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)     

Serum prolactin response to thyrotropin releasing hormone in estrogen treated hypophysial stalk-transected gilts

Twelve crossbred gilts, 169 ± 3 days of age and 72.8 ± 3.4 kg body weight, were hypophysial stalk-transected (HST)1 or sham hypophysial stalk-transected (S-HST). Gilts were ovariectomized 6 days later and assigned to four treatments of 3 gilts each in a 2 × 2 factorial arrangement. One-half of the HST and S-HST gilts received 5 mg estradiolbenzoate (EB) or corn oil vehicle im at 0800 hr daily for 5 days beginning 64 ± 3 days after HST or S-HST. Blood was collected by jugular vein cannula at 0830 and 0900 hr the day after the last injection of EB or oil. Immediately after the 0900 hr sample, 200 μg thyrotropin releasing hormone (TRH) were injected (iv). Mean basal serum prolactin (PRL) concentration was similar for HST (10.3 ± 1.0 ng/ml) and S-HST (12.3 ± 1.7 ng/ml) gilts, however mean basal serum PRL concentration was greater (P<.05) for EB-treated gilts (13.7 ± 1.3 ng/ml) than for oil-treated gilts (8.8 ± .5 ng/ml). Mean serum PRL concentration of all gilts increased within 10 min and returned to approximately 20 ng/ml by 150 min after TRH. Maximum serum PRL concentrations at 10 min after TRH were greater (P<.01) for S-HST (255.9 ± 29.6 ng/ml) than HST gilts (83.4 ± 18.8 ng/ml), but were not different for EB (198.0 ± 50.6 ng/ml) and oil-treated gilts (141.4 ± 36.3 ng/ml). Area under the serum PRL response curve after TRH was greater (P<.005) for S-HST than HST gilts and for EB than oil-treated gilts (P<.05). These results do not eliminate the possible influence of estrogen on PRL secretion at the hypothalamus, but do indicate that estrogen directly stimulated the anterior pituitary gland to secrete PRL.     

Prolactin and luteinizing hormone secretion in the pregnant pig.

Four pregnant, primiparous, crossbred gilts and six gilts from the same population that had been ovariectomized (OVX) for approximately 3 wk were placed in individual pens in an enclosed building. Blood samples were collected every 30 min for 12 h from all gilts via an indwelling jugular vein cannula when the pregnant gilts were at d 30, 50, 70, 90, and 110 of gestation. Serum was quantified for LH and prolactin (PRL) by RIA. The OVX gilts served as controls to ensure that any variations in serum LH and PRL concentrations observed in the pregnant animals were not due to environmental factors unrelated to pregnancy. Within the pregnant gilts, mean serum LH concentrations, mean basal serum LH concentration, and mean serum LH peak height were similar on all days; however, number of LH peaks on d 30, 50, and 70 were greater (P < .05) than on d 90 and 110, and number of LH peaks on d 50 was greater (P < .05) than that on d 70. Within the pregnant gilts, mean serum PRL concentration, mean basal serum PRL concentration, and mean PRL peak height were greater (P < .001) on d 110 than on all other days; however, number of PRL peaks were similar among days. Parameters of LH and PRL secretion in the OVX and pregnant gilts varied independently. Results of this study indicated that 1) LH secretion does not vary appreciably throughout pregnancy and 2) PRL secretion does not vary significantly during the first 90 d of pregnancy, after which it increases markedly on or before 110 d.     

Effect of feeding thyrotropin-releasing hormone to lactating sows

Two experiments were conducted to assess the effects of feeding thyrotropin-releasing hormone (TRH) during lactation on sows. In Exp. 1, sows were fed 0, 1, 10, 100 or 1,000 mg TRH on d 10.8 +/- .4 (mean +/- SE) after parturition. Blood samples were taken from sows every 30 min from -2 h to 8 h and at 10, 12 and 18 h from feeding. Consumption of 100 or 1,000 mg TRH increased mean serum concentrations of thyroxine (T4; P less than .001), 1,000 mg TRH increased growth hormone (GH; P less than .06) and 100 or 1,000 mg TRH increased prolactin (PRL; P less than .01), but insulin (INS; P greater than .10) was unaffected by TRH. Serum concentrations of T4 were elevated within 2 to 4 h after feeding TRH and remained elevated for 12 to 18 h. Concentrations of GH and PRL began to increase immediately after feeding 100 or 1,000 mg TRH and remained elevated for 6 and 8 h, respectively. In Exp. 2, sows were fed 0 or 200 mg TRH from d 111 of gestation to weaning at 27.1 +/- .3 d of lactation. Consumption of TRH elevated concentrations of T4 at all stages of lactation and increased respiration rate on d 10 and d 20, heart rate on d 20, and milk production on d 20 of lactation. Consumption of TRH did not influence number of pigs born, number born alive, survival rate during lactation, sow body weight, heartgirth, backfat depth, feed disappearance, or milk production on d 10 of lactation. Piglets nursing sows fed TRH were similar in weight to piglets nursing sows not fed TRH on d 0 and 5 of lactation, but they were heavier on d 10 (P less than .07), 15 (P less than .001), 20 (P less than .001) and 27 (P less than .0001). Sows fed TRH took longer (P less than .001) to return to estrus after weaning than control sows. Results indicated that feeding TRH elevated T4, GH and PRL and that feeding TRH for the duration of lactation increased milk production on d 20 of lactation and increased weaning weights, but it delayed estrus after weaning.     

Effects of photoperiod on salsolinol‐induced prolactin secretion in goats

The aim of the present study was to clarify the relation between salsolinol (SAL)‐induced prolactin (PRL) release and photoperiod in goats. A single intravenous (i.v.) injection of SAL was given to adult female goats under short (8 h light, 16 h dark) or long (16 h light, 8 h dark) photoperiod conditions at two different ambient temperatures (20°C or 5°C), and the PRL‐releasing response to SAL was compared to that of thyrotropin‐releasing hormone (TRH) or a dopamine (DA) receptor antagonist, sulpiride. SAL, as well as TRH or sulpiride, stimulated the release of PRL promptly after each injection in both 8‐ and 16‐h daily photoperiods at 20°C (P < 0.05). The area under the response curve (AUC) of PRL for the 60‐min period after injections of saline (controls), SAL, TRH and sulpiride in the 16‐h daily photoperiod group was greater than each corresponding value in the 8‐h daily photoperiod group (P < 0.05). There were no significant differences in the AUC of PRL among the values produced after the injection of SAL, TRH and sulpiride in 16‐h daily photoperiod group; however, the values produced after the injection of TRH were smallest among the three in the 8‐h daily photoperiod group (P < 0.05). The PRL‐releasing responses to SAL, TRH and sulpiride under a short and long photoperiod condition at 5°C resembled those at 20°C. These results show that a long photoperiod highly enhances the PRL‐releasing response to SAL as well as TRH or sulpiride in either medium or low ambient temperature in goats.     

Failure of photoperiod to alter body growth and carcass composition in beef steers

In each of two experiments, 70 crossbred steers were blocked by BW and assigned to initial slaughter groups or to treatments in a 2 x 2 design. In Exp. 1, treatments were 168 d of photoperiod (8 h of light [L]:16 h of dark [D] or 16L:8D) and plane of nutrition (high energy [HPN] or low energy [LPN]). On d -22, 67 and 155, blood was sampled every 20 min for 8 h. Relative to LPN, HPN increased (P less than .01) ADG by 28%, carcass weight by 26% and accretion of carcass fat by 109% and carcass protein by 20%. On d 155, compared with LPN, HPN increased (P less than .01) serum insulin (INS; 1.09 vs .64 ng/ml) and lowered (P less than .05) growth hormone (GH; 2.14 vs 3.70 ng/ml), but prolactin was not affected. Photoperiod did not affect BW gains, carcass composition or serum hormones. In Exp. 2, treatments were 113 d of photoperiod (8L:16D or 16L:8D) and Synovex-S implant (presence [IMP] or absence [NONIMP]). On d 93, blood was sampled every 30 min for 10 h. Relative to NONIMP, IMP increased (P less than .01) ADG by 12% and accretion of carcass protein by 16%. Implants did not affect carcass weight or accretion of fat. Compared with NONIMP, IMP increased (P less than .05) GH (3.16 vs 2.39 ng/ml) and INS (.68 vs .46 ng/ml) but did not affect PRL. Photoperiod did not affect BW gain, carcass composition or serum hormones. We conclude that photoperiod fails to influence growth and carcass composition of steers.     

Effect of dose and route of administration of thyroid releasing hormone (TRH) on the concentration of prolactin (PRL) and thyroxine (T4) in cyclic gilts

Our objective was to examine the ability of thyroid releasing hormone (TRH) to stimulate not only the release of the thyroid hormones, but also prolactin (PRL) in the female pig. An experiment was conducted to determine the effect of dose and route of administration of TRH on the concentration of PRL and thyroxine (T4) in cyclic gilts. Six gilts were injected with 0, 5, 25, 125, and 625 micrograms TRH and fed 0, 5, 2.5, 12.5 and 62.5 mg TRH. Gilts received TRH once daily. During the 10-day treatment period, route of TRH administration alternated between i.v. injection and feeding. The dose of TRH progressed from the lowest to the highest. Blood samples were taken prior to TRH injection and thereafter at 15-min intervals for 3 hr. Sampling continued for an additional 3 hr at 30-min intervals when TRH was fed. Concentrations of PRL and T4 were determined by radioimmunoassay. Intravenous injection of gilts with 125 and 625 micrograms TRH resulted in an increase in PRL from 0 to 15 min (P less than .05). All doses of TRH given i.v. elevated T4 over a 2-hr period (P less than .01). TRH failed to increase PRL when TRH was fed (P greater than .5). The feeding of 62.5 mg TRH elevated T4 from 0 to 6 hr (P less than .01). Thus, TRH injection increased PRL rapidly and T4 gradually. When TRH was fed, only a gradual elevation in T4 was observed. We conclude that TRH can elicit the release of both PRL and T4 in the cyclic gilt, but magnitude and duration of the PRL and T4 response depends on the dose and route of TRH administration.     

N-methyl-d,l-aspartate stimulates growth hormone and prolactin but inhibits luteinizing hormone secretion in the pig.

The effects of n-methyl-d,l-aspartate (NMA), a neuroexcitatory amino acid agonist, on luteinizing hormone (LH), prolactin (PRL) and growth hormone (GH) secretion in gilts treated with ovarian steroids was studied. Mature gilts which had displayed one or more estrous cycles of 18 to 22 d were ovariectomized and assigned to one of three treatments administered i.m.: corn oil vehicle (V; n = 6); 10 micrograms estradiol-17 b/kg BW given 33 hr before NMA (E; n = 6); .85 mg progesterone/kg BW given twice daily for 6 d prior to NMA (P4; n = 6). Blood was collected via jugular cannulae every 15 min for 6 hr. Pigs received 10 mg NMA/kg BW i.v. 2 hr after blood collection began and a combined synthetic [Ala15]-h GH releasing factor (1-29)-NH2 (GRF; 1 micrograms/kg BW) and gonadotropin releasing hormone (GnRH; .2 micrograms/kg BW) challenge given i.v. 3 hr after NMA. NMA did not alter LH secretion in E gilts. However, NMA decreased (P < .02) serum LH concentrations in V and P4 gilts. Serum LH concentrations increased (P < .01) after GnRH in all gilts. NMA did not alter PRL secretion in P4 pigs, but increased (P < .01) serum PRL concentrations in V and E animals. Treatment with NMA increased (P < .01) GH secretion in all animals while the GRF challenge increased (P < .01) serum GH concentrations in all animals except in V treated pigs. NMA increased (P < .05) cortisol secretion in all treatment groups. These results indicate that NMA inhibits LH secretion and is a secretagogue of PRL, GH and cortisol secretion with ovarian steroids modulating the LH and PRL response to NMA.     

Serum profiles of progesterone, LH, FSH and prolactin immediately preceding induced puberty in gilts

Two experiments were conducted to determine if the secretory patterns of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) and serum concentrations of progesterone change immediately preceding induced puberty in gilts. To help predict when prepubertal gilts would attain puberty, gilts were induced into puberty by relocation from confinement housing to an outdoor lot and exposure to mature boars. In Exp. 1, 17 prepubertal gilts were bled on two successive days from 0800 to 1200 h before relocation and boar exposure and until the second day of estrus or for 8 d in gilts that failed to exhibit estrus. Blood samples were collected from indwelling cannulas at 20-min intervals for 4 h. In Exp. 2, blood samples were collected from 20 prepubertal gilts at 20-min intervals from 0800 to 1200 h and from 2000 to 2400 h until the second day of estrus or for 6 d if the gilt failed to exhibit estrus. In each experiment, 11 gilts exhibited pubertal estrus 3 to 6 d after relocation and boar exposure. When the frequency of LH spikes in each gilt was normalized to the day of her preovulatory surge of LH (d 0), a decline in the frequency of LH secretory spikes was observed as gilts approached puberty. However, neither the average magnitude of LH spikes nor mean LH concentrations were different among these days. Mean serum concentrations, frequency of spikes or average magnitude of secretory spikes of FSH or PRL did not change on the days preceding the preovulatory peak of LH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reproductive and growth responses of gilts to exogenous porcine pituitary growth hormone

Forty gilts (mean wt = 72 kg) were administered daily either vehicle (C = control) or 70 micrograms porcine growth hormone (pGH)/kg BW. After 30 d of treatment, eight gilts per group (Exp. 1) were slaughtered and blood, uteri and ovaries were collected. Follicular fluid (FFl) was collected and granulosa cells (GC) were cultured. The remaining gilts (Exp. 2) were treated for up to 35 additional days and examined twice daily for estrus. Estrusal gilts were removed from the experiment. Noncyclic gilts (n = 9 of 12 pGH; n = 4 of 12 C) were slaughtered on d 66 and their ovaries were examined. Ovarian weights were not different for pGH and C gilts in either Exp. 1 (P greater than .1) or Exp. 2 (P = .09). Uterine weights were greater for pGH-treated than for C gilts (P less than .007) in Exp. 1, but not in Exp. 2. Concentrations of estradiol (E2) in plasma and FF1 and of progesterone (P) in plasma and FF1 were not different for pGH and C gilts. Concentrations of insulin-like growth factor-I (IGF-I) in FF1 and in serum were greater for pGH than for C gilts (P less than .01). Concentration of P in serum-free medium of cultured GC was lower for GH than for C (P less than .05) in the presence or absence of gonadotropins in Exp. 1. The FSH-stimulated secretion of P was also lower for GC of pGH-treated gilts in Exp. 2, indicating a failure of GC to differentiate in culture. Only one pGH gilts in Exp. 2 manifested estrus, compared with seven C gilts (P less than .025). In Exp. 1, ADG was higher (P less than .03) and feed/gain lower (P less than .07) for pGH gilts. Longissimus muscle area (LMA) was not different (P = .19) between groups. Backfat thickness (BF) was lower (P less than .005) in pGH than in C in both Exp. 1 and 2. We conclude that exogenous pGH increased growth rate, improved feed efficiency and altered carcass traits in gilts. However, these effects were associated with impaired ovarian development of prepubertal gilts and a low incidence of estrus.     

Luteinizing hormone secretion in hypophysial stalk-transected gilts given hydrocortisone acetate and pulsatile gonadotropin-releasing hormone.

The site within the hypothalamic-pituitary axis at which cortisol acts to inhibit luteinizing hormone (LH) secretion was investigated in female pigs. Six ovariectomized, hypophysial stalk-transected (HST) gilts were given 1 microgram pulses of gonadotropin releasing-hormone (GnRH) iv every 45 min from day 0 to 12. On days 6-12, each of 3 gilts received either hydrocortisone acetate (HCA; 3.2 mg/kg body weight) or oil vehicle im at 12-hr intervals. Four ovariectomized, pituitary stalk-intact gilts served as controls and received HCA and pulses of 3.5% sodium citrate. Jugular blood was sampled daily and every 15 min for 5 hr on days 5 and 12. Treatment with HCA decreased serum LH concentrations and LH pulse frequency in stalk-intact animals. In contrast, serum LH concentrations, as well as the frequency and amplitude of LH pulses, were unaffected by HCA in HST gilts and were similar to those observed in oil-treated HST gilts. We suggest that chronically elevated concentrations of circulating cortisol inhibit LH secretion in pigs by acting at the level of the hypothalamus.     

Melatonin and prolactin concentrations in blood of cattle exposed to 8, 16 or 24 hours of daily light

In two experiments, 17-wk-old Holstein bulls exposed to 16 (Exp. 1) or 24 h (Exp. 2) of light daily were compared with bulls given 8 h of light. Blood was sampled at 30-min or 120-min intervals for 48 h at the beginning and again after 4 wk of light treatment. Melatonin concentrations varied episodically in serum, and means were 1.6-fold to 5.1-fold greater during darkness than during light periods. Continuous lighting abolished the nocturnal increase in concentrations of melatonin in three of four calves. Prolactin (PRL) was greater (P less than .05) in calves receiving 16 h (30.9 ng/ml of serum) than in calves receiving 8 h (7.0 ng/ml) of light daily. Prolactin was not different between calves receiving 24 or 8 h of light daily. In a third experiment, one pinealectomized (PX) and two sham PX (SPX) calves were exposed to continuous lighting and infused with melatonin for 16 h/d for 5 wk, and one PX and two SPX calves were infused for 8 h daily. Melatonin infusion increased average concentrations of melatonin in serum 7.2-fold to 18-fold above baseline concentrations. Duration of melatonin infusion did not affect PRL (21.0 vs 20.8 ng/ml of serum). Also, surgical treatment did not affect PRL concentrations. Similarly, in a fourth experiment, PRL in postpubertal heifers fed melatonin to mimic and 8L:16D photoperiod averaged 27.1 ng/ml of serum, which was not different from PRL in heifers receiving 16L:8D and fed vehicle (32.6 ng/ml). We conclude that PRL and melatonin are each affected by photoperiod but are not casually related in cattle.     

N-methyl-d,l-aspartate modulation of pituitary hormone secretion in the pig: Role of opioid peptides

Sixteen ovariectomized (OVX) mature gilts, averaging 139.6 ± 3.1 kg body weight (BW) were assigned randomly to receive either progesterone (P, 0.85 mg/kg BW, n=8) or corn oil vehicle (OIL, n=8) injections im twice daily for 10 d. On the day of experiment, all gilts received either the EAA agonist, N-methyl-d,l-aspartate (NMA; 10 mg/kg BW, iv) alone or NMA plus the EOP antagonist, naloxone (NAL, 1 mg/kg BW, iv), resulting in the following groups of 4 gilts each: OIL-NMA, OIL-NMA-NAL, P-NMA and P-NMA-NAL. Blood samples were collected via jugular cannula every 15 min for 6 hr. All pigs received NMA 5 min following pretreatment with either 0.9% saline or NAL 2 hr after blood collection began and a GnRH challenge 3 hr after NMA. Administration of NMA suppressed (P<0.03) LH secretion in OIL-NMA gilts and treatment with NAL failed to reverse the suppressive effect of NMA on LH secretion in OIL-NMA-NAL gilts. Similar to OIL-NMA gilts, NMA decreased (P<0.03) mean serum LH concentrations in P-NMA gilts. However, in P-NMA-NAL gilts, serum LH concentrations were not changed following treatment. All gilts responded to GnRH with increased (P<0.01) LH secretion. Additionally, administration of NMA increased (P<0.01) growth hormone (GH) and prolactin (PRL) secretion in both OIL-NMA and P-NMA gilts, but this increase in GH and PRL secretion was attenuated (P<0.01) by pretreatment with NAL in OIL-NMA-NAL and P-NMA-NAL gilts. Serum cortisol concentrations increased (P<0.01) in all gilts and the magnitude of the cortisol response was not different among groups. In summary, results of the present study confirmed previous findings that NMA suppresses LH secretion in both oil- and P-treated OVX gilts, but we failed to provide definitive evidence that EOP are involved in the NMA-induced suppression of LH secretion. However, NMA may, in part, activate the EOP system which in turn increased GH and PRL secretion in the gilt.     

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.     

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)     

Scheduled breeding of gilts after estrous synchronization with altrenogest

Fertility of 104 gilts artificially inseminated (AI) at a predetermined time (scheduled AI) after estrous synchronization with altrenogest (15 mg X gilt-1 X d-1 for 18 d) was compared with that of 103 gilts checked for estrus (estrus checked) and inseminated after altrenogest. Scheduled-AI gilts were inseminated once on d 5, 6 and 7 after the last altrenogest feeding (d 0). Estrus-checked gilts were exposed to a boar twice daily at 0830 and 1630 h and inseminated after the second and third estrous detection period following first detected estrus. Percentage of gilts assigned to treatment that farrowed (72.8 vs 67.3%), total pigs farrowed (11 +/- .4 vs 11.3 +/- .4) and pigs born alive (10.1 +/- .4 vs 10.5 +/- .4) were similar for estrus-checked and scheduled-AI gilts, respectively. We conclude that scheduled AI can be used with estrous synchronization for gilts and may have advantages in breeding herd management and the use of AI in swine.     

Prepubertal exposure to dietary zearalenone alters hypothalamo-hypophysial function but does not impair postpubertal reproductive function of gilts

At an average age of 70 d, 60 Yorkshire gilts born either in July (Trial 1; n = 30) or August (Trial 2; n = 30) received a diet containing zearalenone for 0 (control), 45 or 90 d. The concentration of zearalenone in diets was 2 ppm for 2 wk and 1.5 ppm for the remainder of the study. Vulval swelling and reddening was evident within 7 d after zearalenone was first fed. Zearalenone consumption had no effect on BW or backfat depth. Puberty occurred in Trial 1 at 219 +/- 6 d and was not influenced by zearalenone. Gilts in Trial 2 were divided into two groups; blood samples were taken from 12 gilts to assess pulsatile LH patterns and LH response to estradiol benzoate (EB) and 18 were handled similarly to those in Trial 1. Of this latter subgroup, age at puberty was younger (P less than .05) with zearalenone (217 +/- 7.0, 193 +/- 9.1 and 185.6 +/- 8.2 d for 0-, 45-, and 90-d treatments). Prepubertal consumption of zearalenone did not affect conception rates, ovulation rates, number of fetuses or percentage of embryo survival following mating at pubertal estrus. Two days before the 90-d experimental period ended for Trial 2, blood samples were taken from 12 gilts (four/treatment) every 15 min for 4 h prior to injection of EB (10 micrograms/kg) and every 6 h for 108 h after EB. Analysis of pulsatile patterns of LH revealed no influence of zearalenone on the number of peaks/4 h, baseline concentration or peak height.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endocrine changes in sows exposed to elevated ambient temperature during lactation

Seven sows were placed into one of two environmental chambers at 22 C, 5 d prior to farrowing. On day 9 of lactation, one chamber was changed to 30 C (n = 4) and the other remained at 22 C (n = 3). On days 24 and 25, blood samples were collected every 15 min for 9 hr and 7 hr, respectively. On day 24, thyrotropin releasing hormone (TRH) and gonadotropin releasing hormone (GnRH) were injected iv at hour 8. On day 25 naloxone (NAL) was administered iv at hour 4 followed 2 hr later by iv injection of TRH and GnRH. Milk yield and litter weights were similar but backfat thickness (BF) was greater in 22 C sows (P less than .05) compared to 30 C sows. Luteinizing hormone (LH) pulse frequency was greater (P less than .003) and LH pulse amplitude was less (P less than .03) in 22 C sows. LH concentrations after GnRH were similar on day 24 but on day 25, LH concentrations after GnRH were greater (P less than .05) for 30 C sows. Prolactin (PRL) concentrations were similar on days 24 and 25 for both groups. However, PRL response to TRH was greater (P less than .05) on both days 24 and 25 in 30 C sows. Growth hormone (GH) concentrations, and the GH response to TRH, were greater (P less than .0001) in 30 C sows. Cortisol concentrations, and the response to NAL, were less (P less than .03) in 30 C sows. NAL failed to alter LH secretion but decreased (P less than .05) PRL secretion in both groups of sows. However, GH response to NAL was greater (P less than .05) in 30 C sows. Therefore, sows exposed to elevated ambient temperature during lactation exhibited altered endocrine function.     

Reevaluation of the role of progesterone in stimulating sexual receptivity in estrogen-treated gilts

Three studies were conducted to examine the role of progesterone in stimulating sexual receptivity in estrogen-treated, ovariectomized gilts. Progesterone was administered either before, simultaneously with, or 48 h after estrogen. In each study, gilts were treated with either a suboptimal or an optimal dosage of estradiol benzoate (EB). Progesterone treatment (600 micrograms/kg BW-1 X injection-1) on alternate days for a total of four injections produced serum concentrations of progesterone that were maximal at 9.4 ng/ml and remained greater than 1 ng/ml for 15 d. Estradiol benzoate was administered 22 d after the first of these progesterone injections. When progesterone was administered concurrently with or 48 h after EB, the dosage was 100 micrograms/kg BW and produced a maximal serum progesterone concentration of 1.8 ng/ml 4 h after treatment. Gilts were placed in an evaluation pen with a boar for 5 min on d 3 and 4 after EB treatment. Traits of interest were total number of mounts by the boar, mounts before the gilt showed the immobilization response, proportion of gilts that showed the immobilization response, and latency from entry of the gilt into the evaluation pen until the immobilization response. In none of the three studies did progesterone improve any of the traits of interest. In each study the immobilization response was observed in a higher proportion of gilts treated with the optimal than in those treated with the suboptimal dosage of EB. Latency from entry of gilts into the evaluation pen until the immobilization response was less on d 4 than on d 3 after EB in all studies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyrotropin releasing hormone interactions with growth hormone secretion in horses

Light horse mares, stallions, and geldings were used to 1) extend our observations on the thyrotropin releasing hormone (TRH) inhibition of GH secretion in response to physiologic stimuli and 2) test the hypothesis that stimulation of endogenous TRH would decrease the normal rate of GH secretion. In Exp. 1 and 2, pretreatment of mares with TRH (10 microg/kg BW) decreased (P < 0.001) the GH response to exercise and aspartate infusion. Time analysis in Exp. 3 indicated that the TRH inhibition lasted at least 60 min but was absent by 120 min. Administration of a single injection of TRH to stallions in Exp. 4 increased (P < 0.001) prolactin concentrations as expected but had no effect (P > 0.10) on GH concentrations. Similarly, 11 hourly injections of TRH administered to geldings in Exp. 5 did not alter (P > 0.10) GH concentrations either during the injections or for the next 14 h. In Exp. 5, it was noted that the prolactin and thyroid-stimulating hormone responses to TRH were great (P < 0.001) for the first injection, but subsequent injections had little to no stimulatory effect. Thus, Exp. 6 was designed to determine whether the inhibitory effect of TRH also waned after multiple injections. Geldings pretreated with five hourly injections of TRH had an exercise-induced GH response identical to that of control geldings, indicating that the inhibitory effect was absent after five TRH injections. Retrospective analysis of pooled, selected data from Exp. 4, 5, and 6 indicated that endogenous GH concentrations were in fact lower (P < 0.01) from 45 to 75 min after TRH injection but not thereafter. In Exp. 7, 6-n-propyl-2-thiouracil was fed to stallions to reduce thyroid activity and hence thyroid hormone feedback, potentially increasing endogenous TRH secretion. Treated stallions had decreased (P < 0.01) concentrations of thyroxine and elevated (P < 0.01) concentrations of thyroid-stimulating hormone by d 52 of feeding, but plasma concentrations of GH and prolactin were unaffected (P > 0.10). In contrast, the GH response to aspartate and the prolactin response to sulpiride were greater (P < 0.05) in treated stallions than in controls. In summary, TRH inhibited exercise- and aspartate-induced GH secretion. The duration of the inhibition was at least 1 h but less than 2 h, and it waned with multiple injections. There is likely a TRH inhibition of endogenous GH episodes as well. Reduced thyroid feedback on the hypothalamic-pituitary axis did not alter basal GH and prolactin secretion.