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1.
Two experiments were conducted to evaluate the effects of naloxone, an endogenous opioid receptor antagonist, on LH and FSH secretion in postpartum beef cows. In Experiment 1, 24 cows were divided into three equal groups. On day 15 postpartum, all cows were bled for 8 hr at 10 min intervals to evaluate LH secretory parameters. On day 18 postpartum, three treatments were administered: (a) saline at 0730 and 1130 hr; (b) 275 mg naloxone at 0730 and 1130 hr; (c) naloxone as in (b) above, plus this group was also treated with 50 mg progesterone (P4) twice daily from day 16 to day 19. In each treatment, jugular vein samples were collected at 10 min intervals from 0800 to 1600 hr. On day 19 the same treatments were administered at the same times, however, all cows were given 25 micrograms GnRH at 1200 hr to evaluate the LH secretory response. Naloxone increased mean LH concentration (P less than .05) and tended to increase pulse amplitude and frequency compared to controls. However, the most dramatic difference was due to P4 treatment which suppressed mean LH, pulse amplitude and frequency. Treatments had no effect on LH secretion in response to a 25 micrograms dose of GnRH. In Experiment 2, the effects of suckling on the naloxone response were examined in 16 postpartum cows. On day 21 postpartum, blood was collected at 10 min intervals for 8 hr and then calves were removed from half the cows. After 3 days of calf removal, all cows were sampled at 10 min intervals for 4 hr; then naloxone was injected after each 10 min sample at a dose rate of 200 mg/hr (33 mg per injection). Naloxone treatment and sampling continued for an additional 8 hr. Calf removal alone had very little effect on LH pulsatility. However, naloxone resulted in increased pulse frequency and mean LH compared to the control period. We conclude that LH release in the early postpartum cow is partially regulated by endogenous opioid peptides. We were unable to detect any effects on FSH secretion nor on pituitary sensitivity to exogenous GnRH.  相似文献   

2.
Plasma cortisol responses to an intravenous bolus treatment with 250 mg naloxone, 300 mg morphine or a combination, were studied in Holstein-Friesian cows; 4 in early lactation (29-43 d postpartum) and 7 in mid-lactation (90-155 d post-partum). Blood samples were collected every 15 min from 60 min before to 90 min after treatment. Naloxone induced an immediate increase in cortisol concentration, reaching a peak within 30 min. The cortisol response (area under the curve) was positively correlated with pre-naloxone cortisol concentrations (r = 0.7, p < 0.05). The mean increase in cortisol concentration after naloxone appeared to be lower in early lactation (1.8 ng/ml) than in mid-lactation (8.3 ng/ml). In contrast, morphine consistently suppressed mean tonic plasma cortisol concentration by 2.7 ng/ml below baseline for at least 90 min. When given with morphine, naloxone counteracted the suppressive effects; the cortisol response was similar to that after naloxone alone. A cow in mid-lactation, suffering from chronic lameness (joint infection), gave opposite results, i.e., treatment with morphine alone increased cortisol concentration, whereas morphine with naloxone did not result in the expected large increase in plasma cortisol concentration. In conclusion, the hypothalamo-pituitary-adrenal axis of dairy cows appears to be under suppressive opioidergic control. However, the opioidergic system involved in hypothalamo-pituitary-adrenal functions of an animal under chronic stress behaved in an opposite manner.  相似文献   

3.
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.  相似文献   

4.
This study investigated whether the stress associated with a 30-minute journey in a truck could distort the oestradiol-induced surge of luteinising hormone (LH) in dairy cows. Altogether 20 journeys were monitored, 16 to 18 hours after intramuscular administration of 1 mg oestradiol benzoate (OE2). Plasma cortisol concentration was elevated (P less than 0.001) within 30 minutes of the start of each journey, even when the journey was repeated at about weekly intervals, indicating a lack of habituation. The LH surge in response to 11 OE2 treatments in nine non-cycling cows within 30 days after calving was either absent (one cow) or significantly delayed, of shorter duration or of lesser amplitude following transport, compared with untransported OE2-treated controls. However, in six cycling cows, 58 days or more after calving, transport affected the LH surge only once. Even in these cows, the LH surge did not start until the cortisol concentration returned to normal, which may suggest a transient postponement of the LH surge by transport. In conclusion, transport impaired the LH surge in early post partum cows with little or no effect after ovarian cyclicity was resumed. It is hypothesised that endocrine events leading to the onset of the LH surge are more vulnerable to stressors in early post partum cows and in the natural situation this might be responsible for the occurrence of anovulation and cystic ovarian disease.  相似文献   

5.
An experiment was conducted to test the hypothesis that the effect of body fatness on LH pulsatility in post-partum cows is entirely independent of the negative feedback effects of ovarian steroids. Forty beef cows were fed in the last 100 d of gestation so that they achieved either a thin (mean score 1.97) or fat (mean score 2.79) body condition (0 to 5 scale) at calving and were fed after calving to maintain live weight and body condition. At 15 (sd 3.7) d post partum all cows were ovariectomised and half from each body condition score treatment group received a subcutaneous estradiol implant (+EST) while the remainder received no implant (−EST). At weeks 5 and 9 post-partum blood samples were collected via jugular catheter every 20 minutes for 10 hr on two consecutive d and on the third d cows were injected via the jugular vein with 2.5 μg GnRH. Blood samples were collected every 15 minutes for 1 hr before and 2 hr after GnRH injection. At 5 and 9 weeks the fatter cows had significantly higher mean LH concentrations, baseline LH concentrations, LH pulse amplitudes and pulse frequencies (P<0.01). Implantation with estradiol in both fat and thin cows reduced mean LH concentrations, baseline LH concentrations, LH pulse amplitudes and pulse frequencies (P<0.001). The lack of interaction between body condition and the presence or absence of estradiol implies that the effect of body condition on LH release is independent of ovarian steroid feedback mechanisms. Fat cows showed a greater release of LH in response to exogenous GnRH (P<0.01) than thin cows while implantation with estradiol in both fat and thin cows decreased (P<0.01) LH release. The pituitary responsiveness to GnRH with the −EST cows was greater at 9 compared to 5 weeks, but there was no difference with time in the +EST cows. However, there was no such interaction in endogenous LH pulse amplitude suggesting that in the absence of estradiol the magnitude of GnRH pulses declined with time post-partum.  相似文献   

6.
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)  相似文献   

7.
The effects of morphine and the opiate receptor antagonist, naloxone, on the secretory pattern of luteinizing hormone (LH) were assessed in male sheep. Morphine infusion (250 mg/hr) abruptly stopped LH pulsatile secretion in castrates (wethers) and decreased mean serum LH concentrations by nearly 70 percent. Response of the pituitary to exogenous LH releasing hormone was not affected by morphine suggesting that the effects of morphine on LH secretion were mediated through the hypothalamus. Estradiol-implanted wethers, characterized by a nonpulsatile LH secretory pattern, responded to intravenous injection of naloxone (20, 50 and 200 mg Lv.) with an immediate release (pulse) of L.H. Similarly, LH release was significantly increased following naloxone infusion (200 mg/hr for four hours) in intact rams and wethers implanted with testosterone or estradiol. In contrast, naloxone infusion altered the pattern of LH secretion in wethers but without affecting mean serum LH concentrations. These results support the notion that LH secretion in male-sheep is tonically regulated by endogenous opiates and further suggests that opioid modulation of the hypothalamic-pituitary-LH axis in sheep involves an interaction with the steroid negative feedback system.  相似文献   

8.
The influence of the suckling stimulus and ovarian secretions on LH response to naloxone was studied in 16 postpartum anestrous beef cows that were assigned randomly to one of four groups (n = 4/group): intact suckled (IS), intact nonsuckled (IN), ovariectomized suckled (OS) or ovariectomized nonsuckled (ON). Ovariectomy (OS + ON) and calf removal (IN + ON) were performed on d 2, 3 or 4 after parturition. Jugular venous blood was collected at 15-min intervals for 4 h before and 4 h after administration of naloxone (1 mg/kg BW, i.v.) on d 14 and d 28 after parturition. Gonadotropin-releasing hormone (5 micrograms, i.v.) was given 3 h after naloxone. Both IN and OS increased (P less than .05) mean pretreatment LH above IS values (mean +/- SE, ng/ml; IS 1.6 +/- .1 vs IN 2.5 +/- .3 and OS 2.7 +/- .4; P less than .01), whereas ON increased (P less than .01) LH (3.7 +/- .3 ng/ml) even further. Mean LH increased (P less than .05) after naloxone administration in all treatment groups. However, magnitude of this response was variable and dependent on ovarian status. Amplitude of the naloxone-induced LH response was greater (P less than .05) for ovariectomized (5.9 +/- 1.1 ng/ml) than for intact groups (2.7 +/- .5 ng/ml). Gonadotropin-releasing hormone increased mean LH concentrations in all groups. We suggest that ovarian secretions and the suckling stimulus contribute to endogenous opioid inhibition of LH during the postpartum interval.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

9.
This study was designed to evaluate the effects of exogenous prostaglandin F2 alpha (PGF2 alpha) on hormone secretion in cows without a corpus luteum. Blood samples were taken from 10 Friesian dairy cows at frequent intervals from a jugular vein and the caudal vena cava starting between nine and 20 days after parturition. PGF2 alpha (25 mg dinoprost) was injected intramuscularly into five cows after the first eight hours of sampling. Plasma concentrations of 13,14-dihydro 15-keto PGF2 alpha (PGFM) increased rapidly but had returned to baseline by 14 hours after injection. There was no significant effect of the treatment on the time taken by the cows to resume ovarian cycles, and it had no consistent effect on plasma luteinising hormone (LH) patterns; however the amplitude of pulses of LH was temporarily suppressed in two cows and the frequency of pulses of LH was immediately increased in one cow. Treatment with PGF2 alpha had no significant effect on the concentration of oestradiol in blood from the vena cava. It is concluded that any enhancement of the reproductive performance of cows treated with PGF2 alpha after parturition is not due to a direct effect on pituitary-ovarian function.  相似文献   

10.
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.  相似文献   

11.
Effects of testosterone propionate (TP) treatment on plasma concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) before and after an injection of gonadotropin releasing hormone (GnRH) were studied using ovariectomized cows and pony mares. An initial injection of GnRH (1 microgram/kg of body weight) was followed by either TP treatment or control injections for 10 (cows) or 11 (ponies) d. A second GnRH injection was administered 1 d after the last TP or oil injection. Concentrations of LH and FSH were determined in samples of plasma taken before and after each GnRH injection. Control injections did not alter the response to GnRH (area under curve) nor the pre-GnRH concentrations of LH and FSH in ovariectomized cows or ponies. Testosterone treatment increased (P less than .01) the FSH release in response to GnRH in ovariectomized mares by 4.9-fold; there was no effect in cows, even though average daily testosterone concentrations were 59% higher than in pony mares. Testosterone treatment reduced the LH release in response to GnRH by 26% in ovariectomized mares (P less than .05) and by 17% in ovariectomized cows (P approximately equal to .051). These results are consistent with a model that involves ovarian androgens in the regulation of FSH secretion in the estrous cycle of the mare, but do not support such a model in the cow.  相似文献   

12.
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)  相似文献   

13.
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.  相似文献   

14.
Effects of the opiate agonist, morphine, and antagonist, naloxone, on LH release, courtship behavior and ejaculation frequency of mature, sexually active or sexually inactive rams were investigated. Plasma LH concentrations were monitored from blood samples collected every 15 min for 10 hr (0800 to 1800 hr) from eight rams that were isolated from or in contact with estrous females. Plasma LH concentration was higher (P<.05) in sexually active rams exposed to receptive females compared with hormone concentration of rams isolated from ewes. Intravenous infusion of morphine sulphate (1 mg/kg) into rams 4 and 6 hr after exposure to ewes reduced (P<.05) plasma LH concentration as compared to rams given saline. Morphine did not affect (P>.05) courtship behavior (investigatory sniff, mount attempt, foreleg kick, flehmen, vocalization) but diminished (P<.05) number of ejaculations. In another trial, LH concentrations were higher (P<.05) in seven sexually active rams given naloxone iv or when given to three rams through an intracerebroventricular cannula (icv) as compared to LH response of sexually inactive rams. LH did not differ (P>.05) in seven sexually inactive rams before or after administration of naloxone. Investigatory sniffs by sexually active rams were increased (P<.03) after treatment with the opiate antagonist. Four of the seven sexually active rams had more ejaculations after naloxone compared with the pretreatment period, but mean ejaculation frequency after treatment did not differ (P=.31). Naloxone did not stimulate courtship behavior of sexually inactive males. These data suggest that the effect of opiates on sexual behavior and LH secretion depends upon the inherent level of sexual activity among rams.  相似文献   

15.
Involvement of endogenous opioids in inhibition of luteinizing hormone (LH) release and stimulation of prolactin (PRL) release was investigated by injecting the opioid antagonist naloxone into 18 ewes on d 7 and 8, d 12 and 13, and d 18 and 19 postpartum. Compared with control injections of saline, iv naloxone (1 mg/kg) increased serum concentrations of LH and decreased serum PRL in samples collected 15, 30 and 45 min after each injection. Ewes lambing in the spring (March) or autumn (September and October) that nursed one or two lambs did not differ in their LH and PRL responses to naloxone. Autumn-lambing ewes from which lambs were weaned within 1 d after parturition did not differ from ewes of the autumn-nursed group in any of the following characteristics: 1) serum LH increases following naloxone, 2) basal secretion of LH, 3) postpartum interval to first increase in serum progesterone and 4) relative decrease in serum PRL after naloxone despite large differences in basal PRL secretion. In summary, postpartum expression of a naloxone-reversible inhibition of LH release and stimulation of PRL secretion did not depend on suckling stimuli or differ between autumn and spring parturitions.  相似文献   

16.
Recent studies have shown that naloxone (N), an opioid antagonist, increases concentrations of luteinizing hormone (LH) in the postpartum anestrous beef cow. However, the LH response to N was influenced by the postpartum interval. For example, a significant LH response to 200 mg of N occurred on d 42 but not on d 14 or 28 postpartum. The present study was conducted to determine the effect of different doses of N on LH secretion during the postpartum period of beef cows. Twelve cows were given 200, 400 or 800 mg of N on d 14, 28 and 42 postpartum in a Latin square design with repeat measures within cells. On d 14, serum concentrations of LH increased (P less than .01) from .5 +/- .1 ng/ml (mean +/- SE) before N to a peak of 2.0 +/- .5 and 1.4 +/- .5 ng/ml for cows given 400 and 800 mg of N, respectively. In contrast, 200 mg of N had no effect on serum concentrations of LH. On d 28 and 42 all three doses of N elevated (P less than .01) serum concentrations of LH. Therefore, a larger dose of N was required to increase serum concentrations of LH on d 14 postpartum compared with d 28 and 42. Based on these data we suggest that endogenous opioids participate in the regulation of LH secretion in the early postpartum period. The differential response to naloxone may be due to changes in endogenous opioid inhibition of LH secretion during the postpartum period.  相似文献   

17.
The objective of the research was to determine the relationship between circulating 17β-estradiol (E2) and secretion of luteinizing hormone (LH) in cows. A second objective was to determine if response to E2 was influenced by interval between ovariectomy and the start of E2 treatment. Thirty-one nulliparous cows 3 yr of age were randomly assigned to a 2 × 4 factorial arrangement of treatments. Sixteen cows were ovariectomized at 18 mo of age (long term), and the other 15 cows were ovariectomized at 36 mo of age (short term). At the time of ovariectomy of cows in the short term group, 11 cows in the short term group and 12 cows in the long term group were implanted subcutaneously with 1, 2 or 4 polydimethylsiloxane capsules containing E2. The other eight cows served as non-implanted controls (n=4-short term, n=4-long term). All cows were fitted with jugular vein catheters on day 29 of treatment, and on day 30 blood samples were collected at 12-min intervals for 6 hr. At the end of 6 hr, luteinizing hormone-releasing hormone (LHRH) was administered and blood sampling continued at 12-min intervals for an additional hour. Serum was analyzed for LH and E2. Variables of LH secretion analyzed were mean concentration, frequency of pulses, amplitude of pulses and maximum concentration after LHRH. There were no significant interactions for any of the variables of LH among cows ovariectomized for the long and short term. There was a significant linear increase in mean concentration of LH with increased circulating concentration of E2. Frequency of LH pulses was not affected by circulating concentration of E2. As circulating concentration of E2 increased, amplitude of LH pulses increased and response to LHRH increased - resulting in an increase in mean LH. Interval from time of ovariectomy to the start of E2 treatment only had a minor influence on mean concentration of LH and profile of LH concentrations in circulation.  相似文献   

18.
To determine the pattern of follicular growth during oestrus and the relationship with estradiol and luteinizing hormone in ovulating and non-ovulating cows, three groups of (n = 10), thirty cyclic, Bos indicus cows were synchronized with CIDR, consecutively at 9-day intervals. Twenty-four hours after implant withdrawal, all cows synchronized in the same group with other cows displaying estrous behaviour after implant withdrawal were subjected to an intensive period of ultrasonographic observations (every 6 h for 120 h). Blood samples were taken to evaluate LH surge and 17-beta estradiol. No differences were observed in follicular growth, ovulatory diameter and growth average in the three groups of synchronized cows. Cows ovulating (CO) had a better growth average in comparison with the group of cows not ovulating (CNO) (1.4 +/- 0.7 mm vs 0.7 +/- 0.5 mm, p < 0.06). The average time from estradiol release to LH surge was 39.3 +/- 24.6 h. Differences were also observed between CO and CNO with respect to both the first concentration (27.7 +/- 5.2 vs 58.6 +/- 31.9, p < 0.004) and last concentration (79.3 +/- 23.3 vs 99.2 +/- 27.3, p < 0.05) of estradiol above 5 pg/ml. The average time from overt signs of oestrus to LH release was 8.4 +/- 7.7 h. In the CNO, the increase in LH concentration was never above two SD from the basal average. In conclusion, there is a wide variability in follicular growth and ovulatory diameter between CO and CNO, which can affect the intervals of LH release, estradiol peak and ovulation. Yet, LH surge might be a good marker for timing ovulation in Zebu cows.  相似文献   

19.
The luteinising hormone (LH) surge in response to 1 mg oestradiol benzoate intramuscular injection was studied on 67 occasions in 45 cows with cystic ovarian disease 20 to 150 days post partum. Cows diagnosed as having luteal cysts were given 500 micrograms cloprostenol intramuscularly 24 hours before oestradiol, to induce luteolysis. Oestradiol benzoate was also given to eight post partum acyclic and eight cyclic cows and in all these cases a control LH response was characterised for comparison. Eight of 17 cows with luteal cysts (47 per cent), and 10 of 21 cows with follicular cysts (48 per cent), released LH in response to oestradiol. Some cows with cysts were given one of two treatments. Seven cows with follicular cysts were treated with a progesterone-releasing device (PRID) for seven days: all responded to a second oestradiol treatment given 24 hours after removal of the PRID. Luteal cysts in three cows and follicular cysts in nine cows were ruptured manually: only one cow (a luteal case) responded to the second oestradiol treatment given 24 hours after manual rupture. In eight cows initially diagnosed with luteal cysts, cloprostenol was not given and plasma progesterone concentration at the time of oestradiol treatment was high (over 0.9 ng ml-1): none released LH in response to oestradiol. As manual rupture did not improve the LH response to oestradiol, it is concluded that the defective LH response to oestradiol in cows with cystic ovarian disease was not influenced in the short-term by cyst fluid contents.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

20.
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.  相似文献   

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