occurrence of estrus in gilts: decreased secretion of E2 immediately after hCG administration, failure to observe a preovulatory LH surge in some treated animals and earlier production of P4 by newly developed corpora lutea.     

Ovarian response of the hypophysial stalk-transected pig to pregnant mare serum gonadotropin

Hypophysial stalk transection (HST) or sham operation (S-HST) was performed on 14 prepuberal gilts, 169 ± 3 days of age and 72.8 ± 3.4 kg body weight (day of surgery = Day 0). Gilts received 1,000 IU of pregnant mare's serum gonadotropin (PMSG) or saline vehicle (V) intramuscularly (im) on Day 2 resulting in the following groups: S-HST + V (n=3), S-HST + PMSG (n=4), HST + V (n=3) and HST + PMSG (n=4). Ovarian morphology and weights were recorded after ovariectomy on Day 6. Gilts were weighed on Day 59 ± 3. Sequential blood samples were collected via jugular vein cannula from 6 S-HST and 6 HST gilts on Day 60 ± 3, and all gilts were necropsied on Day 86 ± 7. Body weight gain and whole pituitary gland weight were greater (P<0.05) for S-HST than HST gilts. Mean serum LH concentration, basal serum LH concentration, frequency of LH peaks and LH peak amplitude were greater (P<0.005) for S-HST than HST gilts. Serum PRL and GH, were similar for both groups. Total ovarian and follicular fluid weights were greater (P<0.05) in S-HST gilts given PMSG than those of the other three groups which did not differ. Therefore, PMSG stimulated follicular growth in S-HST gilts, but failed to stimulate follicular growth in HST gilts. We suggest that a critical basal serum LH and/or FSH concentration must be maintained to support and promote follicular growth and a pulsatile delivery of GnRH to the anterior pituitary gland by an intact brain-pituitary unit may be required to provide this basal serum gonadotropin concentration.     

Influence of daily injections of porcine somatotropin on growth, puberty, and reproduction in gilts

To determine whether recombinant porcine somatotropin (rpST) alters reproduction, 40 crossbred gilts weighing 59.1 +/- .5 kg at 125 +/- 1 d of age were assigned randomly to an experiment arranged as a 2 x 2 factorial. Eight gilts were given daily injections of diluent until they reached 104 kg BW (DW), and eight received diluent injections until puberty (DP). Twelve gilts were given rpST (4 mg/d) until 104 kg BW (PW) and 12 were given rpST injections until puberty (PP). All gilts were individually fed on an ad libitum basis an 18% CP corn-soybean meal diet (1.2% lysine and 3.1 Mcal/kg of ME). Beginning at 5 mo of age, gilts were exposed 20 min daily to mature boars. Serum concentrations of progesterone were measured weekly from 5 to 8 mo of age to verify age of puberty. Gilts observed in pubertal estrus were mated to two different boars 10 h apart. At 47 +/- 1 d of gestation, gilts were slaughtered to assess fetal development. After 60 d of treatment, serum LH and FSH profiles were determined in blood samples drawn at 20-min intervals for 4 h from eight diluent- and eight rpST-treated gilts fitted with indwelling jugular catheters. By 28 d, feed intake, feed/gain, and blood urea nitrogen were decreased (P less than .005) by rpST. Treatments did not affect (P greater than .05) the proportion of gilts attaining first ovulation (DW = 6/6; DP = 10/10; PW = 7/9; PP = 14/14) or conception rate (DW = 5/6; DP = 7/10; PW = 4/6; PP = 11/12).(ABSTRACT TRUNCATED AT 250 WORDS)     

Function of ovine corpora lutea after administration of luteinizing hormone-releasing hormone

Ewes were treated with an agonistic analog of luteinizing hormone-releasing hormone (LH-RH) during the luteal phase (d 10) of the estrous cycle. Function of natural and hormonally-induced corpora lutea (CL) was evaluated by measurements of progesterone in sera or luteal tissue. Synthesis and secretion of progesterone by natural CL were not chronically altered by LH-RH. Likewise, there was no in vitro effect of LH-RH on luteal function. When natural CL were surgically removed, newly formed CL functioned at a defective level. Hysterectomy shortly after ovulation did not significantly influence such luteal activity. Induction of ovulation by LH-RH during the follicular phase (d 16) in uterus-intact ewes was followed by normal profiles of luteal secretion of progesterone; serum concentrations of progesterone in animals that were hysterectomized increased in association with development of the CL, but then plateaued at a subnormal level. There were no differences in patterns of secretion of luteinizing hormone in response to LH-RH due to stage of the estrous cycle. Follicles stimulated to ovulate during the luteal phase contained low numbers of steroidogenically-deficient granulosal-lutein cells. These results indicate that: ovine CL are not sensitive to exogenous LH-RH; luteal dysfunction is a consequence of ovulation during the luteal phase, and the etiology of this abnormality appears to be linked with the developmental status of the ovulatory follicle; and CL that are formed from ovulation of a matured follicle begin to develop normally, but then function at a defective rate in the absence of the uterus.