Suckling inhibits release of luteinizing hormone-releasing hormone from the bovine median eminence following ovariectomy

The effect of suckling on depletion of hypothalamic LHRH from the median eminence (ME) following ovariectomy (OVX) was determined in cattle. Multiparous, postpartum Holstein cows were assigned randomly to three groups: intact, nonsuckled (INT, n = 4); ovariectomized (3 to 5 d after parturition), nonsuckled (OVX, n = 4); and ovariectomized (3 to 5 d after parturition) and suckled by three calves (OVX-S, n = 5). Blood samples were collected at three periods (1 to 7 d before parturition and 3 to 5 d and 31 to 37 d after parturition) to determine plasma LH concentration. At 31 to 37 d after parturition, all cows were slaughtered and each ME was collected and mid-sagitally sectioned. The left half of each ME was used to determine content and concentration of LHRH. Concentrations of LH and LHRH were determined by RIA. Plasma LH concentration was similar among the three groups at 1 to 7 d before parturition and 3 to 5 d after parturition; however, at 31 to 37 d after parturition, OVX cows had a greater (P less than .05) concentration of LH (2.25 +/- .64 ng/ml) than either INT (.47 +/- .10 ng/ml) or OVX-S (.92 +/- .14 ng/ml) cows. Content of LHRH in the ME of INT (80.12 +/- 15.0 ng) and OVX-S 109.8 +/- 16.4 ng) cows was similar but was greater (P less than .05) than that in OVX cows (48.95 +/- 5.9 ng).(ABSTRACT TRUNCATED AT 250 WORDS)     

Gonadotropin releasing hormone-induced secretion of luteinizing hormone during the milk-ejection reflex in the postpartum beef cow

A study was conducted to determine the effect of the milk-ejection reflex on exogenous gonadotropin releasing hormone (GnRH)-induced release of luteinizing hormone (LH) after short-term calf removal. Twenty-four postpartum multiparous beef cows were assigned randomly to groups arranged in a 2(3) factorial arrangement. Factors consisted of two levels of suckling [suckled (S) or nonsuckled (NS)], treatment with GnRH [saline (C) or 200 micrograms GnRH] and days postpartum (d 1 and 14). Dams were isolated from their calves for 4 h on d 1 and 14 postpartum. At the end of 4 h dams were reunited with their calves in S + C and S + GnRH groups, while dams of calves in NS + C and NS + GnRH groups remained separated an additional 2 h. Cows were injected iv with saline or GnRH following the 4-h isolation period, 5 min after calves had begun suckling or nuzzling the udder. Sera from jugular blood samples collected 15 min prior to the end of the 4-h isolation period, immediately prior to injection (0 h) and at 15 min intervals thereafter for 120 min were analyzed for LH. Serum concentrations of LH in control cows did not differ due to suckling or stage of the postpartum period and averaged 2.3 +/- .1 ng/ml. Pituitary response to GnRH was determined by computing the rate of LH release. Rate of LH release (ng LH.ml-1.min-1) in response to GnRH on d 14 was greater (P less than .001) than on d 1 in both suckled and nonsuckled groups (S + GnRH, 37.1 +/- 3.9 vs 18.3 +/- 5.0; NS + GnRH, 34.7 +/- 5.9 vs 14.5 +/- 1.1). However, GnRH-induced release of LH did not differ between suckled and nonsuckled cows on either d 1 or 14 postpartum. These data indicate that response of the bovine pituitary to GnRH during the postpartum period is not influenced by the act of suckling but is enhanced with time after parturition.     

Endogenous opioid suppression of release of luteinizing hormone during suckling in postpartum anestrous beef cows

Beef cows were used to determine if suckling influences release of LH via endogenous opioids at 28 +/- 4 d after parturition. Cows of similar weight and body condition (6.8 +/- .1, 1 = emaciated, 9 = obese) were assigned randomly to five groups (n = 6 to 7): 1) control-suckled/saline (suckled 15 min every 6 hr for 48 hr); 2) control-suckled/naloxone; 3) calf-removal/saline (calf removal for 52 hr); 4) calf-removal/naloxone; and 5) control-suckled/GnRH (Gonadotropin-Releasing Hormone). At 0 hr, saline was administered to all cows. This treatment was continued at 6 hr intervals for 24 hr. Either naloxone (0.5 mg/kg), GnRH (40 ng/kg) or saline was administered to cows in their respective groups every 6 hr during the ensuing 24-hr period in calf-removal groups, or immediately preceding each suckling episode in the control-suckled groups. Blood samples for analysis of luteinizing hormone (LH) were collected at 15-min intervals for 1 hr prior to and 3 hr after treatment at 0, 24, 36 and 48 hr. Cows were observed for estrus twice daily. All cows in the control-suckled/GnRH group released LH (P less than .05) in response to exogenous GnRH, indicating the presence of releasable quantities of the gonadotropin. Mean concentrations of LH were not effected (P greater than .05) by the control-suckled regime. However, calf-removal alone, or in combination with naloxone, increased (P less than .05) mean concentrations of LH by 48 hr.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cortisol and luteinizing hormone after adrenocorticotropic hormone administration to postpartum beef cows

Cortisol and luteinizing hormone (LH) were measured in serum after the administration of adrenocorticotropic hormone (ACTH) to suckled (S) and nonsuckled (NS) beef cows. Blood was sampled on 2 consecutive days every 2 weeks for four bleeding periods starting 14 days after calving. Cows were injected with 200 IU ACTH or saline in a 2-day switchback design. Serum was collected before ACTH or saline injection and at 30-min intervals thereafter for 8 hours. Average cortisol concentrations in serum were similar in S and NS cows (6.4 +/- .6 and 6.1 +/- .8 ng/ml, respectively) after saline. Average cortisol concentrations in serum collected during an 8-hr period after ACTH on days 14, 28, 42 and 56 postpartum were 24.7 +/- 2.4, 31.8 +/- 3.5, 36.4 +/- 4.2 and 40.7 +/- .5 ng/ml, respectively, for S cows, and 31.1 +/- 2.9, 44.7 +/- 5.2, 45.0 +/- 5.7 and 46.0 +/- 5.4 ng/ml, respectively, for NS cows. Cortisol response to ACTH, measured as area under the response curve, was greater (P less than .05) in NS than in S cows. Amount of cortisol released by 200 IU ACTH was maximal by days 28 to 29 postpartum in NS cows, but the response increased gradually between days 14 to 15 and days 56 to 57 in S cows. overall, LH in serum averaged .55 +/- .08 ng/ml for S cows and .92 +/- .06 ng/ml for NS cows after saline, and .49 +/- .07 ng/ml for S cows and .94 +/- .06 ng/ml for NS cows after ACth. Although mean and peak serum LH concentrations did not differ between cows given ACTH and those given saline, the number of LH peaks and the number of cows having LH after saline. Mean serum LH concentrations were lower (P less than. 05) in S than in NS cows at 28 days postpartum. The number of LH peaks was lower (P less than .05) and the magnitude of the largest LH peak tended to be lower (P less than .06) in S cows at all sampling periods.     

Influence of calf removal on the serum luteinizing hormone response to naloxone in the postpartum beef cow

Twelve anestrous, postpartum beef cows were used to determine the effect of calf removal on the effect of naloxone on serum luteinizing hormone (LH) concentrations. On d 1, six cows were injected iv with saline and six with 200 mg naloxone dissolved in saline. Blood samples were taken at 15-min intervals for 2 h before and 2 h after naloxone or saline administration. At the beginning of blood sampling, calves were removed from three cows in each treatment. At 48 h after calf removal (d 3), all cows were injected iv with 200 mg naloxone and blood samples were collected as on d 1. On d 1, naloxone treatment increased (P less than .01) serum LH concentrations from 1.2 +/- .3 ng/ml at time 0 to 4.3 +/- .6 ng/ml and 4.7 +/- .8 ng/ml at 15 and 30 min, respectively. Injection of saline had no effect on serum LH concentrations. Forty-eight-hour calf removal increased (P less than .01) serum LH concentrations in five of six cows (1.7 +/- .8 vs 4.4 +/- 1.2 ng/ml). Naloxone treatment failed to increase serum LH concentrations in these cows. Injection of naloxone increased (P less than .01) serum LH concentrations in the one cow that did not exhibit an LH increase after calf removal and in six cows whose calves were not removed (1.4 +/- .2 vs 4.4 +/- .5 ng/ml). The present study provides additional evidence that endogenous opioids regulate LH in the postpartum beef cow. We hypothesize that suckling stimulates an opioid inhibition of LH secretion and removal of the suckling stimulus removes the opioid inhibitory tone.     

Effects of estradiol-17 beta, naloxone and gonadotropin releasing hormone on postpartum secretion of luteinizing hormone in fall-lambing ewes

The interaction among exogenous estradiol-17 beta, naloxone and gonadotropin releasing hormone (GnRH) in the control of luteinizing hormone (LH) secretion was studied in intact postpartum ewes nursing their offspring. One-half of 30 fall-lambing ewes were implanted subcutaneously with an estradiol-17 beta containing Silastic capsule between postpartum d 1 and 12 which doubled their serum concentrations of estradiol (16.0 +/- .1 vs 8.4 +/- .1 pg/ml). Blood samples were collected from implanted and non-implanted ewes at 15-min intervals for 5 h on d 3, 8, 13, 20 and 28 postpartum. Pre-injection samples were collected for 1 h, and ewes were injected with saline, naloxone (NAL;1 mg/kg) or GnRH (100 micrograms/ewe). When averaged across all days and implant groups, serum LH in the three post-NAL samples was higher (P less than .05) than in the three pre-NAL samples (3.6 +/- 1.2 vs .6 +/- .2 ng/ml). Post-GnRH concentrations of serum LH were lower (P less than .05) in estradiol-implanted ewes than in non-implanted ewes on d 8 and 13, but there were no differences in any LH characteristics on d 20 and 28 after implant removal on d 12. In non-implanted ewes, serum LH responses to GnRH increased (P less than .05) eightfold from d 3 (3.8 +/- 1.4 ng/ml) to d 8 (31.6 +/- 1.4 ng/ml), remained elevated through d 20, but declined by d 28 (10.8 +/- 1.4 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

Endogenous opioid modulation of luteinizing hormone and prolactin secretion in postpartum ewes and cows

A possible role for endogenous opioid peptides (EOP) in the control of luteinizing hormone (LH) and prolactin (PRL) secretion was studied by injecting the opioid antagonist, naloxone (NAL), into postpartum ewes and cows. Twelve ewes that lambed during the fall breeding season and nursed their lambs were injected iv with NAL (1.0 mg/kg) on d 10, 14, 18, 22 and 26 postpartum. Blood samples were collected at 15-min intervals from 2 h before to 2 h after NAL, and serum concentrations of LH and PRL were quantified. Following treatment on d 10, suckling lambs were removed from 6 of the 12 ewes, creating non-suckled (NS) and suckled (S) treatment groups for subsequent study on d 14 through 26. On d 10, NAL treatment increased LH (P less than .01) but concentrations of PRL were not affected. When averaged across d 14 to 26, post-NAL concentrations of LH were greater (P less than .001) than pre-NAL concentrations (6.5 +/- .7 vs 1.9 +/- .4 ng/ml). In contrast, concentrations of PRL in the post-NAL period were lower (P less than .001) than pre-NAL concentrations (129 +/- 15 vs 89 +/- 10 ng/ml). Compared with S ewes over d 14 to 26, those in the NS group had similar pre-NAL concentrations of LH, tendencies for higher (P less than .10) post-NAL concentrations of LH, lower (P less than .001) mean serum concentrations of PRL (pre- and post-NAL) and similar pre-NAL vs post-NAL differences in serum PRL. Six suckled beef cows on d 24 to 35 were injected iv with either saline or NAL (.5 mg/kg) in a replicated crossover design. Injections of NAL increased serum concentrations of LH (P less than .05), when averaged over all 12 injections in the six cows, but serum PRL was not changed. However, three of six cows did not respond to NAL with increases in serum LH. These non-responding cows were similar to the responding cows in their pre-injection concentrations of LH and PRL, but they tended (P = .10) to have higher serum concentrations of cortisol than responding cows.     

Hypoglycemia alters pulsatile luteinizing hormone secretion in the postpartum beef cow

This study tested the hypothesis that the increased glucose requirement of lactation had effects that were independent of the suckling-dependent inhibition of postpartum endocrine function in beef cows. Mature Hereford cows were either suckled ad libitum and infused with saline iv (n = 9) from d 2 through 4 (d 0 = jugular catherization on d 32 +/- 3 postpartum); were nonsuckled and infused with saline from d 2 through 4 (n = 10); or were nonsuckled and infused with phlorizin (3 g/d) from d 2 through 4 (n = 10). Nonsuckled cows infused with phlorizin had lower (P less than .05) plasma concentrations of glucose and amino acid nitrogen (AAN) on d 2 compared with pre-infusion levels (d 1), but their metabolic profile returned to levels similar to the suckled cows by d 3 and 4. Nonsuckled cows infused with saline had elevated glucose and insulin and lower AAN and free fatty acids (FFA) on d 3 and 4 compared with pre-weaning (d 1) levels (P less than .05). Nonsuckled cows infused with phlorizin did not show this weaning-induced elevation in glucose and insulin. The number of luteinizing hormone (LH) pulses was not affected by treatment. However, in contrast to the large LH pulses observed in the nonsuckled cows infused with saline, both the suckled cows and the nonsuckled cows treated with phlorizin had more small and fewer large amplitude pulses (P less than .01). Treatment did not affect serum concentrations of follicle stimulating hormone, gonadotropin release in response to gonadotropin releasing hormone (25 micrograms) or the number of cows ovulating by 55 d after calving. We conclude that the increased glucose clearance caused by phlorizin infusion or lactation results in depression of LH pulse amplitude in suckled postpartum beef cows.     

Effect of castration on plasma luteinizing hormone concentrations in prepubertal boars

Mean concentrations and the occurrence of pulsatile release of luteinizing hormone (LH) were determined in 14-wk-old crossbred boars (50.5 +/- 1.5 kg) after bilateral or unilateral castration at 10 wk of age. Blood was collected at 10-min intervals for 5 h. Then gonadotropin releasing hormone (GnRH; 40 micrograms) was given and sampling was continued at 5-min intervals for 1 h. Compared with intact boars, bilateral castration increased (P less than .001) mean LH (982 +/- 56 vs 389 +/- 56 pg/ml), pulsatile releases of LH (7.0 +/- .6 vs 2.0 +/- .6 pulses/5 h) and LH pulse amplitude (617 +/- 29 vs 360 +/- 58 pg/ml). Unilaterally castrated boars did not differ from intact boars in any of the above measures of LH secretion. Testis weight increased more between 10 and 14 wk of age in the unilateral castrates than in the intact boars (432 +/- 42 vs 245 +/- 34%; P less than .05). Thus, compensatory hypertrophy occurred within 4 wk of castration. Plasma testosterone was lower for bilateral castrates than for intact animals (.1 +/- .8 vs 3.6 +/- .9 ng/ml; P less than .05) while unilateral castrates (3.8 +/- 1.0 ng/ml) and intact boars did not differ. Plasma estradiol concentrations in bilateral and unilateral castrates were not different from levels found in intact boars (1.8 +/- 1.8, 8.8 +/- 2.1 and 6.0 +/- 1.8 pg/ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of intermittent injections of LHRH on secretory patterns of LH and FSH and ovarian follicular growth during postpartum anovulation in suckled beef cows

Changes in numbers of ovarian follicles and coincident secretion of pituitary gonadotropins were characterized in suckled, anovulatory beef cows injected iv with 500 ng of luteinizing hormone-releasing hormone (LHRH) every 2 h for 48 or 96 h, starting 21.4 +/- .4 d after parturition. Two hours after the last injection, all cows were ovariectomized. Compared with saline-injected controls, LHRH had no effect on baseline or overall concentrations of luteinizing hormone (LH) in serum (P greater than .10), but increased (P less than .05) frequency and decreased (P less than .05) amplitude of LH pulses. Luteinizing hormone-releasing hormone increased (P less than .05) baseline concentration of follicle stimulating hormone (FSH) in serum and frequency of FSH pulses, but decreased (P less than .05) pulse amplitude. Overall concentrations of FSH increased 20% (P less than .10). Exogenous LHRH did not affect diameter of the two largest follicles or numbers of follicles 1.0 to 3.9 mm, 4.0 to 7.9 mm or greater than or equal to 8.0 mm in diameter. These data suggest that increasing the frequency of episodic LH and FSH pulses in postpartum cattle by intermittent administration of LHRH did not increase mean circulating levels of LH, or alter size and numbers of ovarian follicles within the 96-h period of injections. Thus, induction of ovulation in anovulatory cows treated with low-dose injections of LHRH cannot be explained on the basis of an increase in mean concentrations of LH or numbers of antral follicles within 96 h after initiation of injections.     

Opioid control of growth hormone in the suckled sow is primarily mediated through growth hormone releasing factor

Endogenous opioid peptides mediate the effect of suckling on LH and PRL in the domestic pig. However, the role of opioids in modulating GH during lactation in swine is not known. Primiparous sows that had been immunized against GRF(1-29) conjugated to human serum albumin (GRF-HSA, n = 5) or HSA (n = 4) were used to determine changes in GH after naloxone. Treatments were imposed in all sows on day 21 of lactation when antibody titers were 9100 +/- 1629. All sows received (i.v.) naloxone (0.25 mg/kg) or saline (0.0125 ml/kg) at 15 min intervals for 165 min. Active immunization against GRF-HSA during lactation decreased (P less than 0.05) mean concentration (4.8 +/- 0.2 vs 2.6 +/- 0.1 ng/ml) and frequency (1.5 +/- 0.3 vs 0.4 +/- 0.2 peaks/4 hr). Concentrations of LH and PRL were similar in GRF-HSA and HSA immunized sows. Naloxone suppressed (P less than 0.05) GH in all sows. In HSA sows, naloxone abolished episodic release of GH and decreased average, but not basal, concentrations of GH. In sows immunized against GRF-HSA, naloxone decreased (P less than 0.05) average and basal GH but failed to decrease frequency of GH release. Naloxone failed to alter frequency of LH release. Concentrations of PRL decreased (P less than 0.05) after naloxone in all sows. In conclusion, immunization against GRF-HSA blocked most of the effect of lactation on GH. Blocking opioid receptors with naloxone decreased GH and PRL in all sows. In contrast to previous findings naloxone had no effect on LH. Opioids alter concentrations of GH through a GRF dependent and GRF independent pathway.     

Serum concentrations of IGF-I in postpartum beef cows

Four experiments assessed changes in serum IGF-I under various physiologic conditions in postpartum cows. In Exp. 1, anestrous suckled cows (n = 25) were infused for 6 d with either saline or glucose at two different infusion rates. In Exp. 2, anestrous cows (n = 29) received either a saline (weaned and suckled controls) or 3 g/d phlorizin (weaned phlorizin) infusion for 3 d. Calves from the weaned groups were removed from 15 h before and throughout infusions. In Exp. 3, cycling suckled cows (n = 20) received prostaglandin F2 alpha (PGF2 alpha) when the 5-d saline or phlorizin infusion began. In Exp. 4, suckled cows (n = 20) had ad libitum access to feed or received 50% of control feed consumption from 30 to 40 d postpartum. Increasing glucose availability (Exp. 1) increased (P less than .05) serum IGF-I by 30 to 35%. IGF-I remained stable after weaning (Exp. 2) in phlorizin-infused cows (128.8 +/- 12.7 ng/ml), but increased (P less than .05) by 3 d after calf removal in weaned control cows (152.2 +/- 7.5 ng/ml). IGF-I also remained stable in phlorizin-infused cows following PGF2 alpha injection (Exp. 3), but increased in control cows by 2 d after PGF2 alpha (156.8 +/- 18.3 on d 2 vs. 133.7 +/- 9.8 ng/ml pre-injection; P less than .05) and remained elevated (P less than .05) during the periovulatory period. In cows receiving restricted feed intake (Exp. 4), IGF-I decreased by approximately 50% within 4 d of feed restriction (71.3 +/- 9.4 vs 137.4 +/- 16.6 ng/ml; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of naloxone on serum luteinizing hormone, cortisol and prolactin concentrations in anestrous beef cows

Two experiments were conducted with the opioid antagonist naloxone to determine the effect of opioid receptor blockade on hormone secretion in postpartum beef cows. In Exp. 1, nine anestrous postpartum beef cows were used to measure the effect of naloxone on serum luteinizing hormone (LH), cortisol and prolactin concentrations. Cows received either saline (n = 4) or 200 mg naloxone in saline (n = 5) iv. Blood samples were collected at 15-min intervals for 2 h before and after naloxone administration. Serum LH concentrations increased (P less than .01) in naloxone-treated cows from 1.8 +/- .04 ng/ml before treatment to 3.9 +/- .7 ng/ml and 4.2 +/- .5 ng/ml at 15 and 30 min, respectively, after naloxone administration. In contrast, LH remained unchanged in saline-treated cows (1.6 +/- .3 ng/ml). Serum cortisol and prolactin concentrations were not different between groups. In Exp. 2, 12 anestrous postpartum beef cows were used to examine the influence of days postpartum on the serum LH response to naloxone. Four cows each at 14 +/- 1.2, 28 +/- .3 and 42 +/- 1.5 d postpartum received 200 mg of naloxone in saline iv. Blood samples were taken as in the previous experiment. A second dose of naloxone was administered 2 h after the first, and blood samples were collected for a further 2 h. Serum LH concentrations increased (P less than .01) only in cows at 42 d postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postpartum interval in beef cows shortened by enclomiphene

This study was designed to determine whether an anti-estrogen can block the negative effect of estrogens on luteinizing hormone (LH) release and therefore decrease the postpartum interval in suckled beef cows. In Exp. I, eight suckled postpartum beef cows were randomly assigned to treatment and control groups. Treatment cows received 1 g/d clomiphene citrate (im) from d 21 to 28 postpartum, while control cows were injected with saline. On d 28 postpartum, there was no difference (P greater than .05) in mean total and basal LH concentrations or LH pulse frequency between treatment and control cows. All control cows exhibited estrus on d 52 +/- 3; treatment cows exhibited estrus on d 134 +/- 12 (P less than .05). In Exp. II, 17 suckled cows were randomly assigned to three treatment groups: 1) control group (n = 6) receiving one empty implant, 2) 10-cm enclomiphene implant group (n = 5) and 3) 30-cm enclomiphene implant group (n = 6). The silastic implants were placed sc on d 20 and removed on d 29 postpartum. Mean total LH concentrations during d 24 to 29 postpartum in the 30-cm enclomiphene implant group were higher than the 10-cm implant (P less than .05) and control group (P less than .05). The postpartum period in the 30-cm enclomiphene group (45 +/- 6 d) was shorter than the 10-cm implant (94 +/- 24 d) and control (96 +/- 20 d) groups (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of morphine on serum gonadotropin concentrations in postpartum beef cows

Morphine (M), an opioid agonist, was administered to postpartum (PP) Angus cows to investigate opioid modulation of gonadotropin secretion. In Exp. 1, eight PP cows (36.9 +/- 2.3 d) received either M (1 mg/kg; n = 4) or saline solution (S) (n = 4) via i.v. injection 36 h after calf removal. Morphine decreased (P less than .01) the number of serum LH pulses (3.0 +/- 1.1 pre- vs .3 +/- .3 post-pulses/h) and, compared with pretreatment values (3.3 mg/ml), decreased (P less than .05) mean LH at 105 min (2.1 ng/ml) through 270 min 1.9 ng/ml +/- .4). Serum prolactin (PRL) increased (P less than .01) following M from 16.4 ng/ml to a peak of 59.3 ng/ml (+/- 3.9). Serum FSH concentrations were unaffected. In Exp. 2, M (.31 mg/kg i.v. injection followed by .15 mg/(kg.h) infusion; n = 6) or S (n = 6) treatments were given for 7 h beginning 36 h after calf removal. Serum LH was similar between groups during the pretreatment and the first 6 h of infusion, but M decreased (P less than .001) the number of serum LH pulses (.44 +/- .09 vs .06 +/- .04 pulses/h). Morphine increased (P less than .05) serum PRL. It is concluded that M differentially modulated gonadotropin secretion in the cow such that PRL increased, LH decreased and FSH was unchanged.     

Characterization of ovine follicles destined to form subfunctional corpora lutea

A study was done to test whether ovulatory follicles destined to form subfunctional corpora lutea differed from normal ovulatory follicles in steroidogenic function. Twenty-five ewes were treated with prostaglandin F2 alpha on d 11 of the estrous cycle, then unilaterally ovariectomized before (n = 13) or after (n = 12) the surge of luteinizing hormone (LH) at the induced estrus to collect "control" follicles, which would have produced normal corpora lutea. In 15 ewes, the second ovary was removed 63 to 84 h later to collect "treated" follicles before (n = 7) or after (n = 8) the second expected surge of LH. Five ewes (control) were allowed to ovulate from the remaining ovary at first estrus and another five (treated) at the second estrus (3 to 4 d later). Treated ewes had lower serum progesterone than control ewes during the ensuing cycle (P less than .05). Treated follicles contained less estradiol in the theca (4.4 +/- .6 vs 10.0 +/- 2.5 ng; P less than .05), less androstenedione (.1 +/- .1 vs 1.0 +/- .2 ng) and estradiol (.5 +/- .1 vs 2.9 +/- 2.2 ng) in the granulosa (P less than .05) and less progesterone in the follicular fluid (.8 +/- .4 vs 3.3 +/- .8 ng; P less than .05) than control follicles, when removed before the surge of LH. Follicles removed after the surge of LH did not differ. In conclusion, ovulatory follicles with low steroidogenic function became corpora lutea that secreted lower-than-normal quantities of progesterone.     

Elicitation of release of luteinizing hormone by N-methyl-d,l-aspartic acid during three paradigms of suppressed secretion of luteinizing hormone in the female pig.

Two experiments were conducted to determine the minimal effective dose during lactation and site of action of N-methyl-d,l-aspartic acid (NMA) for elicitation of release of luteinizing hormone (LH) in female pigs. In the first experiment, three doses of NMA were given to lactating primiparous sows in which endogenous LH was suppressed by suckling of litters. In the second experiment, ovariectomized gilts were pretreated with estradiol benzoate or porcine antisera against GnRH to suppress LH and then given NMA to determine if it elicited secretion of LH directly at the anterior pituitary or through release of GnRH. In experiment 1, 3 lactating sows (17 +/- 1.5 d postpartum) were each given three doses of NMA (1.5, 3.0 and 5.0 mg/kg body weight [BW]; IV) on 3 consecutive days in a Latin Square design. Blood samples were collected every 10 min from -1 to 1 hr from injection of NMA. NMA at 1.5 and 3.0 mg/kg did not affect (p greater than .5) secretion of LH; however, 5 mg NMA/kg elicited a 114% increase (p less than .001) in circulating levels of LH during 1 hr after treatment. In experiment 2, 8 ovariectomized gilts were given either estradiol benzoate (EB; 10 micrograms/kg BW; IM n = 4) to suppress release of GnRH or porcine antiserum against GnRH (GnRH-Ab; titer 1:8,000; 1 ml/kg BW; IV; n = 4) to neutralize endogenous GnRH. Gilts infused with GnRH-Ab were given a second dose of antiserum 24 hr after the first. Gilts were then given NMA (10 mg/kg BW; IV) 33 hr after EB or initial GnRH-Ab. Blood samples were drawn every 6 hr from -12 to 24 hr from EB or GnRH-Ab treatments, and every 10 min from -2 to 2 hr from NMA. Serum LH declined (p less than .001) after EB (from 1.87 +/- .2 ng/ml at 12 hr before EB to 0.46 +/- .02 ng/ml during 24 hr after EB) and GnRH-Ab (from 1.97 +/- .1 to 0.59 +/- .02 ng/ml). In gilts treated with EB, the area under the curve (AUC) for the LH response (ng.ml-1.min) 1 hr after NMA (38.7 +/- 3) was significantly greater (p less than .01) than the 1 hr prior to NMA (21.3 +/- 1.5). Treatment with NMA had no effect (p greater than .5) on secretion of LH in gilts infused with GnRH-Ab.(ABSTRACT TRUNCATED AT 400 WORDS)     

Peri-oestrus hormone profiles and follicle growth in lactating sows with oestrus induced by intermittent suckling.

This study describes follicle dynamics, endocrine profiles in multiparous sows with lactational oestrus compared with conventionally weaned sows (C). Lactational oestrus was induced by Intermittent Suckling (IS) with separation of sows and piglets for either 12 consecutive hours per day (IS12, n = 14) or twice per day for 6 h per occasion (IS6, n = 13) from day 14 of lactation onwards. Control sows (n = 23) were weaned at day 21 of lactation. Pre-ovulatory follicles (> or =6 mm) were observed in 100% of IS12, 92% of IS6 and 26% of C sows before day 21 of lactation and in the remaining 74% C sows within 7 days after weaning. All sows with pre-ovulatory follicles showed oestrus, but not all sows showed ovulation. Four IS6 sows and one IS12 sow developed cystic follicles of which two IS6 sows partially ovulated. Follicle growth, ovulation rate and time of ovulation were similar. E(2) levels tended to be higher in IS sows (p = 0.06), the pre-ovulatory LH surge tended to be lower in IS12 (5.1 +/- 1.7 ng/ml) than in C sows (8.4 +/- 5.0 ng/ml; p = 0.08) and P(4) levels were lower in IS12 and IS6 than in C sows (at 75 h after ovulation: 8.8 +/- 2.4 ng/ml vs 7.0 +/- 1.4 ng/ml vs 17.1 +/- 4.4 ng/ml; p < 0.01). In conclusion, sows with lactational oestrus induced by IS are similar to weaned sows in the timing of oestrus, early follicle development and ovulation rates, but the pre-ovulatory LH surge and post-ovulatory P(4) increase are lower.     

Endocrine profiles associated with life span of induced corpora lutea in postpartum beef cows

Two experiments were designed to examine whether hormonal profiles were related to luteal life span in pluriparous postpartum anestrous beef cows. Cows (Exp. 1, n = 34; Exp. 2, n = 23) received norgestomet (N) for 9 d or served as controls (C). Each cow received 1,000 IU human chorionic gonadotropin (hCG) 48 h after removal of N (d 0). Blood samples collected every 15 min for 8 h on d -5, 3 and 5 (Exp. 1) or on d -10 and -1 (Exp. 2) were assayed for luteinizing hormone (LH) and follicle stimulating hormone (FSH). Cortisol was determined in hourly samples collected on d -5 and in samples collected every 2 min during suckling on the same day (Exp. 1). Concentrations of 15-keto-13,14-dihydro-PGF2 alpha (PGFM) were determined in samples collected at 15-min intervals for 2 h on d -5, 3, 5 and 10 (Exp. 1). Estradiol-17 beta was measured in samples collected on d -5 (Exp. 1) or on d -10 and -1 (Exp. 2). Life span of induced corpora lutea was longer (P less than .05) in N than C cows. Percentages of N cows in which corpora lutea, formed in response to hCG, exhibited a normal life span were 83% on farm 1 and 25% on farm 2 (Exp. 1), and 90% (Exp. 2), compared with 0% in C cows. Concentrations of FSH were not affected by N but were lower (P less than .05) on d -5 in cows on farm 2 (.6 +/- .1 ng/ml) than in cows on farm 1 (.8 +/- .1 ng/ml). On d -5, a treatment X farm interaction (P less than .05) for mean LH was observed and frequency of pulses of LH was higher (P less than .01) in N than C cows (2.7 +/- .4 vs. .8 +/- .8 pulses/8 h). Neither cortisol nor PGFM was affected by N. Estradiol was increased in d -1 (6.1 +/- .5 vs 2.6 +/- .8 pg/ml; P less than .01) by N. It is suggested that pre-treatment with N enhanced life span of induced corpora lutea, in part, by influencing secretion of LH and development of follicles, but a threshold concentration of FSH was required for N to exert this effect.     

Ovarian compensatory hypertrophy following unilateral ovariectomy in the suckled sow

The effects of unilateral ovariectomy on ovarian compensatory hypertrophy (OCH), endocrine profiles and the pituitary response to gonadotropin releasing hormone (GnRH) were studied in 46 multiparous suckled sows. On d 20 of lactation (d 0 of experiment), sows were subjected to sham ovariectomy (Sham; n = 23) or unilateral ovariectomy (ULO; n = 23). On d 1 (n = 16), 2 (n = 15) or 8 (n = 15) following initial surgery the remaining ovaries in both Sham and ULO sows were removed. Immediately following removal of the remaining ovaries, GnRH (10 micrograms) was administered to each sow. Peripheral blood samples were taken every 10 min for 80 min beginning 20 min prior to GnRH administration. No difference in ovarian weight was observed between ULO and Sham sows until d 8, when ovarian weight was greater (P less than .05) for the remaining ovary from ULO sows (3.96 +/- .21 vs 5.91 +/- .39 g). Ovarian follicular fluid weights from ULO sows were greater (P less than .05) than Sham sows on both d 2 and 8. On d 1, plasma concentrations of follicle stimulating hormone (FSH) were greater (P less than .05) in ULO sows than in Sham sows (2.9 +/- .2 vs 2.1 +/- .1 ng/ml). Plasma FSH concentrations, however, did not differ between Sham and ULO sows on either d 2 or 8. Ovarian venous concentrations of estradiol-17 beta were also greater (P less than .05) in ULO sows compared with Sham sows on d 2 but not d 8.