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)     

Endogenous opioid actions and effects of environmental disturbance on parturition and oxytocin secretion in rats

Blood samples were taken from conscious, chronically-catheterized rats during parturition for measurement of oxytocin by specific radioimmunoassay. After the birth of the 3rd pup, rats were allowed to remain in their nesting cage (undisturbed rats) or were transferred for 45 min to a glass bowl (disturbed rats); at the time of transfer, rats were given an i.v. injection of the opioid antagonist naloxone or saline vehicle. Subsequent parturition was prolonged in saline-treated disturbed rats, but not in naloxone-treated disturbed rats. Parturition was significantly hastened in naloxone-treated undisturbed rats. Naloxone injections were followed by a large rise in plasma oxytocin concentrations in disturbed and undisturbed rats. We conclude, from a statistical analysis of the relationship within experimental groups between plasma oxytocin concentration and speed of parturition, that the effects of disturbance and of naloxone upon parturition may be accounted for, at least in part, by their effects upon oxytocin release. However, the effects of disturbance on parturition may not be mediated entirely by activation of opioid pathways. Naloxone did not potentiate oxytocin release in non-pregnant rats, or on Day 1 post partum, but did potentiate oxytocin release on Day 22 of pregnancy even in rats before the onset of parturition. Endogenous opioid pathways regulating oxytocin release therefore appear to be active during late pregnancy and during parturition itself.     

Effect of pregnancy on oxytocin-induced release of prostaglandin F2 alpha in heifers

The effect of pregnancy on the release of prostaglandin F2 alpha (PGF2 alpha) in response to oxytocin (OT) has been examined. Fourteen cyclic heifers received one intravenous injection of 1 IU OT (n = 6) or 100 IU OT (n = 8) 17, 18, or 19 days (Day 17-19) after the onset of estrus (Day 0). Five of these animals also received 100 IU OT at Days 6 and 13 to determine the effect of OT at different times of the cycle. Frequent blood samples were taken for 60 min before and for 90 min after OT injection for the measurement of 15-keto-13,14-dihydro-PGF2 alpha (PGFM) by radioimmunoassay. The experiment was then repeated using the same animals at Day 17-19 of pregnancy (confirmed by the recovery of an embryo the day after OT injection). Following the injection of 1 IU OT, plasma PGFM reached its peak within 30 min with the increase significantly lower (P less than 0.05) in pregnant (1.13 +/- 0.10-fold) than in nonpregnant animals (2.07 +/- 0.27-fold). However, because only 3 of the 6 cyclic animals showed a response to 1 IU OT, the dose was increased to 100 IU in subsequent experiments. The animals that received 100 IU at Days 6 and 13 had no significant increase in PGFM concentrations (1.18 +/- 0.05-fold and 1.01 +/- 0.04-fold, respectively). At Day 17-19 the increase in plasma PGFM reached its peak 5-15 min after 100 IU OT and the increase was significantly greater in nonpregnant (3.23 +/- 0.17-fold) than in pregnant (1.21 +/- 0.02-fold; P = 0.003) heifers. Six of 11 animals injected at Day 17-19 of the cycle showed a decrease in progesterone (P4) the day after OT administration. These data show that the release of PGF2 alpha in response to OT is suppressed in pregnant animals in vivo, suggesting an antiluteolytic role for the embryo in luteostasis.     

Evidence for opioidergic inhibition of oxytocin release in periparturient mares

In the horse mare, the onset of parturition is associated with an increase in oxytocin secretion, and it has been suggested that the onset of parturition may be triggered by endogenous oxytocin release. To test the hypothesis that oxytocin secretion is regulated by endogenous opioids in the periparturient period, we have 1) characterized oxytocin secretion in response to vaginocervical stimulation and 2) determined the effect of naloxone, an opioid antagonist, on oxytocin secretion induced by vaginocervical stimulation in prepartum mares and in postpartum mares at estrus and diestrus. During the last 2 months of pregnancy, the first diestrus and subsequent estrus post partum, a total of 66 vaginocervical stimulations were performed. Mares were pretreated with naloxone (0.5 mg/kg i.v.) or saline, administered 20 min before vaginocervical stimulation on subsequent days, using a randomized switchback design in which mares served as their own controls. Plasma was collected from 30 min before until 30 min after stimulation and was analyzed for oxytocin concentrations. Vaginocervical stimulation resulted in a significant increase in oxytocin secretion in all mares. Between Days 30 and 20 prepartum, the total amount of oxytocin secreted (calculated as area under the curve for 0 to 10 min after vaginocervical stimulation) was significantly greater in naloxone-treated than in saline-treated mares. From Day 20 prepartum until parturition, the differences between naloxone and saline-treated mares tended to decrease with approaching parturition, and were no longer statistically different. Peak plasma oxytocin concentrations were greater in naloxone-treated mares than in saline-treated mares during the entire prepartum period. During the postpartum period, total amount of oxytocin secreted following vaginocervical stimulation tended to be greater than during the prepartum period, and stimulated oxytocin secretion was significantly greater in naloxone-treated mares than in saline-treated mares. In conclusion, these data suggest that endogenous opioids suppress oxytocin secretion pre and post partum. It appears that opioid inhibition is not limited to the prepartum period, tends to decrease gradually towards parturition and is reinstated after foaling.     

The effect of environment on plasma cortisol and β-endorphin in the parturient pig and the involvement of endogenous opioids

Previous work has indicated that plasma cortisol increases during farrowing in the pig suggesting increasing physiological stress. The aim of this study was to determine changes in plasma cortisol and β-endorphin over farrowing in the pig to obtain a more detailed profile of pituitary and adrenal release at this time and also to investigate the involvement of endogenous opioids in the mediation of the HPA axis. Indwelling jugular catheters were implanted, under general anaesthesia, in 31 Large White×Landrace gilts approximately 15 days before the expected parturition day (EPD). Gilts were moved into either a farrowing crate, without straw (n=15), or a straw-bedded pen (n=16) 5 days before the EPD. Samples were taken during the pre-farrowing period and then during farrowing itself. At 7.5 min after the birth of the first piglet (BFP), gilts either received naloxone, an opioid antagonist, (1 mg kg⁻¹ body weight, i.v.) or a control dose of saline. Plasma β-endorphin increased following the BFP but remained fairly constant over the third and fourth hour of farrowing. Plasma cortisol continued to increase over the 4 h following the BFP. Changes seen in these hormones were generally insensitive to the environment and there was little evidence of opioid mediation of the HPA axis at parturition. From these results it is suggested that certain aspect(s) of parturition itself stimulate the HPA axis. However it is unknown if the rise in plasma cortisol is a result of some stress-inducing factor of the parturition process or whether it reflects a metabolic function. The study also demonstrates the lack of any inhibitory mediation of the HPA axis by endogenous opioids at parturition.     

Serum hormone profiles and return to estrus in early-postpartum spring-lambing ewes treated with somatostatin

After parturition, 10 mature spring-lambing fine-wool ewes producing twins were allotted to one of two treatments. Five ewes received sterile saline (i.v.) twice daily on Days 12 to 15 post partum (PP) while 5 ewes were treated similarly except each injection contained 500 mug somatostatin (SRIF). Jugular blood samples were collected at 15-min intervals for 1 h before to 3 h after morning treatment on Days 12 and 15 PP. Animals were observed twice daily for signs of estrus using vasectomized rams beginning on Day 31 PP and continuing until ewes returned to estrus. Interval from parturition to estrus (mean +/- SEM) was similar (P > 0.40) in ewes receiving SRIF (119 +/- 6.2 d) and in control ewes (113 +/- 6.2 d). Ewes receiving 500 mug SRIF had lower (P < 0.10) serum insulin during the first 45 min after treatment on Day 12 PP; however, on Day 15 PP, serum insulin did not differ (P > 0.40) between treatment groups. Serum growth hormone (GH) did not differ (P > 0.40) between treatment groups 1 h before treatment on Day 12 PP; however, ewes treated with SRIF had lower (P < 0.05) GH levels before treatment on Day 15 PP than control ewes (4.4 and 9.9 +/- 1.5 ng/ml, respectively). After administration of SRIF, serum GH was higher (P < 0.05) in SRIF-treated ewes than in controls (8.2 and 5.3 +/- 2.7 ng/ml, respectively) on Day 12 PP but no differences (P > 0.80) were noted between treatment groups on Day 15 PP. These data indicate that 500 mug SRIF given twice daily from Days 12 to 15 PP neither lowered serum GH nor influenced return to estrus in lactating fine-wool ewes.     

Effect of pregnancy and exogenous ovarian steroids on endometrial prolactin receptor ontogeny and uterine secretory response in pigs

During gestation, pigs have constant circulating levels of prolactin (PRL), and lack decidual PRL and placental lactogens. Effects of PRL on uterine physiology in pigs may be due to changes in endometrial PRL receptors. In this study, effects of the conceptus and cyclic hormonal environment on endometrial PRL receptors were investigated. Endometrial PRL receptor numbers were similar between Days 8 and 15 for cyclic gilts. In contrast, endometrial PRL receptor numbers for pregnant gilts were similar between Days 8 and 11, then increased (p less than 0.05) on Day 12 and remained elevated between Days 14 and 30. This day-by-status interaction approached significance (p less than 0.06) and overall receptor numbers were higher (p less than 0.01) for pregnant than for cyclic gilts. Pig conceptuses secrete estrogen between Days 11 and 12; therefore, regulation of endometrial PRL receptors by acute administration of estradiol was investigated. Uterine flushings and endometrium were collected from one uterine horn of cyclic gilts on Day 11; then, at 1, 6, 12, and 24 h following a single injection of estradiol valerate (EV; 5 mg, into adipose tissue), uterine flushings and endometrium were collected from the second uterine horn. Endometrial PRL receptor numbers were higher (p less than 0.05) at both 1 h and 6 h after treatment with EV and then decreased (p less than 0.02) by 12 h to below pretreatment values. In uterine flushings, total recoverable protein (p less than 0.05), uteroferrin (p less than 0.01), leucine aminopeptidase (p less than 0.05), calcium (p less than 0.03), sodium (p less than 0.01), and potassium (p less than 0.05) increased between 12 and 24 h following EV treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of porcine conceptus secretory proteins on interestrous interval and uterine secretion of prostaglandins

Porcine conceptus secretory proteins (pCSP) were obtained from medium in which pig conceptuses, collected on Day 15 of pregnancy, were cultured for 30 h. Culture medium was pooled, dialyzed, and concentrated by Amicon ultrafiltration for intrauterine infusion. Serum proteins (SP) were obtained from blood collected from a Day 15 pregnant gilt and diluted for intrauterine infusion. Catheters were placed into both uterine horns and the inferior vena cava of cyclic (Day 8) gilts. Single blood samples were collected at 0800 h on Days 9, 10, and 11. On Day 11, all gilts received 1 mg estradiol-17 beta (E2) i.m. at 0800 h. Protein infusions commenced on Day 12 and continued through Day 15, twice daily at 0800 h and 2000 h. Protein infusions per uterine horn were (1) 4.0 mg pCSP + 4.0 mg SP (pCSP, 4 gilts) and (2) 8.0 mg SP (SP, 4 gilts). Blood samples were collected every 15 min on Days 12 through 17 between 0805 h and 1100 h. Single blood samples were collected at 0800 h after Day 17 until gilts exhibited estrus. Concentrations of prostaglandin (PG) E, 13,14-dihydro-15-keto-PGF2 alpha (PGFM), and progesterone (P4) were measured by specific radioimmunoassays. Interestrous intervals for pCSP-treated (18.2 days) and SP-treated (18.0 days) gilts were not different (SEM = 0.8 days) and temporal changes in concentrations of P4 in plasma did not differ between pCSP-treated (29.2 ng/ml) and SP-treated (31.2 ng/ml) gilts.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of prolactin on conceptus survival and uterine secretory activity in pigs

Hypoprolactinaemia was induced by bromocriptine (CB154; 100 mg/day) which decreased circulating prolactin by 40% (P less than 0.06), but did not affect conceptus survival at Day 25 when administered on Days 10-16 when compared to saline:ethanol-treated control gilts. Bromocriptine or vehicle was administered to cyclic gilts on Days 10-11, oestradiol valerate was injected on Day 11 and uterine flushings were collected on Day 12. Total recoverable protein and uteroferrin in uterine flushings were not affected by treatment. However, leucine aminopeptidase activity (P less than 0.02) and total recoverable Ca2+, Na+, K+ and Cl- (P less than 0.05) were decreased in uterine flushings of gilts that received bromocriptine, suggesting that hypoprolactinaemia decreased general secretory activity of the endometrial epithelium and modulated ionic changes, respectively, in the uterine environment of pigs. Subcutaneous administration of pig prolactin (1 mg/12 h) increased (P less than 0.001) serum prolactin 4.5-fold. The interaction between hyperprolactinaemia and progesterone, without oestrogen, on components of uterine flushings were determined using gilts that received progesterone (200 mg/day) and prolactin or saline on Days 4-14 after ovariectomy on Day 4. On Day 15, there were no differences (P greater than 0.05) in any of the uterine secretory components measured. Hyperprolactinaemia (1 mg pig prolactin on Days 6-11) enhanced overall uterine secretory response on Day 12 to oestradiol (5 mg) administered on Day 11 compared to gilts that received 1 ml saline on Days 6-11 of the oestrous cycle. Total recoverable protein and leucine aminopeptidase activity were greater (P less than 0.05) for oestradiol-treated gilts, but effects of prolactin were not significant. Total recoverable glucose (P less than 0.01), PGF-2 alpha (P less than 0.02), uteroferrin (P less than 0.01) and specific activity of uteroferrin (P less than 0.001) were increased by prolactin and oestradiol, but not oestradiol alone. Calcium (P less than 0.05), chloride (P less than 0.05) and potassium (P less than 0.01) were increased in response to oestradiol. These results indicate an interaction between oestradiol and prolactin, but not progesterone and prolactin, which enhances secretion of some products of the pig uterine endometrium.     

A study of prostaglandin F2α as the luteolysin in swine: III effects of estradiol valerate on prostaglandin F, progestins, estrone and estradiol concentrations in the utero-ovarian vein of nonpregnant gilts

Polyvinyl catheters were placed into the right and left utero-ovarian veins and saphenous vein and artery of three control (C) and four estradiol valerate (EV) treated gilts on Day 9 after onset of estrus. The EV treated gilts received 5mg EV/day on Days 11 through 15 after onset of estrus. On Days 12 through 17 utero-ovarian vein blood samples were collected at 15 min intervals from 0700 to 1000 hr and 1900 to 2200 hr and single samples were taken at 1100 and 2300 hr. Peripheral blood samples (saphenous vein or artery) were taken at 0700, 1100, 1900 and 2300 hr from Day 12 until the control gilts returned to estrus or until Day 25 for EV treated gilts and used to measure plasma steroid hormone concentrations. Utero-ovarian vein prostaglandin F (PGF) concentrations (ng/ml, n=1,177) were measured by RIA. Status (control EV treated gilts) by day interactions were detected (P=.10). Curvilinear day trends were detected for plasma PGF concentrations in control (P<.01) but not EV treated gilts. PGF concentrations ( ) for control and EV treated gilts were 1.20 ± 2.08 and .26 ± .84 ng/ml, respectively. PGF peaks (concentrations greater than + 2 S.D.) occured with greater frequency in control gilts (X² = 4.87; P<.05). The interestrus interval ( ) for control and treated gilts was 19.0 ± .6 and 146.5 ± 74.8 days, respectively. Data indicate that estradiol valerate may exert its luteotrophic effect by preventing PGF release from the uterus.     

A study of prostaglandin F2alpha as the luteolysin in swine: III effects of estradiol valerate on prostaglandin F, progestins, estrone and estradiol concentrations in the utero-ovarian vein of nonpregnant gilts

Polyvinyl catheters were placed into the right and left utero-ovarian veins and saphenous vein and artery of three control (C) and four estradiol valerate (EV) treated gilts on Day 9 after onset of estrus. The EV treated gilts received 5mg EV/day on Days 11 through 15 after onset of estrus. On Days 12 through 17 utero-ovarian vein blood samples were collected at 15 min intervals from 0700 to 1000 hr and 1900 to 2200 hr and single samples were taken at 1100 and 2300 hr. Peripheral blood samples (saphenous vein or artery) were taken at 0700, 1100, 1900 and 2300 hr from Day 12 until the control gilts returned to estrus or until Day 25 for EV treated gilts and used to measure plasma steroid hormone concentrations. Utero-ovarian vein prostaglandin F (gf) concentrations (ng/ml, n-1,177) were measured by RIA. Status (control vs EV treated gilts) by day interactions were detected (P=.10). Curvilinear day trends were detected for plasma PGF concentrations in control (P less than .01) but not EV treated gilts. PGF concentrations (X +/- S.D.) for control and EV treated gilts were 1.20 +/- 2.08 and .26 +/- .84 ng/ml, respectively. PGF peaks (concentrations greater than X + 2 S.D.) occurred with greater frequency in control gilts (X2 =4.87; P less than .05). The interestrus interval (X +/- S.E.) for control and treated gilts was 19.0 +/- .6 and 146.5 +/- 74.8 days, respectively. Data indicate tht t estradiol valerate may exert its luteotrophic effect by preventing PGF release from the uterus.     

Opioidergic control of luteinizing hormone release in the female rabbit: influence of ovariectomy and steroid replacement on pulsatile secretion

The influence of ovariectomy and steroid replacement on naloxone-induced changes in pulsatile secretion of luteinizing hormone (LH) in the female rabbit was examined. Blood samples were taken every 5 min through an indwelling catheter in the rabbit ear artery, and plasma was stored until assayed for LH by established radioimmunoassay procedures. In the intact animal, saline injection had no effect on LH secretion. Although naloxone (10 mg/kg) caused a 7-fold increase in mean LH pulse amplitude by 30 min after injection, this increase was not statistically significant because 5 of 11 animals did not respond. In animals ovariectomized 48 h previously, naloxone significantly increased LH concentration by 194% at 23 min after injection. When long-term ovariectomized rabbits were treated with estradiol benzoate and then were given naloxone, no significant increase in LH was observed, although many animals did respond. Treatment of long-term ovariectomized rabbits with 1 microgram estradiol benzoate and 100 micrograms progesterone or 1 mg testosterone propionate on Days 1 and 3 and naloxone on Day 4 resulted in a significant increase in LH 19-24 min later. Although there was an increase in pulse amplitude, no change was detected in pulse frequency after naloxone. These data suggest that the hypothesis of steroid-opioid coupling in the control of LH secretion is not applicable to the female rabbit.     

Opioid control of oxytocin secretion: evidence of distinct regulatory actions of two opiate receptor types

Stress induced oxytocin (OT) secretion was measured in female rats following treatment with various opiate antagonists selective for different types of opiate receptor. Naloxone (mu selective) and MR2266 BS (kappa selective) potentiated the OT response to an emotional stress (1 min. immobilization) whereas the delta selective antagonist ICI 154129 was without effect. Similarly, naloxone and MR2266 BS, but not ICI 154129, potentiated the response to a physical stress (i.p. hypertonic saline). A dose response comparison of the actions of naloxone and MR2266 BS revealed that naloxone was most effective in potentiating the immobilization response whereas MR2266 BS elicited greater responses than naloxone when administered prior to hypertonic saline. The results indicate that the opioid regulation of stress induced OT secretion is primarily mediated via mu and kappa opiate receptor types, the two types differentially regulating the OT response to two different stressors.     

Effect of vascular cannulation on serum concentrations of LH, FSH, prolactin and cortisol in prepubertal gilts

Two experiments were conducted to determine whether cannulation of the jugular vein in gilts alters serum concentrations of LH, FSH, prolactin (PRL) or cortisol (C). In Experiment 1, 12 crossbred prepubertal gilts weighing 95 +/- 1.3 kg were immobilized by snaring, and tygon tubing was threaded into the anterior vena cava through a 12-gauge needle inserted into the jugular vein. Five hours later, blood samples were drawn at 20-min intervals for 4 h (Day 0). Samples were also drawn at 20-min intervals for 4-h periods 24 h (Day 1) and 48 h (Day 2) after cannulation. Serum concentrations of LH were similar (P=0.26) among Day 0 (0.40 ng/ml), Day 1 (0.39 ng/ml) and Day 2 (0.34 ng/ml). Serum PRL was similar (P=0.07) among Day 0 (4.10 ng/ml), Day 1 (3.87 ng/ml) and Day 2 (3.43 ng/ml). Serum concentrations of C were greater (P < 0.001) on Day 0 (8.32 ng/ml) than Day 1 (4.48 ng/ml) or Day 2 (3.54 ng/ml). In Experiment 2, cannulas were placed in 29 prepubertal gilts. Two days after initial cannulation, six blood samples were drawn at 20-min intervals. Gilts were then immobilized by snaring, and a second cannulae was inserted into the contralateral vein. Five blood samples were taken at 2-min intervals during the second cannulation and then six samples were drawn at 20-min intervals. Serum LH and FSH were not altered by cannulation or elevated during the subsequent 2-h sampling period (P>0.05). In contrast, serum concentrations of PRL rose slowly (P<0.05) during cannulation and remained elevated for 60 min before returning to baseline. Serum concentrations of C rose within 6 min of cannulation, remained elevated for 30 min, and then declined over the next 90 min. From these two experiments, it appears that secretory patterns of LH and FSH can be accurately assessed immediately after cannulation in prepubertal gilts. Measurements of serum PRL and C that reflect nonstressed conditions, however, cannot be obtained until at least 2 h or 1 d after cannulation, respectively.     

Growth hormone is secreted by ectopic pituitary grafts and stimulates maternal behavior in rats

The onset of maternal behavior at parturition in rats is hormonally regulated. Recently, we reported that treatment of behaviorally inexperienced, hypophysectomized (hypox), ovariectomized (ovx) rats with a sequential steroid treatment of progesterone (P) and estradiol (E2), and either ectopic anterior pituitary grafts or prolactin (PRL), stimulated maternal responsiveness toward foster young. That growth hormone (GH) has a number of PRL-like activities led us to ask whether the actions of PRL on maternal behavior were specific to PRL or might be shared by other PRL-like protein hormone, i.e., GH. In Experiment 1 we quantified plasma concentrations of GH and PRL by RIA in groups of hypox female rats that were ovariectomized and treated with a combination of ectopic pituitary grafts (Days 1-23) and Silastic capsules filled with P (Days 1-11) and E2 (Days 11-23). Blood samples were collected from Days 1 to 23 of treatment. Both plasma PRL and GH levels increased after grafting, initially rising 10- to 60-fold by Day 4 and gradually declining throughout the remainder of the 23-day sampling period. Throughout the 3-week period after grafting plasma GH levels were as high or higher than those of PRL. In Experiment 2 the behavioral effects of exogenously administered ovine (o)-GH were measured in groups of hypox, ovx rats that were treated with P and E2 as in Experiment 1. Experimental rats were injected twice daily with 0.25 mg oGH beginning on Day 1. Testing for maternal behavior toward foster young was conducted daily from Day 12 to Day 22. In steroid-treated rats, GH treatment stimulated a more rapid onset of maternal behavior (latencies of 3 vs greater than 10 days for vehicle-injected controls). These data indicate that GH, like PRL, is secreted by ectopic pituitary grafts and is capable of stimulating maternal behavior.     

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)     

Effects of estrogen and prostaglandin on progesterone-delayed farrowing

Effects of estradiol benzoate and prostaglandin F(2alpha) (PGF(2alpha)) on concentrations of progesterone and estrogen in serum and the percentage of live births were determined in 21 gilts treated with exogenous progesterone in late gestation. All gilts received progesterone (25mg s.c. four times daily) from Days 108 through 113 of gestation. Gilts receiving no other treatments (controls) had elevated levels of progesterone through 1800 h on Day 114 (29.2 +/- 11.4 ng/ml) and farrowed at 115.6 +/- 0.3 d of gestation with a relatively low percentage of live births (66.8 +/- 17.3). Gilts treated with PGF(2alpha) administered at 0600 h on Day 114 had less (P<0.01) progesterone by 1800 h (7.0 +/- 1.3 ng/ml) relative to that of the controls, but they had similar gestation lengths (115.5 +/- 0.3) and percentages of live births (50.0 +/- 16.2). Administration of estradiol benzoate (10 mg) to gilts at 0600 h on Day 114 did not reduce progesterone on Day 114 or the gestation length relative to that of the control gilts, but it did increase (P<0.05) the percentage of live births (100%).     

The impact of dose of FSH (Folltropin) containing LH (Lutropin) on follicular development, estrus and ovulation responses in prepubertal gilts

FSH is favored over chorionic gonadotropins for induction of estrus in various species, yet little data are available for its effects on follicle development and fertility for use in pigs. For Experiment 1, prepubertal gilts (n = 36) received saline, 100 mg FSH, or FSH with 0.5 mg LH. Treatments were divided into six injections given every 8 h on Days 0 and 1. Proportions of gilts developing medium follicles were increased for FSH and FSH-LH (P < 0.05) compared to saline, but follicles were not sustained and fewer hormone-treated gilts developed large follicles (P < 0.05). No gilts expressed estrus and few ovulated. Experiment 2 tested FSH preparations with greater LH content. Prepubertal gilts (n = 56) received saline, FSH-hCG (100 mg FSH with 200 IU hCG), FSH-LH5 (FSH with 5 mg LH), FSH-LH10 (FSH with 10 mg LH), or FSH-LH20 (FSH with 20 mg LH). FSH-LH was administered as previously described, while 100 IU of hCG was given at 0 h and 24 h. Hormone treated gilts showed increased (P < 0.05) medium and large follicle development, estrus (>70%), ovulation (100%), and ovulation rate (>30 CL) compared to saline. There was an increase (P < 0.05) in the proportion of hormone-treated gilts with follicular cysts at Day 5, but these did not persist to Day 22. These gilts also showed an increase in poorly formed CL (P < 0.05). FSH alone or with small amounts of LH can induce medium follicle growth but greater amounts of LH at the same time is needed to sustain medium follicles, stimulate development of large follicles and induce estrus and ovulation in prepubertal gilts.     

Ovarian steroid involvement in endogenous opioid modulation of LH secretion in seasonally anoestrous mature ewes

In June, 16 mature ewes were ovariectomized and allocated to four groups: 1, saline; 2, naloxone; 3, progesterone implant plus naloxone; 4, oestrogen implant plus naloxone. Steroids were implanted at the time of ovariectomy. At 5 days after ovariectomy, the animals were intravenously infused with saline for 8 h and naloxone (50 mg/h) in saline for 8 h the following day. Three intact ewes were given naloxone in a similar way. During infusions and for 8 h on the day after naloxone, jugular venous blood samples were taken every 15 min and assayed for LH. Naloxone resulted in significant increases in mean LH concentration (P less than 0.01), LH episode frequency and episode height (P less than 0.05) in Group 3 ewes, but was without effect in any other group. These results provide evidence that the progesterone status of the ewe affects its response to naloxone, that progesterone negative feedback on LH release may be mediated by an opioid system, and that increased oestradiol negative feedback during seasonal anoestrus is unlikely to work via increased opioid inhibition of LH.     

Proteins secreted by the sheep conceptus suppress induction of uterine prostaglandin F-2 alpha release by oestradiol and oxytocin

In Exp. I, 0.5 mg oestradiol or vehicle (0.5 ml absolute ethanol + 0.5 ml 0.9% NaCl) was injected i.v. at 08:00 h on Day 14 (onset of oestrus = Day 0). Blood samples were obtained via a jugular catheter at 30 and 1 min before oestradiol and every 30 min for 10 h afterwards. Plasma was obtained and assayed for 15-keto-13,14-dihydro-PGF-2 alpha (PGFM) by radioimmunoassay. Before oestradiol, PGFM basal values were higher (P less than 0.01) in pregnant (N = 10) than nonpregnant (N = 6) ewes (193 +/- 30 vs 67 +/- 8 pg/ml). However, at 4-10 h after oestradiol, pregnant ewes (N = 5) had less variable (P less than 0.01) PGFM values than did nonpregnant ewes (N = 5). In Exp II, conceptus secretory proteins (CSP) were obtained by pooling medium from cultures of Day-16 sheep conceptuses (N = 40). Ewes received 750 micrograms CSP + 750 micrograms plasma protein (N = 6) or 1500 micrograms plasma protein (N = 6) per uterine horn at 08:00 h and 18:00 h on Days 12-14. All ewes received 0.5 mg oestradiol at 08:00 h on Day 14 and blood samples were collected as in Exp. I and assayed for PGFM. On Day 15, 3 ewes in each group received 10 i.u. oxytocin and 3 received saline i.v. at 08:00 h and blood samples were taken continuously from 10 min before to 60 min after treatment. Mean PGFM response to oestradiol was suppressed (P = 0.05) in CSP- vs plasma protein-treated ewes (371 +/- 129 vs 1188 +/- 139 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)