Response of the bovine corpus luteum to increased secretion of luteinizing hormone induced by exogenous gonadotropin releasing hormone

Two experiments were conducted to investigate the response of the bovine corpus luteum to surges of luteinizing hormone (LH) induced by natural gonadotropin-releasing hormone (GnRH) administered twice during the same estrous cycle. In experiment 1, eight mature beef cows, each cow serving as her own control, were injected intravenously (iv) with saline on days 2 and 8 of the cycle (day of estrus = day 0 of the cycle), then with 100 micrograms GnRH on days 2 and 8 of the subsequent cycle. Jugular blood samples were taken immediately prior to an injection and at 15, 30, 45, 60, 120 and 240 min postinjection, to quantitate changes in serum luteinizing hormone. Blood was also collected on alternate days after an injection until day 16 of the cycle, to characterize changes in serum progesterone concentrations. Although exogenous GnRH caused release of LH on days 2 and 8 of the cycle, the quantity of LH released was greater on day 8 (P less than .025). Serum levels of progesterone after treatment with GnRH on day 8 of the cycle did not differ significantly from those observed during the control cycles of the heifers. Because exposure of the bovine corpus luteum to excess LH, induced by GnRH early during the estrous cycle, causes attenuated progesterone secretion during the same cycle, these data suggest that a second surge of endogenous LH may ameliorate the suppressive effect of the initial release of LH on luteal function. Duration of the estrous cycle was not altered by treatment (control, 20.4 +/- .5 vs. treated, 20.4 +/- .4 days).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of subluteal concentrations of progesterone on luteinizing hormone and ovulation in lactating dairy cows

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.     

Endocrine and body growth traits in heifers exposed to testosterone-propionate during early fetal development

This study was conducted to determine the effects of testosterone-propionate exposure during fetal development on sexual differentiation and growth rates in heifers. Ten pregnant cows were given subcutaneous injections of testosterone-propionate (250 mg/injection) every other day during d 40 to 60 of gestation. Four cows aborted after the end of testosterone treatment, while four heifers (androgenized females) and two bulls (androgenized males) were produced from the six remaining pregnant, testosterone-propionate treated cows. Calves from cows that did not receive exogenous hormone treatment were used as controls. At 8 mo of age, the androgenized heifers and control heifers and control steers were challenged with 1 mg estradiol-17 beta to induce a preovulatory luteinizing hormone (LH) surge. Two weeks later, pituitary responsiveness to exogenous luteinizing hormone releasing hormone (LHRH; 75 micrograms) was evaluated in androgenized heifers and in control heifers and control steers. To monitor growth rates, all animals were weighed at 28-d intervals from birth to 380 d of age. Androgenized females exhibited a partially masculinized phenotype as well as internal male reproductive structures. Treatment with estradiol-17 beta first depressed (P less than .05) serum LH concentrations in all animals, then induced (P less than .05) a preovulatory-like LH surge in control and androgenized females. Control steers did not (P greater than .05) exhibit a preovulatory-like LH surge following administration of estradiol-17 beta. Exogenous LHRH treatment stimulated peak LH concentrations (P less than .05) to a greater extent in control and androgenized females than in control steers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cyclic release of luteinizing hormone and the effects of luteinizing hormone-releasing hormone injection in Asiatic elephants.

Cyclic changes in serum concentration of luteinizing hormone (LH) were observed throughout the estrous cycle of Asiatic elephants (Elephas maximus). The increase in serum LH was correlated with a slight increase in serum estradiol concentration and the onset of behavioral heat (willingness to mate). In a second series of studies, injection of luteinizing hormone-releasing hormone after 3 days of estrone administration induced an increase in serum LH. These studies indicate that the Asiatic elephant exhibits a cyclic LH release that can be experimentally induced by estrone and luteinizing hormone-releasing hormone administration.     

Concentrations of ovarian and pituitary hormones following prostaglandin F2 alpha-induced luteal regression in ewes varies with day of the estrous cycle at treatment

Prostaglandin F2 alpha (PGF2 alpha) was injected on d 5, 8 or 11 postestrus in ewes to determine how stage of the estrous cycle would affect PGF2 alpha-induced changes in concentrations of ovarian and pituitary hormones and intervals to the onset of estrus and the preovulatory surge of luteinizing hormone (LH). Initial concentrations of progesterone and average values during the 12 h after PGF2 alpha were related positively to the day of cycle on which PGF2 alpha was administered. Patterns of decline in progesterone after injection of PGF2 alpha were similar among the 3 d. Concentrations of LH in plasma increased in a similar manner from 0 to 12 h in all ewes. After 12 h LH continued to increase, plateaued or declined in ewes treated on d 5, 8 or 11, respectively. Initial concentrations of follicle stimulating hormone (FSH) in plasma were related positively to day of treatment. After treatment with PGF2 alpha, FSH increased within 2 h on d 5 but declined by that time on d 8 or 11. Concentrations of estradiol following treatment did not vary with day. The onset of estrus and the preovulatory surge of LH occurred at 36 and 35, 40 and 45, and 48 and greater than 48 h in ewes treated on d 5, 8 or 11, respectively. It is concluded that: 1) the initial increase in LH is dependent on a decrease in plasma progesterone and 2) differences in patterns of secretion of gonadotropins before the preovulatory surge of LH might be caused by differences in progesterone or progesterone:-estradiol ratio when luteal regression is induced on different days of the estrous cycle.     

Pulsatile or continuous infusion of luteinizing hormone-releasing hormone and hormonal concentrations in prepubertal beef heifers

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.     

Effect of FSH treatment on LH and FSH receptors in chronic cystic-ovarian-diseased dairy cows

This experiment was conducted to 1) determine whether chronic cystic-ovarian-diseased (CCOD) cows fail to respond to luteinizing hormone (LH) treatment because of a lack of adequate ovarian LH receptors and 2) determine the effect of follicle stimulating hormone (FSH) treatment on ovarian LH and FSH receptors in ovaries of CCOD cows. The CCOD cows were those that did not resume cyclic ovarian activity after repeated treatment with human chorionic gonadotropin (hCG) and(or) LH-releasing hormone (LHRH) and were considered chronic by veterinarians. Thirteen CCOD cows were purchased from producers; six of them were injected with 5 mg FSH twice daily for 3 or 5 d (TCCOD) and the remaining seven remained untreated. Seven control (noncystic) cows in the luteal phase of the estrous cycle were injected with Lutalyse approximately 48 to 50 h before slaughter so they would be in the follicular phase (FP) of the cycle at the time of slaughter. Analysis of serum and pituitaries showed no differences (P greater than .05) in mean concentrations of serum or pituitary LH and FSH or pituitary LHRH receptor concentration and affinity among FP, CCOD and TCCOD cows. Ovarian follicle wall concentrations of receptors for LH (3.2 +/- .6; 13.0 +/- 2.5; 22.4 +/- 5.1 fmol/mg protein) and FSH (10 +/- 2.6; 43 +/- 7.2; 29 +/- 6.7 fmol/mg protein) were lower (P less than .05) in CCOD cows compared with FP and TCCOD cows, respectively. The same pattern was observed for concentrations of granulosa cell LH and FSH receptors.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pituitary-testicular responses of estradiol-17 beta-implanted bull calves to continuous versus pulsatile infusion of luteinizing hormone releasing hormone

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.     

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.     

Effects of estradiol-17β, para-chlorophenylalanine and quipazine on tonic and LHRH-induced secretion of luteinizing hormone in ovariectomized ewes

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.     

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.     

Production of estradiol by each ovary during the estrous cycle of cows

The objective of our experiment was to examine changes in serum concentrations of estradiol in each utero-ovarian vein before, during and after gonadotropin surges. Four cows were given prostaglandin F2 alpha (PGF2 alpha) during diestrus and three cows were allowed to cycle spontaneously. All cows had a cannula in each utero-ovarian vein and in one jugular vein. Most cows had two transient rises in estradiol, primarily coming from a single ovary, preceding and after luteinizing hormone (LH) surges. The first rise in estradiol began after luteal regression and was sustained from 48 h before a pre-ovulatory LH surge to the end of the LH surge. The second rise in estradiol was sustained from 72 to 168 h after the end of an LH surge. To determine how rapidly asymmetrical production of estradiol began during luteolysis, several cows were injected with PGF2 alpha during the luteal phase. Blood samples were taken from a jugular and both utero-ovarian veins at hourly intervals before and after PGF2 alpha. Asymmetrical production of estradiol began within 3 h after an injection of PGF2 alpha. We concluded: (1) that a single ovary was responsible for the sustained increases in concentration of estradiol that occur during proestrus to estrus and early diestrus in cows and (2) that cows may have at least one follicle capable of producing estradiol during most days of an estrous cycle, thus little delay in selection of which follicle eventually ovulates occurs after luteal regression.     

Follicular phase gonadotropin secretion in cyclic postpartum beef cows with phlorizin-induced hypoglycemia

Twenty mature, lactating Hereford-cross cows were used to determine the effect of phlorizin-induced hypoglycemia on gonadotropin secretion following prostaglandin-induced luteolysis. Cows were 43 to 108 d postpartum and had a functional corpus luteum (CL) at the start of infusion treatment (d 1). Infusions consisted of either saline (control) or 3 g/d of phlorizin infused continuously from the time of prostaglandin injection at 1000 on d 1 until 0800 on d 5. Blood samples were collected for determination of plasma concentrations of insulin, glucose and free fatty acids (FFA) and for serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and progesterone. Plasma concentrations of insulin (P less than .05) and glucose (P less than .05) were lower, whereas FFA concentrations increased (day X treatment, P less than .05) over the infusion period in phlorizin-treated cows compared with saline-infused controls. Mean serum concentrations of LH (1.17 +/- .10 vs 1.53 +/- .20 ng/ml; P less than .05) and LH pulse amplitude (1.69 +/- .14 vs 2.47 +/- .37 ng/ml; P less than .10) were lower in phlorizin-infused compared with saline-infused cows during the 0 to 24-h period immediately preceding the ovulatory gonadotropin surge. The FSH pulse frequency increased (.33 +/- .11 to .55 +/- .12 pulses/h) in saline-infused cows, but decreased (.61 +/- .10 to .41 +/- .11 pulses/h) in phlorizin-infused cows before the gonadotropin surge. Other characteristics of gonadotropin secretion were similar among phlorizin-infused and saline-infused cows. All but one phlorizin-infused cow ovulated and formed functional CL similar to controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Shrinkage in the horizontal dimensions of the vulva (vulvar shrinkage) as an indicator of standing heat in the beagle

During the proestrous and estrous periods in 12 beagles, the following parameters were measured daily: the horizontal dimensions of the vulva, vaginal cytology, and serum luteinizing hormone (LH) and progesterone concentrations. Measurements of serum LH concentrations allowed for the identification of the LH surge and the optimal time for artificial insemination (AI). Nine out of the 12 beagles became pregnant through AI and completed a gestation. Shrinkage in the horizontal dimensions of the vulva (i.e., vulvar shrinkage) was primarily observed prior and subsequent to the LH surge. In six of the nine (66.7%) beagles that became pregnant, vulvar shrinkage was observed on the days in which the LH surge was confirmed, and the rate of vulvar shrinkage tended to be greater at higher serum LH concentrations. Further vulvar shrinkage was identified in all nine beagles within two days of the LH surge. An increase in the serum progesterone concentration was observed after the LH surge in each of the beagles that became pregnant, together with clinical signs of estrous behavior (i.e., standing heat) as well as a change in vulva condition from swollen to soft. This demonstrates that vulvar shrinkage is induced in response to the onset of the LH surge and that the LH surge can be predicted through the measurement of the horizontal dimensions of the vulva, vaginal cytology, and the assessment of serum progesterone concentrations in beagles.     

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.     

Endocrine patterns in the postpartum beef cow associated with weaning: a comparison of the short and subsequent normal cycles

Levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), progesterone and estradiol-17 beta were measured in five Polled Hereford cows. Blood samples were collected once or twice daily for 5 d, then every 6 h from 1 d before weaning (d 28 to 38 postpartum) until 10 d after the second postweaning estrus. Blood samples were again collected at daily intervals until the third postweaning estrus. All cows exhibited estrus within 4 d after weaning, a second estrus 8 to 10 d after the first and a third estrus 16 to 23 d after the second. All cows had peaks in serum concentrations of LH during the first (22.6 to 81.7 ng/ml) and second (4.4 to 149.0 ng/ml) postweaning estrus. Mean levels of LH in serum during the peak and the area under the LH curve during the first and second postweaning estrus did not differ. Serum levels of LH and FSH during the first 4 d of the short cycle did not differ from LH and FSH levels the first 4 d of the subsequent normal cycle. Levels of LH in serum for 4 d before the first LH surge, associated with the first postweaning estrus, did not differ from levels of LH found 4 d before the second Lh surge, associated with the second postweaning estrus. However, serum levels of FSH during the 4 d before the first ovulatory LH surge were lower (P = .05) than those observed during the 4-d period before the second ovulatory surge of LH. Progesterone levels were similar the first 6 d after the first and second estrous periods, but were lower after d 6 of the first (short) cycle than after d 6 of the second (normal) cycle. Estradiol peaks of 1.2 to 2.8 pg/ml were detected during the first postweaning estrus and 1.4 to 12.5 pg/ml during the second postweaning estrus, but due to the variability among cows mean levels of estradiol during first estrus did not differ from second estrus. These data agree with previous reports that postpartum anestrous cows had short cycles if they exhibit estrus in response to weaning. The early decline of progesterone after the first estrus apparently did not stem from lack of LH in serum, but the lower levels of FSH observed before this first ovulation may have been an important factor contributing to the reduced life span of the subsequent corpus luteum.     

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)     

Effects of feed restriction on reproductive and metabolic hormones in ewes

The goal of this study was to determine the effects of short-term feed withdrawal on reproductive and metabolic hormones during the luteal phase of the estrous cycle in mature ewes. Mature ewes observed in estrus were assigned randomly to control and fasted groups (n = 10 per group Trials 1 and 2). For Trials 1 and 2, control ewes had ad libitum access to feed, whereas fasted ewes were not fed from d 7 through 11 of their estrous cycle; on d 12, all ewes were treated with 10 mg of PGF2alpha, and fasted ewes were gvien ad libitum access to feed. For Trial 1, blood samples were collected daily through fasting and at 2-h intervals following PGF2alpha for 72 h. Serum concentrations of insulin (P < or = 0.002) and IGF-I (P < or = 0.01), but not GH (P > or = 0.60), were decreased during fasting compared with fed ewes. Serum concentrations of 29 (P = 0.02) and 34 kDa (P = 0.04) IGFBP were greater in fasted ewes at 96 h after initiation of fasting than in control ewes. Two control and four fasted ewes in Trial 1 did not exhibit a preovulatory surge release of LH by 72 h. Therefore, Trial 2 was conducted so that the timing of the LH surge could be predicted following the collection of blood samples at 2-h intervals for 112 h and then at 6-h intervals until 178 h following PGF2alpha administration and realimentation. The magnitude of the preovulatory LH surge in Trial 2 was decreased (P = 0.009) and delayed (P = 0.04), and serum concentrations of estradiol were diminished (P < or = 0.03) 12 h before the LH surge in fasted ewes. Ovulation rates were not influenced (P > or = 0.32) by fasting in Trials 1 and 2. Serum concentrations of progesterone in both Trials 1 and 2 were, however, greater (P < 0.001) in fasted than in control ewes. A third trial with ovariectomized ewes was conducted to determine whether the increased serum concentrations of progesterone observed in fasted ewes during Trials 1 and 2 were ovarian-derived. Ovariectomized ewes were implanted with progesterone-containing intravaginal implants and allotted to control (n = 5) or fasted (n = 5) treatment groups and fed as described for Trials 1 and 2. Similar to intact ewes, serum concentrations of progesterone were approximately twofold greater (P < 0.001) in fasted than in control implanted ovariectomized ewes. In summary, feed withdrawal for 5 d during the luteal phase of the estrous cycle increased serum concentrations of progesterone and evoked endocrine changes that could perturb the subsequent estrous cycle.     

Associated luteinizing hormone-releasing hormone and luteinizing hormone secretion in ovariectomized gilts.

The secretion of luteinizing hormone-releasing hormone (LHRH) and its temporal association with pulses of luteinizing hormone (LH) was examined in ovariectomized prepuberal gilts. Push-pull cannulae (PPC) were implanted within the anterior pituitary gland and LHRH was quantified from 10 min (200 microliters) perfusate samples. Serum LH concentrations were determined from jugular vein blood obtained at the midpoint of perfusate collection. Initial studies without collection of blood samples, indicated that LHRH secretion in the ovariectomized gilt was pulsatile with pulses comprised of one to three samples. However, most pulses were probably of rapid onset and short duration, since they comprised only one sample. Greater LHRH pulse amplitudes were associated with PPC locations within medial regions of the anterior pituitary close to the median eminence. In studies which involved blood collection, LH secretion was not affected by push-pull perfusion of the anterior pituitary gland in most gilts, however, adaptation of pigs to the sampling procedures was essential for prolonged sampling. There was a close temporal relationship between perfusate LHRH pulses and serum LH pulses with LHRH pulses occurring coincident or one sample preceding serum LH pulses. There were occasional LHRH pulses without LH pulses and LH pulses without detectable LHRH pulses. These results provide direct evidence that pulsatile LHRH secretion is associated with pulsatile LH secretion in ovariectomized gilts. In addition, PPC perfusion of the anterior pituitary is a viable procedure for assessing hypothalamic hypophyseal neurohormone relationships.     

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.