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Two trials were conducted to determine whether feeding excess degradable intake protein (DIP) during a synchronized estrous cycle and the first 5 d after breeding alters early embryonic development, ovarian steroids, or BUN concentrations in ewes. Ewes were group-fed in Trial 1 (T1) and individually fed in Trial 2 (T2) either 100 (control; T1, n = 15; T2, n = 12) or 200% (high-protein; T1, n = 16; T2, n = 12) of the NRC protein recommendation for maintenance during a synchronized estrous cycle until surgery in the next cycle. Ampullae (AMP), isthmi (IST), and uterine horns (UT) of high-protein and control ewes were removed on d 2 (T1), 3 (T2), 4 (T1), or 5 (T2) after breeding. In T1, jugular blood samples were taken once daily starting on d 2 of the synchronized cycle, and in T2 on d 2, 9, 15, 16, and 17, and in both trials from estrus (d 0) to the day of surgery. Ampullae, IST, and UT flushings were examined microscopically for the presence of embryos, embryo condition, and embryo cell number. There was no trial × treatment interaction (P≥ 0.10), so data for both trials were pooled. Concentrations of BUN were higher (P< 0.05) in high-protein-fed ewes than in control ewes during the synchronized cycle and the first 5 d of the next cycle. Progesterone concentrations of the synchronized cycle did not differ (P> 0.10) between treatments. During the first 5 d of the next cycle, estradiol-17βconcentrations were lower (P= 0.06) in high-protein-fed than in control ewes. Progesterone increased (P< 0.05) to higher concentrations by d 5 in high-protein-fed ewes than in control ewes. More (P< 0.05) embryos were found in AMP of high-protein-fed ewes than in AMP of control ewes on d 4. Fewer (P= 0.05) embryos were found in UT of high-protein-fed ewes than in UT of control ewes on d 4. More embryos were found in UT of high-protein-fed ewes than in UT of control ewes on d 5. Fewer (P= 0.05) embryos were found in IST of high-protein ewes than in the IST of control ewes on d 5. Embryos of high-protein-fed ewes had more (P< 0.05) cells than embryos from control fed ewes on d 5. Feeding ewes excess DIP protein during an estrous cycle and the first 5 d after breeding initially impeded embryo transport; thereafter, embryo transport and development through the oviduct was accelerated.

Gross anatomical and histometric characteristics of oviducts and uteri were evaluated during the pubertal transition in ewe lambs. Lambs were hysterectomized prepubertally (PP; n = 10) or 26 ± 2 h after onset of first (FE; n = 13) or third estrus (TE; n = 12), or estrus in mature pluriparous ewes (ME; n = 4). Gross characteristics included diameters, lengths, and weights of oviducts; diameters of uterine cornua; and weights of uteri. Histometric characteristics of ampullae, isthmi, and uterine cornua included epithelial cell volume, total luminal surface area, and total number of cells per ampulla or isthmus and area of the muscularis. Side of the reproductive tract did not affect (P> 0.10) any gross or histometric characteristic. Gross uterine characteristics increased (P< 0.05) dramatically between PP ewes and FE ewes, and then increased (P< 0.05) to a lesser degree between FE and TE ewes, and again (P< 0.05) between TE and ME ewes. Histological characteristics of uteri followed a similar developmental pattern: large changes (P< 0.05) between PP and FE ewes, slight increases between FE and TE ewes, and no change (P> 0.10) between TE and ME ewes. Oviductal weight and length showed little change (P> 0.10) at puberty or by third estrus, but they were greater (P< 0.05) in ME ewes than in the other groups. The diameters of ampullae increased (P< 0.05) at puberty, showed no change between FE and TE ewes, and were greatest (P< 0.05) in mature ewes. These changes seemed to be due to increases (P< 0.05) in mucosal cell height and muscularis area at puberty, and to muscularis area and submucosal thickness between TE and ME ewes. The surface area of the ampullae increased (P< 0.05) at puberty or by third estrus in a linear manner between PP, FE, TE, and ME ewes. The diameters of isthmi did not change (P> 0.10) at puberty but increased (P< 0.05) between FE and TE, and were greatest (P< 0.05) in ME ewes. The histological characteristics of isthmi followed the pattern observed in the ampullae. However, the surface area of the isthmi showed no change (P> 0.10) at puberty or by third estrus and was largest (P< 0.05) in ME ewes. Results of this study indicate that gross morphological characteristics of uteri and oviducts increase at puberty with either slight increases or changes after two estrous cycles. This relationship is also reflected by histological characteristics of these organs during the pubertal transition of sheep.

Peripheral serum progesterone concentrations were evaluated in beef heifers following breeding at puberal (E1, n=63) or third (E3, n=45) estrus. A blood sample was collected on d 6 ± 1, 9 ± 1 and 12 ± 1 (estrus = d 0) after the puberal estrus of all heifers and after the third estrus of E3 heifers. Progesterone concentrations were higher (P<.05) for heifers in E1 compared with heifers in E3 on d 6, 9 and 12 after breeding to a fertile bull. Progesterone concentrations on d 6, 9 and 12 did not differ (P>.10) between pregnant heifers in E1 and E3; however, non-pregnant heifers in E1 had higher (P<.05) concentrations of progesterone compared with non-pregnant heifers in E3 on each day. Concentrations of progesterone did not differ (P>.10) between non-pregnant heifers in E1 and heifers of E3 during their puberal cycle. Pregnant heifers in E1 and E3 had higher (P<.05) concentrations of progesterone on each day than non-pregnant heifers in their respective treatments. There were no interactions (P>.10) between treatment, pregnancy status and day-of-estrous cycle for concentrations of progesterone. Results of this study indicated that luteal function differed between heifers that failed to conceive at their puberal estrus and heifers that failed to conceive at third estrus. However, concentrations of progesterone did not differ between heifers that conceived at puberal or third estrus. The relationship of changes in luteal function from the puberal through the third estrous cycle and pregnancy is not clear.

Two experiments were conducted with an-estrous postpartum beef cows (1) to determine the effects of human chorionic gonadotropin (hCG) and gonadotropin releasing hormone (GnRH) on the proportion of cows that formed corpora lutea and on conception rates of those cows at a subsequent estrus, and (2) to examine the effects of progestogen and estrogen on the life span and function of corpora lutea induced by hCG. In Exp. 1, conducted with three herds, ovaries of lactating cows that were 30 or more days postpartum were palpated per rectum. On the day of examination (d 0), those cows without a corpus luteum were injected im with either hCG (2,500 IU) or GnRH (200 µg) or served as controls. Cows with a palpable corpus luteum 12 d after the administration of these treatments were given prostaglandin F2α (PGF2α; 33.4 mg tromethamine salt, im). All cows were observed for estrus twice daily, on d 8 through 20 after treatment with gonadotropin in two herds and on d 12 through 21 in the third herd. Twelve hours after estrus, cows were inseminated artificially. Treatment with GnRH or hCG increased (P<.05) the proportion of cows in estrus on d 8 through 12 (11 of 37 vs one of 19 control cows) and the proportion of cows with corpora lutea on d 12 (18 of 45 vs four of 30). The overall conception rate was 56% and did not differ among groups. In Exp. 2, 48 anestrous beef cows (19 to 33 d postpartum) were assigned to eight groups of six each. Three factors were studied in sequence: (1) an ear implant of norgestomet (3.35 mg) for 9 d or sham implantation; (2) estradiol-17β (400 µg; im) or corn oil 24 h after removal of the implant, and (3) a second implant of norgestomet for 10 d or sham implantation. Each cow received hCG (1,000 IU; im) 36 h after removal of the first implant, at which time the animals were an average of 3 7 d postpartum. The second implant was inserted 4 d after the administration of hCG. Ovaries were palpated before the insertion and at the time of removal of the first implant of norgestomet and 4, 7 and 14 d after hCG. Jugular samples for analyses of serum progesterone were taken at the time of each palpation, at the time of administration of hCG and 18 d after hCG. Follicular size at the time of removal of the first implant did not differ between the implanted and sham-implanted cows. Among the cows that formed corpora lutea (29 of 48), those receiving the first implant of norgestomet had a profile of serum progesterone that was higher over the 18 d after hCG than that for sham-implanted cows (P<.05). Neither estradiol nor the second implant of norgestomet altered the life span or level of function of the induced corpora lutea.

In ewe lambs peripheral progesterone increases for a 1–4 day period prior to puberty. The source of this increase was investigated in 15 spring-born ewe lambs. Ewes were checked twice daily with a teaser ram throughout the experiment but no signs of behavioral estrus were observed. Daily samples of jugular plasma were assayed for progesterone on the day of collection. Basal concentrations of progesterone (ng/ml; x ± SEM) averaged 0.3 ± 0.1 for all ewes and increased to 1.1 ± 0.1 during the first rise. The duration of the first rise in 5 ewes was 2.5 ± 0.5 days. Progesterone then decreased to 0.4 ± 0.1 for 4 ± 1 days and rose again to 1.9 ± 0.3 ng/ml.Six to 8 h after progesterone had been elevated in 2 consecutive daily samples during the first (5 ewes) and second (5 ewes) rises, ewes were laparotomized, bilateral ovarian venous samples were drawn and ovariectomy was performed. Five ewes that had not exhibited any rise in progesterone were sampled and ovariectomized at the same time as ewes ovariectomized during the first rise. Concentrations of progesterone were higher (150 ± 18 ng/ml) in venous plasma from ovaries containing luteal tissue than from ovaries that did not contain luteal tissue (1 ± 0.8 ng/ml; P<0.05). Luteal tissue was observed grossly and microscopically in ovaries removed during a rise in progesterone. No ovulation papillae (stigmata) were apparent on luteal structures (7.0 ± 1.7 mm in diameter) in ovaries removed during the first rise in progesterone and no corpora albicantia were observed. Definitive stigmata were observed on corpora lutea (8.2 ± 1.5 mm in diameter) in ovaries removed during the second rise in progesterone and corpora albicantia were present.After ovariectomy, progesterone decreased to basal concentrations in ewes that had shown either the first or second rise in progesterone, but remained unchanged in those ewes that had not shown a rise. Neither rise in progesterone was preceded by behavioral estrus.It is concluded that the increase in circulating progesterone prior to puberty in ewe lambs is produced by luteal tissue in the ovary.

Two trials were conducted to determine whether 7-d progestogen treatment beginning on d 17 of the estrous cycle altered 1) ovarian follicular development, 2) serum concentration of estradiol-17β(E2) and progesterone (P4), and 3) patterns of release of luteinizing hormone (LH). In both trials, Angus, Angus × Holstein, or Holstein cows 2 to 6 yr of age were randomly assigned to receive either melen-gestrol acetate (MGA, .5 mg•animal−1•d−1; n = 23), a progesterone-releasing intravaginal device (PRID, n = 26) or to serve as untreated Controls (n = 14). Ultrasonography and blood sampling were performed daily throughout the experiment beginning on d 3 (Trial 1) or d 9 (Trial 2) of the estrous cycle. In Trial 2, blood samples were collected every 15-min for 6 h on d 17 (all cows) and d 20 and 23 (MGA and PRID cows) for determination of LH. Estrous cycle length was 3 to 5 d greater (P< .05) for MGA- and PRID-treated cows characterized by two (MGA-2 and PRID-2) or three (MGA-3 and PRID-3) dominant follicles than for control cows exhibiting two (Control-2) or three (Control-3) dominant follicles. A greater proportion (P< .05) of MGA- than of PRID-treated cows ovulated the follicle that was dominant at the beginning of treatment on d 17 (10 of 23 vs 1 of 26). Serum P4concentrations declined 3 d earlier in Control-2 and MGA-2 cows than in Control-3, MGA-3 or PRID-3 cows. Throughout the treatment period (d 18 to 24) serum E2concentrations were higher (P< .05) in MGA-2 cows than in MGA-3 or PRID-3 cows. Mean and baseline LH concentration and amplitude of LH pulses did not differ (P> .10) among treatments on d 17, 20, and 23. The LH pulse frequency did not differ (P> .10) among treatments on d 17 or 23; however, LH pulse frequency was greater (P< .03) on d 20 in MGA-2 cows than in MGA-3 or PRID-3 cows (4.3 ± .6 vs 2.6 ± .3 and 3.2 ± .4, respectively). In conclusion, treatment with MGA extended the growth phase of ovulatory follicles, which resulted in a premature increase in both serum E2concentration and LH pulse frequency, whereas the follicle that was dominant at the beginning of PRID treatment underwent atresia and a preovulatory follicle emerged after the initiation of PRID treatment.

The objective of this study was to determine if pregnancy rates (PR) differed between beef heifers bred to fertile bulls on either their puberal (E1, n = 89) or third (E3, n = 67) estrus. Heifers were obtained from two lactations (Manhattan, LI; and Miles City, L2), and the experiment was conducted at Miles City. Heifers were assigned randomly within location to either E1 or E3. Heifers were fed to gain .56 kg•head−1•d−1and observed twice daily for estrus. After exhibiting first estrus (puberty) and breeding, each heifer in E1 was palpated rectally on d 6, 9 and 12 ± 1 d (estrus = d 0) for the presence of a corpus luteum, and a venous blood sample was collected for assay of progesterone by radioimmunoassay. Heifers in E3 were palpated and bled on the same schedule as heifers in E1 after first estrus and after being bred to a fertile bull at third estrus. Pregnancy rates were determined by rectal palpation at approximately 38 d post-breeding. Location of origin did not affect (P>.10) weight at puberty or weight at breeding; however, heifers from L1 were younger (P<.05) than heifers from L2 at puberty and breeding. Pregnancy rates were 57 and 78% for heifers in E1 and E3, respectively (P<.05). Weight at breeding did not influence (P>.10) pregnancy rates. The probability of heifers in E1 becoming pregnant increased (P<.05) with increasing age, while age was not a factor (P>.10) for heifers in E3. These results indicated that fertility of puberal estrus in beef heifers is lower than third estrus. Higher fertility of third estrus may be related to maturational changes associated with cycling activity.

The objective of this study was to determine if biostimulation of prepuberal beef heifers by mature bulls would alter proportions of heifers exhibiting puberty, or age or weight at puberty. Angus (A), A × Hereford (H) and Tarentaise × HA heifers (n = 103) were stratified by age and weight within breed-type and location of birth and allotted randomly to the following treatments: 1) heifers exposed to mature bulls (T1;n = 52) or 2) heifers isolated from bulls (T2; n = 51). At the start of the experiment, heifers in T1 and T2 were 287 ± 2 and 286 ± 2 d of age, respectively. Male-to-female ratio for T1 was 1:26. Heifers in T1 and T2 were maintained in drylots separated by .5 km. Heifers were observed for estrus twice daily for 152 d. Puberty was characterized by the following criteria: 1) behavioral estrus, 2) presence of a palpable corpus luteum (d 9; estrus = d 0) and 3) a rise in serum progesterone above 1 ng/ml (d 9). Proportions of heifers reaching puberty by 11, 12, 13, 14 and 15 mo of age did not differ (P>.10) between treatments. Percentages of heifers reaching puberty by the end of the experiment were 84 and 89% for T1 and T2, respectively. Age and weight at puberty did not differ (P>.10) between treatments and averaged 370 ± 7 d and 293 ± 4 kg, respectively. Results from this experiment indicated that presence of mature bulls did not alter proportions of beef heifers reaching puberty, or age and weight at puberty.

Four hundred seventy-four ewe lambs (5 to 6 mo of age) were assigned within breed to two postweaning feed treatments; 1 = alfalfa pellets ad libitum and 2 = alfalfa pellets plus 20% barley or wheat ad libitum. Ten days prior to the start of breeding, approximately one-half of the ewe lambs within each feed treatment were treated with a single injection of 2.5 mg of estradiol valerate and 1.5 mg of norgestomet and implanted with 3 mg of norgestamet for 8 d. At the start of breeding, fertile Suffolk rams were fitted with marking harnesses and penned with ewe lambs; evidence of estrus and breeding was determined on a weekly basis by visual examination for breeding marks. In the second year of the study, 7 to 13 d after recording estrous activity, all marked ewe lambs were bled; and blood was assayed for progesterone. In 1983, 60% of the ewe lambs showed estrus and 11% lambed compared with 48% exhibiting estrus and 30% lambing in 1984 (P<.01). More (P<.01) ewe lambs on feed treatment 1 displayed estrus, but more (P<.05) lambed in the feed treatment 2 group. Steroid treatment resulted in more (P<.01) ewe lambs showing estrus but fewer lambing (P<.01). Examination of progesterone concentrations for evidence of ovulation and corpus luteum development indicated that treatment with steroids caused a large percentage of ewe lambs to exhibit estrus. However, many of these failed to develop a corpus luteum and become pregnant. Furthermore, pregnancy rate was reduced (P<.05) in steroid-treated ewe lambs that developed a corpus luteum.

Luteinizing hormone-human chorionic gonadotropin (LH-hCG) binding capacity for testes of boars and receptor sites per Leydig cell were estimated during pubertal development from 70 to 250 days of age, and changes in these two traits were correlated with morphological and endocrine parameters. Binding capacity increased linearly from 70 to 160 days of age, remained constant through 250 days of age, and was correlated (P<0.05) with paired testes weight, Leydig cell number and weight per paired testes, and serum estradiol-17β(E2) concentrations. LH-hCG receptor sites per Leydig cell were constant at all ages except for an increase observed at 160 days of age and were correlated (P<0.05) to in vitro maximum testosterone (T) production and sensitivity of E2production per Leydig cell in response to hCG stimulation. Number of LH-hCG receptor sites was correlated (P<0.05) with Leydig cell surface area, and sites per unit surface area increased with age. Equilibrium association constants did not differ with age, and they averaged 8.6 ± 1.0 × 109M−1. Results from the present study indicate that LH-hCG receptor capacity per paired porcine testes increases throughout pubertal development primarily as Leydig cell numbers increase.

Crossbred gilts were ovariectomized (OVX) at 120, 150, 180 and 210 d of age to determine whether various characteristics of luteinizing hormone (LH) concentrations are influenced by age and reproductive state (prepuberal vs postpuberal). All 120-d-old gilts were prepuberal and all 210-d-old animals were postpuberal, whereas gilts 150 and 180 d old included both prepuberal and postpuberal animals. Blood was collected at 15-min intervals for 2 h, 2 d before OVX (d −2), and 2 (d +2), 8 (d +8) and 14 (d +14) d after OVX. Mean LH concentrations for prepuberal gilts were similar among age groups (P>.05) on d −2 and +2; however, LH increased (P<.05) from d −2 to +2. No change in LH secretion was found in postpuberal gilts during these two periods. After OVX, LH increased from d +2 to +14 in both prepuberal and postpuberal gilts in all age groups. In postpuberal gilts, LH increased linearly (P<.05) between d +2 and +14; rate of increase accelerated with advancing age (P<.01). In prepuberal gilts, LH increased in a nonlinear manner, but it did not increase between d +2 and +8. The increase observed in prepuberal and postpuberal gilts after OVX resulted primarily from an increase in magnitude of peak concentrations of LH. Implants of estradiol-17β(E2) were used to determine whether the postovariectomy increase in LH is affected differently by E2in prepuberal and postpuberal gilts during advancing ages. Estradiol-17βsuppressed mean LH concentrations (P<.05)in 120-d-old gilts; whereas in 150-d-old prepuberal gilts mean LH was suppressed (P<.05) on d +2 and +8, but then increased (P<.05) by d +14. In prepuberal gilts, E2implants suppressed (P<.05) both frequency and amplitude of LH peaks at 120 d old, but only frequency was suppressed (P<.05) in 150-d-old animals. In postpuberal gilts, 150 and 180 d old, E2did not alter (P>.05) either the postovariectomy increase in mean LH, or frequency and amplitude of LH peaks. Observations of the present study suggest that sensitivity of the hypothalamic-pituitary axis to ovarian and estrogen negative feedback regulation of LH secretion decreases as gilts progress from the prepuberal to the postpuberal state.

The pattern of concentrations of progesterone in plasma was characterized by two transient increases prior to puberty. The source of these increases of progesterone was studied in beef heifers. Basal concentrations of progesterone (ng/ml; x̄ ± SE) averaged .7 ± .1 in all heifers. Progesterone increased to 2 ± .2 during the first elevation, the duration of which was 7 ± 2 days, then decreased to .9 ± .2 for 4 ± 1 days after which it increased again to 2 ± .2. Twenty-four to 30 hr after progesterone had increased in two consecutive samples during the first (four heifers) and second (four heifers) elevations, ovariectomy was performed via a supravaginal incision and the ovaries were examined grossly and histologically for the presence of luteal tissue. Seven heifers which had not shown increases in progesterone were ovariectomized as controls.After ovariectomy, concentrations of progesterone in plasma from heifers that had shown a prior increase returned immediately to concentrations seen in those that had not shown any increase (.6 ± .2 ng/ml). Neither the first nor the second elevation of progesterone was accompanied by the formation of a palpable corpus luteum or grossly visible luteal structure on the ovaries. Ovaries were examined histologically in 10 sections of 12 µm each, taken at 1,800 µm intervals. Microscopic examination revealed the presence of compact luteal tissue in three of four heifers that had exhibited the first increase and in three of four heifers that had exhibited the second increase of progesterone in plasma. The approximate diameters of these luteal tissues observed ranged from 1.5 to 6 millimeters. It is concluded that the first increase of progesterone prior to puberty was produced by luteal tissue embedded within the ovary, but not palpable or observable grossly on the ovarian surface. The second increase probably originated in a similar manner within the ovary.

The level and pattern of growth hormone (GH) secretion were investigated in mature ovariectomized gilts after hypophysial stalk transection and sham operation. A nylon disk was inserted between severed ends of the stalk to prevent vascular regeneration. Blood samples were collected via indwelling jugular catheters at 15-min intervals for 3 hr, 2 days before surgery (Day −2) and 2 days after surgery (Day +2), and at 4-hr intervals from Day +3 to Day +8. Mean overall serum concentrations of GH after hypophysial stalk transection remained similar (P> 0.05) to presurgical levels. These mean concentrations also were similar to those in shamoperated and unoperated controls. However, hypophysial stalk transection significantly dampened (P< 0.05) the episodic secretion of GH and resulted in elevated basal blood concentrations of the hormone as compared with either presurgical levels or those in the two control groups. These results indicate that synthesis and secretion of GH continue in the absence of hypothalamic control in hypophysial stalk-transected gilts. Thus, the hypothalamus is required for regulation of both episodic release and the tonic inhibition of basal secretion of growth hormone in the pig.