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1.
An experiment was conducted to determine if exogenous luteinizing hormone-releasing hormone (LHRH) administered iv intermittently as pulses (P) or by continuous sc infusion (I) using osmotic minipumps could sustain pulsatile LH release and induce estrous cyclicity in prepubertal heifers. Prepubertal heifers were assigned randomly to: 1) receive pulses of LHRH (n = 6; 2.5 micrograms LHRH/2 h for 72 h), 2) be infused with LHRH (n = 11; 1.25 micrograms LHRH/h for 72 h), or 3) serve as controls (n = 16). Blood was collected at 20-min intervals for 8 h (0900 to 1700 h) from six heifers in each group on d 1, 2, 3 (during treatment), and on d 4 (during 8 h after terminating LHRH treatments). Heifers given LHRH had higher (P less than .01) LH concentrations than controls. Preovulatory-like LH surges occurred in three I, two P and no control heifers during treatment. Pulse frequencies of LH (no. LH pulses/8 h) were greater (P less than .001) for P heifers than for I and control heifers due to pulsatile LHRH treatment. Serum estradiol was higher (P less than .01) during treatment for LHRH-treated heifers than for controls. Serum follicle-stimulating hormone, cortisol, and progesterone were unchanged during treatment. High levels of cortisol on d 1 declined (P less than .001) to baseline by d 2. Characteristic progesterone rises or short luteal phases occurred within 10 d of treatment initiation in more (P less than .05) LHRH-treated heifers (I = 45%, P = 33%) than controls (6%), although days to first observed estrus and first ovulation were unaffected by treatments. Although both continuous and pulsatile administration of LHRH successfully induced LH and estradiol release as well as preovulatory-like LH surges in some heifers, earlier initiation of estrous cycles was not achieved. Estrous cycles appeared to be delayed by exposure to continuous LHRH infusions during the peripubertal period.  相似文献   

2.
Changes in metabolism of serotonin (5-HT) might mediate the reduced tonic luteinizing hormone (LH) and increased pituitary responsiveness to luteinizing hormone releasing hormone (LHRH) caused by estradiol-17β (estradiol). Two experiments were conducted to determine effects of estradiol, para-chlorophenylalanine (PCPA), an inhibitor of synthesis of 5-HT, and quipazine, an agonist of 5-HT, on tonic and LHRH-induced secretion of LH in ovariectomized ewes during the summer. Tonic levels of LH were reduced, the interval from LHRH to peak of the induced surge was longer and the magnitude of release of LH was greater in ovariectomized ewes treated with estradiol than in controls. Neither PCPA nor quipazine affected tonic secretion of LH. In ovariectomized ewes not receiving estradiol, PCPA and quipazine increased the magnitude of the LHRH-induced release of LH. However, PCPA reduced pituitary sensitivity to LHRH when administered concomitantly with estradiol; treatment with quipazine attenuated this effect of PCPA. The interval to the peak of the induced surge of LH was not affected by PCPA or quipazine in estradiol-treated or control ovariectomized ewes. Based on these results it appears that 5-HT mediates or is required for estradiol to increase pituitary responsiveness to LHRH.  相似文献   

3.
The luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone response of bull calves implanted with estradiol-17 beta to continuous and pulsatile infusion of luteinizing hormone releasing hormone (LHRH) has been examined. Estradiol-17 beta reduced serum LH and FSH concentrations and suppressed testosterone secretion and testicular growth when compared with sham-implanted bulls. Pulsatile iv infusion of LHRH [500 ng every 2 h (6 micrograms/d)] for a 4-wk period to estradiol-17 beta-implanted bulls resulted in elevated mean serum LH and testosterone concentrations that were characterized by discrete secretory episodes. Mean serum FSH was also increased by LHRH pulse infusion, but LHRH-coupled secretory episodes were not apparent. Continuous infusion of LHRH (6 micrograms/d) did not increase the low serum gonadotropin levels observed in estradiol-17 beta-implanted calves. Testicular growth was normal in LHRH pulse-infused calves, but was markedly curtailed in continuously infused calves. These results suggest that estradiol-17 beta inhibits testicular development by blocking gonadotropin release at the level of the hypothalamus because pulsatile administration of LHRH can override the inhibitory effect by increasing LH and FSH secretion.  相似文献   

4.
The objectives of this study were 1) to evaluate the ability of trenbolone acetate (TBA) administered in tandem with LHRH immunization to suppress reproductive function in bulls and 2) to examine the effects of LHRH and androgen (TBA) signaling on pituitary gland function. Forty-four Angus × Hereford crossbred calves (BW=225 ± 2 kg; age=187 ± 6 d) received castration, LHRH immunization, or TBA administration in a 2 × 2 × 2 factorial design. Treatment groups receiving LHRH immunization contained 6 animals, whereas other treatment groups contained 5 animals. Animals immunized against LHRH received a primary injection and 2 booster injections of ovalbumin-LHRH-7 fusion protein on d 0, 42, and 196, respectively. Animals treated with TBA were implanted on d 224. Serum LHRH antibodies increased (P<0.05) after each booster for immunized animals, but were negligible in nonimmunized animals throughout the experiment. Serum testosterone concentration (P<0.001) and scrotal circumference (P<0.05) were depressed in LHRH-immunized bulls compared with nonimmunized bulls by d 84 and 168 of the experiment, respectively. Treatment with TBA tended (P=0.08) to decrease serum testosterone concentrations of nonimmunized bulls. Weights of testes at slaughter were decreased (P<0.001) for LHRH-immunized (232 ± 41 g) compared with nonimmunized (752 ± 45 g) bulls, but did not differ (P=0.80) between TBA-implanted (500 ± 49 g) and nonimplanted bulls (484 ± 36 g). Both LHRH immunization and castration decreased pituitary gland stores of LH and FSH (P<0. 001). There was no effect (P>0.10) of TBA on pituitary gland FSH content and only a tendency (P=0.09) to increase pituitary gland LH content. Immunization against LHRH decreased expression of LH β-subunit and common α-subunit genes (P<0.001). Castration increased expression of LH β-subunit and common α-subunit genes (P=0.02). Treatment with TBA further suppressed (P=0.04) α-subunit mRNA expression in LHRH-immunized steers. In summary, LHRH immunization decreased synthesis and storage of LH and decreased storage, but not synthesis of FSH in bulls. The increased synthesis of LH and FSH in nonimmunized, but not LHRH-immunized steers suggests that castration removes the negative feedback on gonadotropin synthesis but that LHRH is still needed for release of these hormones. Androgen replacement with TBA did not restore the negative feedback control of gonadotropin synthesis.  相似文献   

5.
Opioid modulation of LH and prolactin (PRL) concentrations in Angus steers was investigated. In Exp. 1, morphine sulfate (M) was administered at either 1, 2 or 3 mg/kg BW (n = 4) as an i.v. injection. Blood samples were obtained at 15-min intervals for 4 h pre- and post-treatment for serum hormone analyses. Mean serum LH concentration and number of LH secretory pulses decreased (P less than .1) for 2 h after M (4.1 to nadir of 2.4 ng/ml, and .33 vs. .21 pulses/h; pre- vs post-treatment). Luteinizing hormone pulse amplitude decreased (P less than .01; 7.3 vs 2.6 ng/ml; pre- vs post-treatment) during the 2 h following M. Prolactin concentrations increased 126.6%, 170.6% and 187.6% following 1, 2 and 3 mg M/kg BW, respectively (P less than .05, 1 vs 2; P less than .01, 1 vs 3). In Exp. 2, either saline solution (S, n = 6) or M (.31 mg/kg BW, i.v. injection followed by .15 mg/(kg.h) infusion; n = 6) was given for 7 h. Concentration of LH was unaffected. Response of LH to naloxone was determined in Exp. 3. Blood samples were obtained for 2 h pre- and post-administration of either naloxone (1 mg/kg BW, i.v. injection; n = 5) or S (n = 5). Response of LH at 15, 30 and 45 min posttreatment was greater (P less than .05) in naloxone- compared with S-treated steers. In summary, M had no significant effect on serum LH concentration or LH pulse frequency, but it decreased pulse amplitude and increased serum PRL concentrations. In contrast, naloxone increased LH secretion. These observations taken together indicate a physiological role for opioid modulation of LH and PRL secretion in the steer.  相似文献   

6.
Hourly pulses of gonadotropin-releasing hormone (GnRH) or bi-daily injections of estradiol (E2) can increase luteinizing hormone (LH) secretion in ovariectomized, anestrous pony mares. However, the site (pituitary versus hypothalamus) of positive feedback of estradiol on gonadotropin secretion has not been described in mares. Thus, one of our objectives involved investigating the feedback of estradiol on the pituitary. The second objective consisted of determining if hourly pulses of GnRH could re-establish physiological LH and FSH concentrations after pituitary stalk-section (PSS), and the third objective was to describe the declining time trends of LH and FSH secretion after PSS. During summer months, ovariectomized pony mares were divided into three groups: Group 1 (control, n = 2), Group 2 (pulsatile GnRH (25 μg/hr), n = 3), and Group 3 (estradiol (5 mg/12 hr), n = 3). All mares were stalk-sectioned and treatment begun immediately after stalk-section. Blood samples were collected every 30 min for 8 h on the day before surgery (DO) and 5 d post surgery (D5) to facilitate the comparison of gonadotropin levels before and after pituitary stalk-section. Additionally, jugular blood samples were collected every 12 hr beginning the evening of surgery, allowing for evaluation of the gonadotropin secretory time trends over the 10 d of treatment. On Day 10, animals were euthanized to confirm pituitary stalk-section and to submit tissue for messenger RNA analysis (parallel study). Plasma samples were assayed for LH and FSH by RIA. Mean LH secretion decreased from Day 0 to Day 5 in Groups 1 and 3, whereas LH secretion tended (P < 0.08) to decrease in Group 2 mares. On Day 5, LH was higher (P < 0.01) in Group 2 (17.26 ± 3.68 ng/ml; LSMEANS ± SEM), than either Group 1 (2.65 ± 4.64 ng/ml) or group 3 (4.28 ± 3.68 ng/ml). Group 1 did not differ from Group 3 on Day 5 (P < 0.40). Similarly, mean FSH levels decreased in all groups after surgery, yet Group 2 mares had significantly (P < 0.001) higher FSH concentrations (17.66 ± 1.53 ng/ml) than Group 1 or Group 3 (8.34 ± 1.84 and 7.69 ± 1. 63 ng/ml, respectively). Regression analysis of bi-daily LH and FSH levels indicated that the time trends were not parallel. These findings indicate: 1) Pituitary stalk-section lowered LH and FSH to undetectable levels within 5 d after surgery, 2) pulsatile administration of GnRH (25 μg/hr) maintained LH and FSH secretion, although concentrations tended to be lower than on Day 0, and 3) E2 did not stimulate LH or FSH secretion.  相似文献   

7.
Two experiments were conducted in ovariectomized, pituitary stalk-transected ewes to determine if dopamine (DA), norepinephrine (NE) or serotonin (5-HT) alter secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL). In experiment 1, ewes were infused (iv) with saline (control), DA (66 micrograms/kg/min), NE (6.6 micrograms/kg/min) or 5-HT (6.6 micrograms/kg/min). Treatments did not alter pulse frequency, but 5-HT increased (P less than .05) amplitude of pulses of LH and mean concentrations of LH, DA and NE were without effect on basal secretion of LH. DA but not NE or 5-HT decreased (P less than .05) the release of LH in response to gonadotropin hormone-releasing hormone (GnRH, 25 micrograms, im). Concentrations of FSH were not affected by treatments. Secretion of PRL was reduced (P less than .05) by treatment with DA and NE but not 5-HT. Each amine reduced (P less than .05) the release of PRL in response to thyrotropin-releasing hormone (TRH; 3 micrograms, im). In experiment 2, ewes were given DA at doses of 0, 0.66, 6.6 or 66.0 micrograms/kg/min, iv. No dose altered basal LH, but each dose reduced (P less than .05) basal and TRH-induced release of PRL. Key findings from these studies include direct pituitary action for: (1) 5-HT enhanced basal secretion of LH, (2) suppression of GnRH-induced secretion of LH by DA. (3) DA and NE inhibition of PRL secretion, and (4) DA, NE and 5-HT inhibition of release of PRL in response to TRH.  相似文献   

8.
Bovine infundibular (stalk median eminence) explants were incubated in vitro to test the hypothesis that calcium (Ca) is involved in the release of luteinizing hormone-releasing hormone (LHRH) from LHRH neuron terminals in cattle. Right and left infundibular halves from individual heifers and/or steers were randomly assigned to either control or treated (EGTA [a Ca chelator] or verapamil [an L-type Ca channel antagonist]) groups. Each half was incubated in 600 μl of KrebsRinger bicarbonate medium (KRB) in the presence or absence of a treatment agent for 180 min. At 30-min intervals, 500-μl samples were removed from each incubate and replaced with fresh media. Spontaneous (basal) and depolarization-induced (60 mM potassium) LHRH release was evaluated by radioimmunoassay of the LHRH content in the media incubated from 91 to 120 and 121 to 150 min of culture, respectively. The effect of treatment on depolarization-induced LHRH release was analyzed by comparing the differences between spontaneous and depolarization-induced LHRH release in control and treated groups. Spontaneous LHRH release was not different between control and 1.25 mM EGTA- or 100 μM verapamil-treated halves from steers. In contrast, steer infundibular halves incubated with EGTA (replacing Ca in KRB and chelating any Ca in the media) released less LHRH during depolarization than did control halves. In addition, verapamil-treated (to block Ca uptake by the terminal) infundibular halves from steers or heifers released less LHRH in response to depolarization than did control halves. In conclusion, these results: 1) support the hypothesis that Ca is involved in LHRH release from the bovine infundibulum, 2) suggest that the involvement of Ca may be independent of the reproductive state, and 3) demonstrate that bovine infundibular halves incubated in vitro are useful for studying selected mechanisms regulating bovine hypothalamic neurohormone release (exocytosis) from neuron terminals.  相似文献   

9.
To examine the effect of diet on luteinizing hormone (LH) secretion, basal and luteinizing hormone releasing hormone (LHRH)-induced LH release was compared in intact or castrated-estradiol-17 beta implanted Finn-Dorset lambs. Ten to 12 wk old ram (n = 20) and ewe lambs (n = 20) were maintained under a 8L:16D photoperiod and fed for high (HG, 163 to 168 g/d) or low (LG, 76 to 103 g/d) rates of gain. Eight to 10 wk later, baseline LH concentrations were determined in blood samples collected at 20 min intervals for 7 h. The following day, lambs were given an iv injection of 5 micrograms of estradiol-17 beta followed within 4 h by LHRH (.5 or 2.5 micrograms). Baseline concentrations of LH for HG ewes were threefold greater than for LG ewes (4.2 vs 1.4 ng/ml), respectively. Time to peak response was inversely related to dietary energy level (P less than .025). Basal LH levels were similar across diets in rams. Total LH release following LHRH was dose-dependent (P less than .005). Effects of gonadal feedback were tested in a second group (n = 24) of castrated lambs. Changes in LH secretion were not different between diets within 3 to 4 wk after castration. A subcutaneous silastic implant (22 mm) of estradiol-17 beta inhibited (P less than .01) LH concentrations across diets in both ewes and rams. No differences in estradiol feedback on LH secretion (at the dose of steroid tested) were detected between HG and LG lambs. Within 8 d, however, basal LH concentrations were 60% lower (P less than .01) in HG vs LG ewes. Furthermore, peak LHRH-induced LH release was greater (P less than .025) in LG vs HG lambs of both sexes. Estradiol inhibited basal LH secretion in ewes and rams but facilitated LH release in lambs with a reduced rate of gain.  相似文献   

10.
We tested the hypothesis that rapidly expressed inhibitory effects of estradiol (E) on luteinizing hormone (LH) release in the male are attributable, in part, to suppression of luteinizing hormone-releasing hormone (LHRH) release. Hypophyseal-portal cannulated, castrated male sheep were infused with E (15 ng/kg/hr) or vehicle. Portal and jugular blood samples were collected at 10-min intervals for 4 hr before, and for either 12 hr (E, n = 4; vehicle, n = 4) or 24 hr (E, n = 8; vehicle, n = 3) after the start of infusion. In animals sampled for 16 hr, temporal changes in both LHRH and LH were assessed. In animals sampled for 28 hr, only LH data were analyzed. Before either the 12-hr or 24-hr infusion, LHRH and/or LH mean concentrations, pulse amplitude and interpulse interval (IPI) did not differ between E- and vehicle-infused animals. In animals sampled for 16 hr, no effects of time or steroid × time interactions were detected for mean LHRH and LHRH pulse amplitude; however, both were greater (P < 0.01) in vehicle-infused than in E-infused males. LHRH IPI was unaffected by infusion. In contrast, both mean LH and LH pulse amplitude declined (P < 0.01) within 4–8 hr after the start of E infusion, whereas mean LH IPI was unaffected. In animals sampled for 28 hr, an effect of time (P < 0.01) and a steroid × time interaction (P < 0.01) was detected for mean LH, and there was an effect of time (P < 0.01) on LH pulse amplitude. Mean LH IPI was not affected. Our results show that in male sheep E rapidly reduces LH release in the absence of a detectable change in LHRH release.  相似文献   

11.
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)  相似文献   

12.
Nutritionally induced anovulatory cows were ovariectomized and used to determine the relationships between dose, frequency, and duration of exogenous gonadotropin-releasing hormone (GnRH) pulses and amplitude, frequency, and concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in serum. In Experiment 1, cows were given pulses of saline (control) or 2 micrograms of GnRH infused i.v. during a 0.1-, 1.25-, 5-, 10-, or 20-min period. Concentrations of LH and FSH during 35 min after GnRH infusion were greater than in control cows (P < 0.01), and FSH concentrations were greater when GnRH infusions were for 10 min or less compared with 20 min. In Experiment 2, the effect of GnRH pulse frequency and dose on LH and FSH concentrations, pulse frequency, and pulse amplitude were determined. Exogenous GnRH (0, 2, or 4 micrograms) was infused in 5 min at frequencies of once every hour or once every 4th hr for 3 d. There was a dose of GnRH x frequency x day effect on LH and FSH concentrations (P < 0.01), indicating that gonadotropes are sensitive to changes in pulse frequency, dose, and time of exposure to GnRH. There were more LH pulses when GnRH was infused every hour, compared with an infusion every 4th hr (P < 0.04). Amplitudes of LH pulses were greater with increased GnRH dose (P < 0.05), and there was a frequency x dose x day effect on FSH pulse amplitude (P < 0.0006). We conclude that LH and FSH secretion in the bovine is differentially regulated by frequency and dose of GnRH infusions.  相似文献   

13.
Two experiments were conducted to determine if administration of progesterone within a low, subluteal range (0.1-1.0 ng/mL) blocks the luteinizing hormone (LH) surge (experiments 1 and 2) and ovulation (experiment 2) in lactating dairy cows. In experiment 1, progesterone was administered to cycling, lactating dairy cows during the luteal phase of the estrous cycle using a controlled internal drug release (CIDR) device. CIDRs were pre-incubated in other cows for either 0 (CIDR-0), 14 (CIDR-14) or 28 days (CIDR-28). One group of cows received no CIDRs and served as controls. One day after CIDR insertion, luteolysis was induced by two injections of prostaglandin (PG) F(2alpha) (25 mg) at 12 h intervals. Two days after the first injection, estradiol cypionate (ECP; 3 mg) was injected to induce a LH surge. Concentrations of progesterone after luteolysis were 0.11, 0.45, 0.78 and 1.20 ng/mL for cows treated with no CIDR, CIDR-28, CIDR-14, and CIDR-0, respectively. LH surges were detected in 4/4 controls, 4/5 CIDR-28, 2/5 CIDR-14 and 0/5 CIDR-0 cows following ECP. In experiment 2, progesterone was administered to cycling, lactating, Holstein cows during the luteal phase of the estrous cycle as in experiment 1. Luteolysis was induced as in experiment 1. The occurrence of an endogenous LH surge and ovulation were monitored for 7 days. Concentrations of progesterone after luteolysis were 0.13, 0.30, 0.70 and 1.20 ng/mL for cows treated with no CIDR, CIDR-28, CIDR-14 and CIDR-0, respectively. LH surges and ovulation were detected in 5/5 controls, 3/7 CIDR-28, 0/5 CIDR-14 and 0/5 CIDR-0 cows. It was concluded that low concentrations of progesterone can reduce the ability of either endogenous or exogenous estradiol to induce a preovulatory surge of LH and ovulation.  相似文献   

14.
1. Furazolidone or nitrofurazone were given orally to laying turkeys at doses of 7.5, 15 or 30 mg/kg for 7 d. Plasma concentrations of luteinising hormone (LH), prolactin (PRL) and egg production were measured before, during and after treatment. 2. Both drugs produced dose-dependent decreases in LH concentration which were statistically significant at doses of 15 and 30 mg/kg. Plasma PRL concentration was significantly increased in birds receiving 15 or 30 mg/kg of nitrofurazone, and tended to increase in the other treated groups, but this was not statistically significant. 3. Egg production was lowered in a dose-dependent manner by both drugs. However, nitrofurazone appeared to be more potent in reducing egg production than furazolidone. 4. Birds given 15 mg/kg of either drug were injected intramuscularly with luteinising hormone releasing hormone (LHRH) at a dose of 5 micrograms/kg and blood was collected immediately before and 30 min after LHRH administration. 5. Nitrofurazone significantly reduced the rise in LH induced by LHRH. Seven days after withdrawing the drug, the LHRH-induced LH release was not significantly different when compared to that in the control group or that seen on day 7 of treatment.  相似文献   

15.
The objective of the present study was to determine if postpubertal boars (12-13 months of age; 156 +/- 8 kg) with large testes had altered hypothalamic control of secretion of luteinizing hormone (LH). Seven boars with the highest estimated 150 d, paired testis weights from a line selected for large testes (769 +/- 60 g = mean weight of excised testes) and 8 boars from a control group (control, 544 +/- 20 g) were tethered in stalls and fitted with indwelling jugular catheters. Males were bled when they were intact, 14 days after castration and during administration of sodium pentobarbital anesthetic (subsequent to castration) to block secretion of endogenous LH-releasing hormone (LHRH). Blood samples were collected at 12-min intervals for 6 hr before and 1 hr after intravenous injection of LHRH in intact and castrated males. During anesthesia, LHRH was administered 4 times at 1-hr intervals and blood samples were collected every 6 min. All samples were analyzed for concentrations of LH and pooled samples were analyzed for concentrations of 17-beta estradiol (E2) and testosterone (T). In intact and castrated males, mean concentrations of LH, frequency and amplitude of pulses of LH, and concentrations of E2 and T were not different between boars of the two groups (P greater than .10). Response to exogenous LHRH was less (P less than .05) in intact males with large testes than in corresponding males from the control group (P less than .05). Fourteen days after castration, males that had larger testes before castration had less of a response to LHRH than males from the control group (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

16.
This study evaluated the effectiveness of a LHRH fusion protein vaccine on endocrine changes, feedlot performance, and carcass quality of bulls compared with steers and hormone-implanted steers. Crossbred bulls (n = 30; mean weight, 179 +/- 4 kg; mean age, 130 +/- 2 d) were randomly assigned to three treatment groups: 1) castrated (castrated; n = 10); 2) castrated-implanted with trenbolone acetate (implanted; n = 10); and 3) immunized against a cocktail of recombinant fusion proteins, ovalbumin-LHRH-7 and thioredoxin-LHRH-7 (immunized bulls; n = 10). Blood was collected every 2 wk to evaluate antibody and hormone concentrations. Serum LHRH antibodies (P < 0.001) were detected in animals of the immunized group, which had reduced serum LH concentrations (P < 0.001) compared with the castrated groups and serum FSH concentrations, which did not decrease but were significantly different when compared with castrated and implanted animals. Serum testosterone concentrations in the immunized bulls were not different from the two castrated groups (P > 0.05) by d 60 after primary immunization. Initial mean scrotal circumference of the immunized bulls was 18.0 +/- 0.6 cm on d 0 and increased to 22.6 +/- 1.3 cm by d 310. No differences (P > 0.05) in ADG were observed among treatment groups. Immunized animals had an intermediate BW gain (P > 0.05) when compared with the castrates, whereas the castrated groups differed (P < 0.05) from each other. Carcass characteristics were similar (P < 0.05) among the three groups. Vaccinating bulls against a LHRH fusion protein cocktail suppressed LH and testosterone, which led to reduced testicular development and no bullock carcasses. Growth and carcass characteristics of the immunized animals were similar to the steers.  相似文献   

17.
This study evaluated the effect of microencapsulated LHRH agonist (D-Trp6-LHRH) on gonadotropin release and occurrence of estrus in early postpartum beef cows. Angus cows (n = 54) were assigned randomly to two treatment groups at d 5 postpartum. Group 1 received a single i.m. injection of D-Trp6-LHRH (LHRH-A) encapsulated in poly-DL-lactide-coglycolide, calculated to release 15 micrograms of LHRH-A per day for 30 d (n = 23). Group 2 received vehicle only (control, n = 31). Blood samples (15-min intervals for 6 h) were obtained on d 5, 10, 20, 30, and 40 postpartum for evaluation of LH and FSH concentrations (n = 12 per group). Days to first postpartum estrus were reduced by treatment with LHRH-A (Group 1, 43.7 +/- 4.2 d vs Group 2, 55.9 +/- 4.7 d; P < .05). However, days to conception were similar between groups (68.9 +/- 7.9 vs 76.7 +/- 6.7 d, respectively). On the day of treatment, cows treated with LHRH-A had higher mean concentrations of LH and FSH than did controls (8.3 +/- 1.4 vs 2.0 +/- .4 ng/mL for LH and 211.0 +/- 8.6 vs 51.2 +/- 2.7 ng/mL for FSH (P < .05). There were no differences in mean concentrations of LH or FSH between treatment groups on d 10, 20, 30, and 40 postpartum. Cows given LHRH-A had more (P < .05) LH pulses on d 10 and 30 postpartum than did controls. This study demonstrated that microencapsulated D-Trp6-LHRH reduced the postpartum anestrous interval in suckled beef cows.  相似文献   

18.
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)  相似文献   

19.
Plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) were determined over a 24-h period using radioimmunoassay in sheep injected with corn oil (control) or various doses of zeranol or estradiol-17 beta. Injection of .333, 1 or 10 mg of zeranol caused dose-related increases (P less than .01) in plasma PRL (peak levels at 12 to 18 h) and LH (peak levels at 12 to 20 h) in ovariectomized ewes. Similarly, PRL and LH increased following doses of 33 or 100 microgram of estradiol. Before the LH surge, plasma LH levels were significantly depressed (4 to 8 h). Plasma FSH levels were significantly decreased 4 to 8 h after zeranol and estradiol injection. Slight surges of FSH were observed at times similar to those of LH, but the peak level was never greater than control levels. Injection of 1 mg of zeranol or 100 microgram of estradiol into wethers resulted in a 24-h pattern of PRL secretion not significantly different of LH concentration and significantly prolonged inhibition of FSH secretion. These results indicate similarities in the effects of zeranol and estradiol on anterior pituitary hormone secretion within groups of animals of the same sex or reproductive state. Differences in secretion and plasma concentrations of LH, FSH and PRL due to underlying sexual dimorphism are maintained and expressed even when animals are challenged with structurally different compounds of varying estrogenic potencies.  相似文献   

20.
The influence of varying doses of human chorionic gonadotropin (hCG) on the preovulatory luteinizing hormone (LH) surge, estradiol-17 beta (E2) and progesterone (P4) was studied in synchronized gilts. Altrenogest (AT) was fed (15 mg X head-1 X d-1) to 24 cyclic gilts for 14 d. Pregnant mares serum gonadotropin (PMSG; 750 IU) was given im on the last day of AT feeding. The gilts were then assigned to one of four groups (n = 6): saline (I), 500 IU hCG (II), 1,000 IU hCG (III) and 1,500 IU hCG (IV). Human chorionic gonadotropin or saline was injected im 72 h after PMSG. No differences in ovulation rate or time from last feeding of AT to occurrence of estrus were observed. All gilts in Groups I and II expressed a preovulatory LH surge compared with only four of six and three of six in Groups III and IV, respectively. All groups treated with hCG showed a rapid drop (P less than .01) in plasma levels of E2 11, 17, 23 h after hCG injection when compared with the control group (35 h). The hCG-treated gilts exhibited elevated P4 concentrations 12 h earlier than the control group (3.1 +/- .5, 3.4 +/- .72, 3.1 +/- .10 ng/ml in groups II, III and IV at 60 h post-hCG vs .9 +/- .08 ng/ml in group I; P less than .05). These studies demonstrate that injections of ovulatory doses of hCG (500 to 1,500 IU) had three distinct effects on events concomitant with occurrence of estrus in gilts: decreased secretion of E2 immediately after hCG administration, failure to observe a preovulatory LH surge in some treated animals and earlier production of P4 by newly developed corpora lutea.  相似文献   

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