Opioid inhibition of luteinizing hormone secretion during the postpartum period in suckled beef cows

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.     

Effects of body condition and estradiol on luteinizing hormone secretion in post-partum beef cows

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.     

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

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

Influence of the ovary and suckling on luteinizing hormone response to naloxone in postpartum beef cows

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)     

Effects of feeding diets containing endophyte-infected fescue seed on luteinizing hormone secretion in postpartum beef cows and in cyclic heifers and cows.

Two experiments were conducted to investigate the effect of feeding endophyte (Acremonium coenophialum)-infected fescue (Festuca arundinacea Shreb.) seed on LH secretion in postpartum beef cows and in cycling heifers and cows. In Exp. 1, spring-calving primiparous Angus cows (n = 16) were pair-fed for 75 d diets that contained endophyte-free or endophyte-infected (95%) fescue seed that contained 1.3 micrograms/g of ergovaline and 5.2 mg/g of saturated pyrrolizidines. Serial blood samples for basal and GnRH-stimulated serum LH analysis were obtained on d 7, 28, 42, and 56 of the study. The endophyte had no effect on LH secretion (basal, pulse frequency, and amplitude) or milk production. Average daily gain was decreased (P < .05) in cows that consumed infected fescue seed compared with controls (-.20 vs -.01 kg, respectively). Basal serum prolactin concentrations were reduced (P < .01) in treated compared with control cows (8.9 vs 25.4 ng/mL, respectively) on d 70. In Exp. 2, cycling Angus heifers (n = 8; age = 2 yr) and cows (n = 8; age = 4 yr) stratified by age were pair-fed for 40 d diets that contained the noninfected or the highly infected fescue seed. Estrus was synchronized by prostaglandin F2 alpha (d 18 and 28). Serial blood samples for serum LH analysis were obtained on d 28 (luteal phase) and d 30 (follicular phase). The endophyte did not affect LH (P > .28) or prolactin (P > .16) secretion, whereas ADG was decreased (P < .05) in treated compared with control animals (.32 vs .70 kg/d, respectively).     

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

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

Hypoglycemia alters pulsatile luteinizing hormone secretion in the postpartum beef cow

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

Hypothalamic deafferentation in prepuberal beef heifers: Effects of gonadotropin-releasing hormone and estradiol benzoate on luteinizing hormone secretion

Hypothalamic control of luteinizing hormone (LH) secretion was investigated in crossbred beef heifer calves by comparing anterior (AHD), posterior (PHD), and complete (CHD) hypothalamic deafferentation with sham operated controls (SOC). Heifers (n = 16) were fitted with an indwelling jugular catheter for 6 days before cranial surgery, and assigned randomly to treatments. Blood for radioimmunoassay of LH was collected sequentially at 15-min intervals during an 8-h period on days ? 1 before and day 6 after hypothalamic deafferentation or sham operation. On the day of surgery, blood samples were collected sequentially at 15-min intervals 2 h before induction of anesthesia and throughout surgery and early recovery. Seven months after hypothalamic deafferentation, all experimental and sham operated heifers were ovariectomized and treated with vegetable oil (i.m.) plus saline (i.v.), vegetable oil plus gonadotropin releasing hormone (GnRH), estradiol benzoate (EB, 1 mg) in vegetable oil. After ovariectomy basal plasma concentrations of LH increased (P < 0.01) compared with the low circulating hormone levels before ovariectomy. The amplitude of LH response to GnRH was greater (P < 0.01) in CHD and PHD when compared with SOC and AHD heifers. Injection of EB failed to induce a LH surge in CHD and PHD 900–1100 min later when compared with the robust response seen in SOC and AHD heifers. Injection of EB plus GnRH elicited LH release in all deafferentated and sham operated heifers. These results indicate a transient change in LH secretion after AHD or CHD in prepuberal heifers with intact ovaries. After OVX, the integrity of the neural connection of the posterior hypothalamus is required for EB-induced LH release in beef heifers.     

Effect of metoclopramide on luteinizing hormone secretion in postpartum anestrous cows.

The effect of metoclopramide (MC), a dopamine antagonist on luteinizing hormone (LH), was examined in anestrous primaparous cows. Metoclopramide has been found to be beneficial in overcoming fescue toxicosis; increasing LH secretion stimulates return to ovulatory function after parturition. Consequently, if MC had negative effect on LH secretion, it would indicate that administration of MC to reproducing animals might be limited. Of 14 postpartum (47 to 66 days) cows, 7 were given MC (4 mg/kg of body weight, IV), and 7 served as controls. Blood was obtained via jugular cannulas at 15-minute intervals for 8 hours; MC was given at the end of the first hour, and gonadotropin-releasing hormone (GnRH, 7 mg/kg), was given IV at the end of hour 7 as a challenge stimulus for LH secretion. Prior to GnRH administration, MC did not have significant effect on LH secretion, as judged by mean serum LH concentration, LH pulse frequency, and LH pulse amplitude. Administration of MC resulted in greater (P less than 0.05) LH response to GnRH, indicating enhanced secretory ability when the pituitary gland was challenged. Serum prolactin concentration was increased (P less than 0.01) by MC administration. Therefore, MC did not have adverse effect on LH secretion in postpartum cows.     

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.     

Ovulation in postpartum beef cows treated with estradiol

The effect of implants of estradiol on initiation of ovarian cycles postpartum was studied in 201 anestrous beef cows. Cows from four farms were used over a 2-yr period in a 2 x 3 factorial arrangement of treatments with estradiol implants and stage postpartum as main effects. Cows were assigned at random within date of calving within farm to receive an ear implant containing estradiol-17 beta (24 mg) for 21 d or to serve as controls. Stages postpartum at implantation were divided into less than or equal to 25, 26 to 39, and greater than or equal to 40 d, three stages that should reflect potential changes in hypothalmic-hypophysial sensitivity to estradiol. Blood samples for determination of progesterone were obtained and rectal examinations of the ovaries performed at implant insertion, 14 d after insertion, at implant removal (d 21), and 14 d after removal (d 35) to assess ovulatory response to treatment. Circulating concentrations of estradiol on d 14 of treatment averaged 3.2 +/- 1.0 and 23.1 +/- 4.7 pg/ml for control and estradiol-treated cows, respectively. Compared with control cows, treatment with estradiol initiated after d 26 postpartum increased the proportion of cows that ovulated during the experimental period. No differences were seen in the average days postpartum when cows were first determined to have ovulated.     

Luteinizing hormone concentrations in serum of postpartum beef cows injected with microencapsulated luteinizing hormone-releasing hormone analog

Twenty-five cows were divided equally into five groups to determine whether [D-Trp6]-luteinizing hormone releasing hormone (LHRH-A) microencapsulated in poly (DL-lactide co-glycolide) would increase basal serum concentrations of LH during the postpartum period. On d 5 postpartum, cows were injected i.m. with 2 ml of vehicle alone (Group 1) or vehicle containing microcapsules calculated to release .4, 1.6, 6.4 or 25.6 micrograms LHRH-A per day for approximately 30 d (Groups 2, 3, 4 and 5, respectively). Cows were bled every 15 min for 4 h immediately before and after injection and every 15 min for 4 h at weekly intervals for the next 4 wk to evaluate serum profiles of LH. Estrus was determined by twice daily observations and confirmed by serum progesterone. More cows in Groups 2, 3, 4 and 5 exhibited pulsatile patterns of LH after LHRH-A injection than in Group 1 (P less than .06). More pulses of LH were observed after LHRH-A injection in Groups 4 and 5 than in Group 1 (P less than .01). Mean concentrations of LH within treatment groups did not change during the initial injection, except in Group 5. All cows in Group 5 had a surge of LH immediately after injection. The induced surge of LH in two cows in Group 5 cows resulted in progesterone profiles similar to those during a normal luteal phase. Days to first postpartum estrus were not different among the five treatment groups. Microencapsulated LHRH-A given at a dose estimated to release 25 micrograms LHRH-A/d was effective in elevating LH concentrations following injection. However, effectiveness of this hormonal treatment in shortening postpartum anestrus was not substantiated.     

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

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

Relationship between weaning and secretion of luteinizing hormone, cortisol and transcortin in beef cows

The effects of suckling on secretion of luteinizing hormone, cortisol and transcortin were investigated in anovulatory postpartum cows. On d 35 postpartum, calves were separated from 12 cows to prevent suckling and eight calves continued to suckle their dams ad libitum. Between 35 and 41 d postpartum, samples of jugular blood were collected every 15 min for two periods of 6 h/d. In non-suckled cows, frequency of pulses and basal luteinizing hormone increased but amplitude of pulses did not change. Concentrations of total cortisol in serum of cows were not altered during 3 d after weaning calves and did not differ among intervals before, during and after a suckling event. Affinity of transcortin for cortisol was not affected by postpartum interval or treatment. Capacity of transcortin to bind cortisol tended to increase after weaning. We found no evidence to support the hypothesis that suckling reduces binding capacity of transcortin or increases unbound cortisol. Differences in preovulatory secretion of luteinizing hormone between suckled and non-suckled cows could not be accounted for by differences in secretion of cortisol. In beef cows that are fed to satisfy requirements for energy and have average body condition, we conclude that negative modulation of luteinizing hormone by suckling is not mediated by cortisol.     

Reduced postpartum anestrus of suckled beef cows treated with microencapsulated luteinizing hormone-releasing hormone analog.

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.     

Effects of body condition score at parturition and postpartum supplemental fat on metabolite and hormone concentrations of beef cows and their suckling calves

To determine the effects of BCS at parturition and postpartum lipid supplementation on blood metabolite and hormone concentrations, 3-yr-old Angus x Gelbvieh beef cows, which were nutritionally managed to achieve a BCS of 4 +/- 0.07 (479.3 +/- 36.3 kg of BW) or 6 +/- 0.07 (579.6 +/- 53.1 kg of BW) at parturition, were used in a 2-yr experiment (n = 36/yr). Beginning at 3 d postpartum, cows within each BCS were assigned randomly to be fed hay and a low-fat control supplement or lipid supplements with either cracked high-linoleate or high-oleate safflower seeds until d 61 of lactation. The diets were formulated to be isonitrogenous and isocaloric, and the safflower seed supplements were formulated to achieve 5% DMI as fat. On d 31 and 61 of lactation, blood samples were collected preprandially and then hourly postprandially (at 0, 1, 2, 3, and 4 h). Serum insulin (P = 0.27) and glucose (P = 0.64) were not affected by BCS at parturition. The mean concentrations of plasma NEFA (P = 0.08) and beta-hydroxybutyrate (P = 0.08) tended to be greater, and serum IGF-I was greater (P < 0.001) in BCS 6 than BCS 4 cows. Conversely, serum GH was greater (P = 0.003) for BCS 4 cows, indicating that regulation of IGF by GH may have been uncoupled in BCS 4 cows. The postpartum diet did not affect NEFA (P = 0.94), glucose (P = 0.15), IGF-I (P = 0.33), or GH (P = 0.62) concentrations. Oleate-supplemented cows had greater (P = 0.03) serum insulin concentrations, whereas control cows had greater (P = 0.01) plasma beta-hydroxybutyrate concentrations. Concentrations of NEFA (P = 0.05) and glucose (P < 0.001) were greater, and beta-hydroxybutyrate tended (P = 0.07), to be greater at d 3, whereas serum IGF-I was greater (P = 0.003) at d 6 of lactation. Similar concentrations of NEFA, glucose, GH, and IGF-I indicate that the nutritional status of beef cows during early lactation was not influenced by lipid supplementation. However, perturbations of the somatotropic axis in BCS 4 cows indicate that the influence of energy balance and BCS of the cow at parturition on postpartum performance should be considered when making managerial decisions.     

Pituitary receptors for GnRH and estradiol, and pituitary content of gonadotropins in beef cows. II. Changes during the postpartum period

Pregnant beef heifers (n = 24) were assigned randomly to four groups and slaughtered at day 1, 15, 30 or 45 postpartum. The day prior to slaughter blood samples were taken from each cow every 15 min for 8 hr. The anterior pituitary gland, preoptic area (POA) and medial basal hypothalamus (HYP) were collected from each cow. Contents of gonadotropin-releasing hormone (GnRH) in extracts of POA and HYP, and luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in extracts of anterior pituitary were quantified by radioimmunoassay. In the anterior pituitary gland, membrane receptors for GnRH were quantified by a standard curve technique and cytosolic receptors for estradiol were quantified by saturation analysis. Concentrations of LH, FSH and prolactin in serum were quantified by radioimmunoassay. Only one cow of eight had a pulse of LH during the 8 hr bleeding period on day 1 postpartum. This increased to 8 pulses in 6 cows on day 30 postpartum. Contents of GnRH in POA (15.0 +/- 3.2 ng) and HYP (14.0 +/- 2.0 ng) did not change significantly during the postpartum period. Pituitary content of LH was low following parturition (.2 +/- .1 mg/pituitary) and increased significantly through day 30 postpartum (1.2 +/- .1 mg/pituitary). Pituitary content of FSH did not change over the postpartum period. Receptors for both GnRH (.9 +/- .2 pmoles/pituitary) and estradiol (5.0 +/- .9/moles/pituitary) were elevated on day 15 postpartum, possibly increasing the sensitivity of the anterior pituitary gland to these hormones and leading to an increased rate of synthesis of LH that restored pituitary content to normal by day 30 postpartum.