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Biomedical subjects

G B Rampacek

Publications and source records attributed to G B Rampacek.

At least 73 records · Page 4Linked to original sources

Absence of an estradiol-induced surge of luteinizing hormone in pigs receiving unvarying pulsatile gonadotropin-releasing hormone stimulation.

The goal of this study was to pharmacologically block central nervous system (CNS) input to gonadotropes in mature ovariectomized gilts to determine the direct actions of estradiol (E2) on pituitary LH release when given at a dose sufficient to elicit a gonadotropin surge. Feeding AIMAX [N-methyl-N'-(1-methyl-2-propenyl)1,2-hydrazinedicarbothioamide; 125 mg/day] for 7 days reduced serum LH concentrations from 1.25 +/- 0.13 (mean +/- SE) to less than 0.18 ng/ml, abolished LH pulses, but did not compromise LH release in response to exogenous GnRH. Serum FSH concentrations were reduced by 27%, whereas serum concentrations of PRL, GH, thyroid hormones and cortisol were not affected after 7 days of AIMAX treatment. Behavior was not altered, aside from a slightly reduced appetite. The LH surge that peaked 48-80 h after injecting E2 benzoate (E2B) into control gilts was blocked in five of eight gilts given AIMAX. Giving GnRH pulses (1 microgram every 45 min) to AIMAX-treated gilts restored mean serum LH concentrations as well as the frequency and amplitude of LH pulses to those of untreated ovariectomized gilts. E2B suppressed the LH response to these GnRH pulses by 88% at 12 h, whereas from 24-96 h after E2B treatment, the LH response to GnRH and mean serum concentrations of LH were again similar to those of controls not given estradiol. These data indicate that induction of the gonadotropin surge by E2 in the gilt requires CNS input. The action of E2 on the pituitary in the presence of unvarying GnRH pulsation may, however, be limited to an early transient inhibition of responsiveness to GnRH, with no subsequent direct stimulation during the period of the surge.

Animals↗

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)

17-Hydroxysteroid Dehydrogenases↗

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)

Animals↗

Effect of photoperiod and temperature on prolactin secretion in ovariectomized gilts.

Five ovariectomized (OVX) gilts were placed in each of two chambers at 20 C with a photoperiod of 12 h light and 12 h dark for 8 d (12L:12D). On d 1, blood samples were collected via jugular cannula every 30 min from 0830 to 1630. At 1630, 200 micrograms of thyrotropin releasing hormone (TRH) were injected iv and blood samples taken every 10 min for 1 h and every 30 min for the next 2 h. On d 2, samples were taken every 30 min from 0830 to 0930 and from 1530 to 1630. Temperature was changed to 10 C or 30 C on d 3. Samples were taken from 0830 to 1630 on d 3, 4 and 9. At 1630 on d 9, the TRH challenge was repeated. Mean basal serum concentrations of prolactin (PRL) were similar for all gilts and for all periods. However, serum PRL response (ng PRL X ml-1 X 150 min-1) to TRH increased (P less than .0001) after exposure to 30 C, while exposure to 10 C failed to alter PRL response. In Exp. 2, six ovariectomized gilts were assigned to each chamber. The protocol of Exp. 1 was followed through d 3, except temperature and photoperiod were changed to 10 C and 8L:16D or 30 C and 16L:8D. On d 34 the TRH challenge was repeated. Mean basal serum concentration of PRL was similar for all gilts and all periods. However, simultaneous increases in temperature and photoperiod increased (P less than .005) serum PRL response to TRH, whereas simultaneous decreases in temperature and photoperiod failed to alter PRL response to TRH.

Animals↗

Opioid inhibition of luteinizing hormone secretion in the postpartum lactating sow.

Twelve lactating sows were used at 22.4 +/- 0.8 days postpartum to determine whether endogenous opioid peptides (EOP) are involved in the suckling-induced inhibition of luteinizing hormone (LH) secretion. Four sows each received either 1, 2, or 4 mg/kg body weight of naloxone (NAL), an opiate antagonist, in saline i.v. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. All sows were then given 100 micrograms gonadotropin-releasing hormone (GnRH) in saline i.v., and blood samples were collected for an additional h. Pigs were weaned after blood sampling. At 40 h after weaning, sows were treated and blood samples collected as during suckling. Serum concentrations of LH after treatment with NAL were similar for all doses; therefore, the data were pooled across doses. During suckling, serum concentrations of LH were 0.41 +/- 0.04 ng/ml before NAL treatment, increased to 0.65 +/- 0.08 ng/ml at 30 min after NAL treatment, and remained elevated above pretreatment concentrations for 120 min (p less than 0.05). Naloxone failed to alter serum concentrations of LH after weaning. These data indicate that EOP may be involved in the suckling-induced suppression of LH secretion and that weaning may either decrease opioid inhibition of LH secretion or decrease pituitary LH responsiveness to endogenous GnRH released by NAL.

Animals↗

Influence of stage of the estrous cycle on endogenous opioid modulation of luteinizing hormone, prolactin, and cortisol secretion in the gilt.

Fourteen gilts that had displayed one or more estrous cycles of 18-22 days (onset of estrus = Day 0) and four ovariectomized (OVX) gilts were treated with naloxone (NAL), an opiate antagonist, at 1 mg/kg body weight in saline i.v. Intact gilts were treated during either the luteal phase (L, Day 10-11; n = 7), early follicular phase (EF, Day 15-17; n = 3), or late follicular phase (LF, Day 18-19; n = 4) of the estrous cycle. Blood was collected at 15-min intervals for 2 h before and 4 h after NAL treatment. Serum luteinizing hormone (LH) concentrations for L gilts averaged 0.65 +/- 0.04 ng/ml during the pretreatment period and increased to an average of 1.3 +/- 0.1 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum prolactin (PRL) concentrations for L gilts averaged 4.8 +/- 0.2 ng/ml during the pretreatment period and increased to an average of 6.3 +/- 0.3 ng/ml (p less than 0.05) during the first 60 min after NAL treatment. Serum PRL concentrations averaged 8.6 +/- 0.7 ng/ml and 7.6 +/- 0.6 ng/ml in EF and LF gilts, respectively, prior to NAL treatment, and decreased (p less than 0.05) to an average of 4.1 +/- 0.2 ng/ml and 5.6 +/- 0.4 ng/ml in EF and LF gilts, respectively, during the fourth h after NAL. Naloxone treatment failed to alter serum LH concentrations in EF, LF, or OVX gilts and PRL concentrations in OVX gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The relationship between 13,14-dihydro-15-keto PGF2 alpha and LH secretion in bulls.

Half-life (t1/2), volume of distribution (Vd) and total body clearance (TBC) of 13,14-dihydro-15-keto PGF2 alpha (PGFM) were measured in order to determine optimal sampling frequency for accurate measurement of PGFM. Three yearling Holstein bulls (349.2 +/- 6.7 kg) and 3 yearling Holstein steers (346.7 +/- 7.0 kg) were utilized in a 3 X 3 Latin square design. Animals were given 0, 25 or 50 micrograms PGF2 alpha I.V.; blood samples collected every 2 min and plasma PGFM determined. The t1/2, Vd and TBC of PGFM were 2.3 +/- .2 min, 43.3 +/- 3.3 liters and 13.7 +/- 1.9 liters/min, respectively and were similar for 25 and 50 micrograms doses. To determine the relationship between endogenous PGFM and LH secretion in bulls, blood samples were collected every 2 min for 12 h in 4 yearling Angus bulls (489.1 +/- 11.6 kg). All animals elicited at least one LH surge and PGFM concentrations were measured in samples coincident with the LH surge. Mean plasma PGFM concentrations were greater prior to the LH surge than during the LH surge. In addition, mean plasma PGFM concentration and frequency of PGFM peaks appeared to increase prior to the LH surge suggesting an association between PGFM and pulsatile LH secretion in the bull.

Animals↗

Inhibition of pregnancy with indomethacin in mature gilts and prepuberal gilts induced to ovulate.

Twenty prepuberal (P) gilts, 56.5 +/- 1.1 kg body weight, were induced to ovulate with 1000 IU of pregnant mare's serum gonadotropin followed 72 h later by 500 IU of human chorionic gonadotropin (hCG), and bred by artificial insemination (AI) with 50 ml fresh pooled boar semen the day after hCG treatment (Day 0). Eighteen mature (M) gilts, 120.6 +/- 1.7 kg body weight, were bred by AI each day of estrus using pooled semen from the same boars (onset of estrus = Day 0). One-half of each group was fed the prostaglandin (PG) synthesis inhibitor indomethacin (IND), at 10 mg/kg body weight, or control (C) feed twice daily on Days 10 to 25. Blood samples taken by venipuncture on Days 10, 15, 20 and 25 were quantitated for progesterone (P4) and 13,14-dihydro-15-keto-PGF2 alpha (PGFM) by radioimmunoassay. Ovaries were examined on Day 26. All M-C gilts were pregnant, whereas 3 of 9 M-IND gilts (P less than 0.05) and none of the P gilts (P less than 0.01) were pregnant. Three of the 6 nonpregnant M-IND gilts displayed estrus on Day 21. The 3 remaining M-IND gilts had maintained corpora lutea (CL) on Day 26. Only corpora albicantia were present in P gilts on Day 26. Serum P4 concentrations for M-C gilts, nonpregnant M-IND gilts with maintained CL, and pregnant M-IND gilts were not different. Serum P4 for all nonpregnant gilts in which CL had regressed by Day 25 decreased to less than 5 ng/ml on Day 20.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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

The effect of daily injections of human chorionic gonadotropin (HCG) on luteal maintenance in hysterectomized prepuberal gilts induced to ovulate and in hysterectomized mature gilts was studied. Twenty-four pre-puberal gilts, 120 to 130 d of age, were induced to ovulate with 1,000 IU pregnant mare serum gonadotropin followed 72 h later with 500 IU HCG. Nine of the 24 prepuberal gilts (bred controls) were artificially inseminated on d 0 (d 0 = d after HCG). Mature gilts that had displayed one or more estrous cycles of 17 to 22 d were used (d 0 = onset of estrus). All gilts, except the bred controls, were totally hysterectomized on d 6 to 9 and their corpora lutea (CL) marked with charcoal. From d 10 through 29, eight prepuberal and 10 mature hysterectomized gilts received daily injections of 500 IU HCG in saline while seven prepuberal and eight mature hysterectomized gilts received daily injections of saline vehicle. Jugular blood samples were quantitated by radioimmunoassay for estrogen and 13,14-dihydro-15-keto prostaglandin F2 alpha (PGFM), a metabolite of prostaglandin F2 alpha. One bred control gilt was pregnant on d 30, indicating that the prepuberal gilts used in the experiment were prepuberal. All mature gilts and six of seven prepuberal gilts that received saline had maintained CL to d 30. Eight of 10 mature gilts that received HCG had maintained CL to d 30, while only two of eight (P less than .05) prepuberal gilts that received HCG maintained CL to d 30. All gilts receiving HCG had numerous follicles and accessory luteal structures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Luteinizing hormone receptors and progesterone content in porcine corpora lutea after prostaglandin F2 alpha.

The effect of prostaglandin F2 alpha (PGF2 alpha) on luteinizing hormone (LH) receptors, weight and progesterone content of corpora lutea (CL), and serum progesterone concentrations was studied in gilts. Fifteen gilts were hysterectomized between Days 9 to 11 of the estrous cycle. Twelve gilts were injected i.m. with 10 mg of PGF2 alpha and 3 with saline on Day 20. Ovaries were surgically removed from each of 3 gilts at 4, 8, 12 and 24 h following PGF2 alpha treatment and from the 3 control gilts 12 h following saline injection. Jugular blood samples for progesterone analysis were collected from all gilts at 0, 2 and 4 h following treatment and at 8, 12 and 24 h for gilts from which ovaries were removed at 8, 12 and 24 h, respectively. Mean serum progesterone and CL progesterone concentrations decreased within 4 h after PGF2 alpha treatment (P less than 0.05) and remained low through 24 h after treatment. The number of unoccupied LH receptors decreased by 4 h (P less than 0.05) and this trend continued through 24 h. There were no differences in luteal weight or affinity of unoccupied LH receptors of luteal tissue at 4, 8 12 and 24 h after PGF2 alpha when compared to luteal tissue from controls. These data indicate that during PGF2 alpha-induced luteolysis in the pig, luteal progesterone, serum progesterone concentrations and the number of LH receptors decrease simultaneously.

Animals↗

The effect of adrenocorticotropin or hydrocortisone on serum luteinizing hormone concentrations after adrenalectomy and/or ovariectomy in the prepuberal gilt.

The possible role of ACTH and the adrenal gland in modulating LH secretion in prepuberal gilts was studied. Fifty-one gilts, 170-175 days of age, were randomly assigned to 12 treatments in a 2 X 2 X 3 factorial design. The main treatments were adrenalectomy (ADX) or sham-ADX, ovariectomy (OVX) or sham-OVX, and ACTH, hydrocortisone acetate (HCA), or vehicle (V) administration. ACTH, HCA, or V was administered from days 3-10 after surgery. Beginning at 0800 h on day 10, blood samples were collected every 15 min for 16 h via jugular cannulae. At 1600 and 2000 h, all gilts were injected iv with a pharmacological dosage of 400 micrograms GnRH. ADX and OVX did not influence subsequent serum cortisol (CS) concentrations, detected by RIA. HCA elevated serum CS concentrations in all four surgical groups. ACTH treatment elevated serum CS and progesterone concentrations only in the sham-ADX groups. Every 3 days after surgery, all ADX gilts received 10 mg deoxycorticosterone acetate, im, as an electrolyte maintenance treatment, which may have been detected in the peripheral blood by the CS assay since the cross-reaction of deoxycorticosterone with the first antibody of the CS assay was 17.1%. Serum LH concentration, peak frequency, and peak magnitude were greater in V-treated OVX gilts than in V-treated sham-OVX gilts in both ADX and sham-ADX groups. Chronic ACTH treatment blocked the increase in basal serum LH concentration, peak frequency, and peak magnitude after OVX only when the adrenal glands were present. In contrast, HCA blocked the postcastration increase in the basal serum LH concentration and peak magnitude in the presence or absence of the adrenal glands. However, HCA had no effect on the increased frequency of LH peaks that occurred after OVX in V-treated gilts. The serum LH responses after both GnRH challenges were similar for all gilts, and the LH response to the second GnRH challenge was less than that observed after the first challenge. These data indicate that ACTH and HCA suppressed the postcastration increase in LH secretion. However, the effect of ACTH was mediated through the adrenal gland, and the inhibiting influence of ACTH and HCA on LH secretion was apparently not mediated at the pituitary level in the prepuberal gilt.

Adrenalectomy↗

Comparison of physiological indicators of chronic stress in confined and nonconfined gilts.

Two experiments were conducted to determine if confinement-induced delayed puberty in gilts was due to chronic physiological stress imposed by confinement housing. In both experiments, crossbred gilts, raised in total confinement, were moved to an outside dirt lot (nonconfined) or to a single pen in a confinement finishing unit (confined) at 100 to 110 d of age. Beginning at 150 d of age, estrus was checked daily with a boar to determine age at first estrus. Gilts were necropsied at 270 d of age. In Exp. I, 19 confined and 19 nonconfined gilts were cannulated by jugular puncture at 185 d of age. The day after cannulation, blood samples were collected for 4 h, 200 IU porcine adrenocorticoptropic hormone (ACTH) was injected via the cannulae and blood samples were collected for an additional 8 h. Serum cortisol, progesterone, luteinizing hormone (LH) and prolactin (PRL) concentrations were determined. In Exp. II, both jugular veins of six confined and six nonconfined gilts were cannulated at 204 d of age. The day after cannulation, blood samples were collected for 4 h and cortisol was continuously infused for the last 2 h of the blood collection period. Cortisol metabolic clearance rate (MCR) and secretion rate (SR) were determined. By 270 d of age, 21 of 28 (75%) nonconfined gilts and 11 of 31 (35.5%) confined gilts (P less than .01) in Exp. I and 18 of 25 (72%) nonconfined gilts and 12 of 25 (48%) confined gilts (P less than .06) in Exp. II had exhibited estrus and ovulated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum luteinizing hormone and estrogen profiles before puberty in the gilt.

The hypothesis that an increase in serum luteinizing hormone (LH) concentration occurs before the onset of puberty in the gilt was tested. Blood samples were collected from 14 gilts, 166 d of age and 72.6 +/- 1.8 kg body weight, every 15 min for 8 h 1 d after jugular cannulation. Gilts were checked daily for estrus with a boar. The sampling procedure was repeated 21 and 33 d later, by which time three gilts had attained puberty (first estrus with continued regular estrous cycles), and then every 7 d thereafter until an additional five gilts attained puberty. Serum LH and estrogen (E) concentrations were quantitated by radioimmunoassay. Bleeding periods were grouped into seven common physiological ages before puberty; age 1 greater than or equal to 57 d (n = 4), age 2 = 43 to 50 d (n = 5), age 3 = 31 to 38 d (n = 4), age 4 = 22 to 26 d (n = 5), age 5 = 17 to 19 d (n = 4), age 6 = 10 to 12 d (n = 5) and age 7 = 3 to 5 d (n = 5). Mean serum LH concentration (ng/ml, mean +/- SE) at age 7 (1.0 +/- .1) was greater (P less than .01) than at ages 2, 3, 4 and 5 (6 +/- .1) but not ages 1 and 6 (.8 +/- .1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum luteinizing hormone in prepuberal gilts after ovariectomy or adrenalectomy.

Serum luteinizing hormone (LH) concentrations after ovariectomy (OVX) and adrenalectomy (ADX) were studied in the prepuberal gilt. In Exp.I, gilts, 170 to 175 d of age and 80 to 85 kg body weight, were OVX (n = 5) or sham-OVX (n = 5). Blood samples were collected via jugular vein cannulae every 30 min for 8 h on d 1, 3, 5, 7 and 21 after surgery. In Exp. II, blood samples were collected via jugular vein cannulae every 30 min for 12 h on d 3, 5, 7 and 14 after surgery from five ADX, five sham-ADX and five nonsurgical control gilts of similar ages and weights as in Exp. I. In Exp. I, basal serum LH concentrations (means +/- SE, ng/ml) over all days were greater (P less than .05) in OVX (2.9 +/- .1) than in sham-OVX (1.1 +/- .2) gilts. Average basal serum LH concentrations were greater (P less than .05) on d 1 for both treatments than all other days sampled. The frequency of LH peaks (means +/- SE/8 h) was also greater (P less than .01) for OVX (3.5 +/- .3) than sham-OVX gilts (1.7 +/- .2). Similarly, the mean concentration of the LH peaks was greater (P less than .01) for OVX (4.1 +/- .2 ng/ml) than sham-OVX gilts (2.1 +/- .2 ng/ml). In Exp. II, mean basal serum LH concentrations, frequency of LH peaks and mean concentration of the LH peaks were similar for all treatments on each day sampled. The frequency of LH peaks (means +/- SE/12 h) was greater (P less than .05) on d 3 (3.4 +/- .3) than on d 5 (2.3 +/- .3) and d 7 (2.1 +/- .4), but similar to d 14 (2.8 +/- .5) in all treatments. In prepuberal gilts, ADX failed to influence serum LH concentration, whereas OVX caused a significant increase in serum LH concentration. We suggest that the ovary is the major steroid-secreting gland having a negative feedback on pituitary gonadotropin production in the prepuberal gilt.

Adrenal Glands↗

Serum concentrations of pituitary and adrenal hormones in female pigs exposed to two photoperiods.

Serum concentrations of pituitary and adrenal hormones were determined in lactating sows and ovariectomized (OVX) gilts exposed to 8 h (8L:16D) or 16 h of light (16L:8D). In addition serum prolactin (PRL) concentrations were determined after a thyrotropin releasing hormone (TRH) challenge. At 103 +/- 2 d of gestation or 3 wk after ovariectomy of nulliparous gilts on d 7 to 9 of the estrous cycle (d - 10), blood samples were collected from jugular vein cannulae at 30-min intervals for 8 h beginning at 0800 h. Immediately after the last sample, 13 sows and five OVX gilts were assigned to 8L:16D and 14 sows and five OVX gilts were assigned to 16L:8D/d and placed in two identical chambers in the farrowing house. Blood sampling was repeated on d 7, 14 and 21 of lactation in the sows and on d 7, 14, 21 and 28 in the OVX gilts. In Exp. 1, serum cortisol (C) concentrations were similar for sows exposed to 8L:16D (n = 7) and 16L:8D (n = 6) treatments, whereas in Exp. 2, serum C concentrations for sows exposed to 8L:16D (n = 6) were lower than those exposed to 16L:8D (n = 6) on d 7, 14 and 21. Photoperiod failed to influence serum concentrations of PRL, luteinizing hormone (LH) and growth hormone in the lactating sows or PRL in the OVX gilts. Photoperiod also failed to affect mean basal serum concentrations, peak height and peak frequency for PRL and LH in the lactating sows or for PRL in the OVX gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cytoplasmic estrogen receptors in bovine uterus and uterine tube (oviduct).

The effects of progesterone (P) or estradiol benzoate (EB) on unfilled uterine and uterine tubal (oviductal) cytoplasmic estrogen receptors (ER) were studied in nulliparous heifers. Progesterone (4.4 mg/kg of body weight) in oil EB (350 micrograms) in oil, or oil vehicle only (C) were injected IM 24 hours after the end of estrus. The heifers were euthanatized 36 hours later. There was a difference (P less than 0.005) in the concentration of ER among treatment groups, but no difference (P greater than 0.05) between the ER concentrations in the uterus and uterine tube within each treatment group. The affinity constant (KA) of the uterine tubal ER was similar among the treatment groups (P greater than 0.15), and there was no difference (P greater than 0.05) in the KA between the uterus and uterine tubal ER within the P and C treatment groups. The KA of the uterine ER of the EB-treated heifers was greater (P less than 0.001) than that in either P- or C-treated heifers.

Animals↗

Failure of the orally active progestin, Regu-mate, to overcome confinement-induced delayed puberty in gilts.

Thirty-three crossbred gilts that were raised in total confinement were randomly allotted to two adjacent pens in a finishing unit at 144.7 +/- .5 days of age and 58.0 +/- 1.7 kg body weight. At approximately 253 days of age, 16 gilts were group fed a daily dose of 20 mg of Regu-mate per gilt for 18 days and 17 control gilts were group fed the same diet without Regu-mate for 18 days. Ovarian morphology was examined on 11 or 12 days after the last feeding of Regu-mate. Based on estrous behavior and ovarian morphology only one Regu-mate gilt displayed an estrus but did not ovulate and only three of the control gilts displayed estrus and ovulated at least once before the start of treatment. Three of the 16 Regu-mate gilts displayed estrus and ovulated 7.3 +/- .3 days after the last feeding and within the same time period the 3 control gilts, which previously displayed estrus, continued to have estrous cycles. One additional control gilt displayed estrus and ovulated 5 days after the last feeding of the control diet. Therefore, the proportion of gilts that displayed estrus and ovulated by the end of the experimental period were similar for the treated (25.0%) and control (23.5%) groups. Based on these results we conclude that treatment of gilts in a state of confinement-induced delayed puberty with 20 mg Regu-mate daily for 18 days failed to result in a synchronized onset of puberty in a significant proportion of gilts.

Journal Article↗

Alteration of the estrous cycle of gilts by movement to a confinement housing system.

Thirty-six crossbred gilts were maintained in outside dirt lots for 2 or more estrous periods. Eighteen of the gilts were moved to another outside dirt lot (non-confined) and the other eighteen were moved to a single pen in a confinement finishing building (confined). A blood sample was collected on the day of movement and every 7 days thereafter for 12 weeks and quantitated for progesterone to verify the occurrence of each ovulation. Any estrous cycle shorter than 18 days or longer than 23 days was classified as abnormal. The duration of estrous cycles of non-confined gilts were not different before, during or after movement, whereas the duration of estrous cycles were greater (P=.005) during movement than before movement in the confined gilts. The duration of estrous cycles of confined gilts were greater (P=.020) than those of non-confined gilts during movement. The percentage of abnormal estrous cycles were greater during movement than before (P=.007) or after (P=.052) movement for the confined gilts, whereas the percentage age of abnormal estrous cycles were greater (P=.050) during movement than before movement in non-confined gilts. Therefore, the greatest percentage of abnormal estrous cycles occurred during movement in both groups. A single incident of silent estrus followed by normal estrous cycles was observed. In addition, an estrus occurred while plasma progesterone concentration was elevated (51 ng/ml) and was followed by normal estrous cycles.

Journal Article↗