OBJECTIVE To determine whether luteinizing hormone receptors (LHRs) are expressed in canine femoral head subchondral bone (FHSB), hip joint round ligament (RL), cranial cruciate ligament (CCL), and femorotibial joint synovium (FJS) specimens. SAMPLE 1 specimen each of the FHSB, RL, CCL, and FJS obtained from the left hind limbs of 19 fresh canine cadavers. PROCEDURES 1 section of each FHSB, RL, CCL, and FJS specimen was processed with rabbit polyclonal IgG anti-human LHR antibody, and 1 section was treated with negative control reagents. Percentage immunoexpression of LHRs in FHSB and FJS sections was analyzed by assessment of 100 bone marrow cells or synoviocytes in 3 adjacent hpf (400×). In each RL and CCL section, immunoexpression of LHRs in fibrocytes was semiquantitatively analyzed on the basis of the mean of the product of percentage staining score (from 0 [no staining] to 3 [> 50% of cells stained]) and staining intensity score (from 0 [no staining] to 2 [moderate to strong staining]) for 3 adjacent hpf. RESULTS All tissues examined had variable LHR expression. Expression of LHRs in FHSB, CCL, or FJS specimens did not differ between sexes or between sexually intact and gonadectomized dogs. However, RL specimens from female dogs had significantly greater LHR expression scores, compared with findings for male dogs. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that LHRs are expressed in structural support tissues of canine hip and femorotibial joints. Further research is required to determine the LHRs' function, mechanism of action, and potential contribution to the pathogenesis of hip dysplasia or CCL rupture in dogs.

Changes in luteinizing hormone (LH) secretion after 17beta-estradiol (E2) injection were evaluated during sexual maturation in 10 prepubertal Nelore heifers. Heifers were divided into 2 groups: intact (I) and ovariectomized (OVX). 17beta-estradiol (2 micrograms/kg) was administered to both groups at 10, 13, and 17 mo of age. Only at 10 mo of age was there a greater mean LH concentration in OVX heifers (1.33 +/- 0.29 ng/mL) compared with the I group (0.57 +/- 0.15 ng/mL). At 13 and 17 mo of age there was no significant difference between the 2 groups in any of the evaluated variables (number of peaks, total peak area, greatest peak area, and time to greatest peak occurrence). This suggests a decrease in negative E2 feedback associated with an increase in positive feedback to LH secretion during sexual maturation, and these were likely the key factors that determined the time of first ovulation in Nelore heifers.

Dairy goats were given IM injections of 12 micrograms of cloprostenol sodium on day 6 of the estrous cycle (prostaglandin F [PGF] 6, n = 22) or day 12 of the estrous cycle (PGF 12, n = 26). Mean +/- SE hours from injection to onset of behavioral estrus and proportion of goats responding were 46 +/- 4.2 (range, 12 to 88 hours) and 95% and 48 +/- 2.9 (range, 34 to 68 hours) and 100% for groups PGF 6 and PGF 12, respectively. There was no significant difference between the groups in mean time to onset of estrus, but variances about the means were different. Of the does in groups PGF 6 and PGF 12, 67 and 85%, respectively, had signs of onset of estrus between 36 and 60 hours after administration of PGF. Mean (+/- SE) hours from injection to time of peak concentrations of luteinizing hormone (LH) were 62 +/- 3.1 and 64 +/- 2.1 for groups PGF 6 and PGF 12, respectively. Of the does in groups PGF 6 and PGF 12, 86 and 100%, respectively, had LH peaks. Of the does in groups PGF 6 and PGF 12, 68 and 77%, respectively, had peak concentrations of LH between 48 and 72 hours after administration of PGF. All does in groups PGF 6 and PGF 12 had concentrations of progesterone > 1.0 ng/ml on the day of administration of PGF. Concentrations decreased to < 1.0 ng/ml by 48 hours after injection in all does except 1 in group PGF 6. Prostaglandin was equally effective for induction of estrus on day 6 or day 12 of the estrous cycle in dairy goats, but resulted in a more predictable time to estrus when injection was done on day 12.

The effects of coliform endotoxin (E) and recombinant ovine tumor necrosis factor a (TNF) were compared with respect to clinical signs of disease and changes in plasma metabolite and pituitary and pancreatic hormone concentrations in calves. In addition, changes in plasma TNF concentration during each challenge exposure were quantitated by use of radioimmunoassay. Healthy Holstein bull calves with mean body weight of 90 kg were each given, in order, on different days, saline solution (5.0 ml, IV, day 1, n = 4), E (type 055:B5, 1.0 microgram/kg of body weight IV, day 2, n = 4) and TNF (5.0 microgram/kg IV, day 9, n = 3). Jugular venous blood samples, rectal temperature reading, and PCV were obtained at hourly intervals before (2 hours) and after challenge exposure. The PCV increased (P < 0.05) after E and TNF administrations for the first 5 hours, then returned to normal in calves given E, but decreased and remained low in calves given TNF through 24 hours. Plasma triglyceride and nonesterified free fatty acids concentrations were increased through 10 hours (P < 0.05) after E administration, whereas triglyceride and nonesterified free fatty acids concentrations were not significantly affected by TNF administration. Increase in blood glucose concentration at 1 hour after administration of E and TNF was followed by prolonged hypoglycemia that lasted through 6 hours. Changes in plasma insulin concentration paralleled the observed changes in glucose concentration, initially increased at 2 hours after E and TNF (P < 0.05) administrations, but then tended to decrease below control values thereafter. Plasma growth hormone and luteinizing hormone concentrations decreased after E and TNF administrations to almost nondetectable values through 4 hours after dosing, returning to normal values by 8 hours. The data indicate similarities in physiologic response of calves to E and TNF and suggest a role for acute production of TNF as a mediator of E responses.

Body and testis weights, serum luteinizing hormone, follicle-stimulating hormone, and prolactin values and volume fractions of Sertoli cells, spermatogonia, early and late primary spermatocytes, and round and long spermatids were evaluated in 70-day-old male rats treated orally with 20 mg of zearalenone/kg of body weight daily for 5 weeks. A significant (P < 0.05) increase in serum prolactin concentration was consistently observed during the 5 weeks of treatment with zearalenone. Significant changes were not observed in any of the other variables evaluated.

At initiation of a 140-day postweaning weight gain test, Angus bulls were assigned in equal numbers (n = 5) to 1 of 3 treatment groups to determine effects of implantation with zeranol, an estrogenic growth promotant, on selected reproductive characteristics. The bulls, whose age (mean +/- SD) was 233 +/- 20 days at initiation of the test (day 0), were implanted with 36 mg of zeranol on day 0, on days 0 and 60, or were not implanted. At day 140, scrotal circumference and testicular consistency were unaffected by zeranol implantation. Zeranol implantation did not affect the morphologic characteristics of semen samples collected by electroejaculation on day 139. There was no effect of zeranol treatment on paired weights of testes, epididymides, or vesicular glands from bulls at slaughter 47 to 68 days after day 140. Microscopic lesions associated with estrogenic exposure were not observed in accessory sex glands or epididymides of any bull. Histopathologic changes in the seminiferous epithelium were not induced by zeranol treatment. Implantation with zeranol did not affect body weight or hip weight at day 140 or carcass weight at slaughter. Plasma concentration of luteum hormone was increased (P = 0.04), whereas testosterone concentration tended to be less (P = 0.08) in both groups of zeranol-implanted bulls after administration of gonadotropin-releasing hormone on day 140.

Existence of ultradian variation in serum progesterone concentration and the relation between progesterone and luteinizing hormone (LH) secretory patterns were investigated in nonpregnant and pregnant mares. Blood samples were taken every 15 minutes for a 24-hour period on day 8 of the estrous cycle and day 18 of pregnancy, respectively. Progesterone and LH concentrations were determined by radioimmunoassay. Progesterone was secreted in pulsatile manner in nonpregnant and pregnant mares. Luteinizing hormone also was secreted in a pulsatile manner in both groups of mares. There was little temporal relation between LH and progesterone pulses in either pregnant or nonpregnant mares.

Luteinizing hormone (LH) and ACTH concentrations were measured in plasma from 7 cows to determine whether ACTH secretion changes with the phase of the estrous cycle, and to determine whether any ACTH peaks are associated with LH peaks. Blood was collected every 5 minutes for 190 minutes during the luteal and follicular phases of the estrous cycle. Radioimmunoassays were used to measure ACTH and LH in plasma. Mean concentration of ACTH in all cows did not differ significantly between luteal (35.1 +/- 8.0 pg/ml) and follicular (37.5 +/- 9.4 pg/ml) phases of the estrous cycle. Mean concentration of luteal-phase LH of all cows (2.0 +/- 1.1 ng/ml) was significantly (P < 0.01) lower than mean concentration of follicular-phase LH (5.4 +/- 1.6 ng/ml). Frequency of peaks in ACTH concentration was low during the sampling period. Mean number of luteal-phase ACTH peaks (0.29 +/- 0.49) was not significantly different from that of follicular-phase samples (0.43 +/- 0.53). Unlike ACTH, mean frequency of LH peaks was significantly (P < 0.05) higher in plasma from cows in the follicular phase of the estrous cycle (2.9 +/- 0.7), compared with that from cows in the luteal phase (0.29 +/- 0.49).

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 < 0.05) LH response to GnRH, indicating enhanced secretory ability when the pituitary gland was challenged. Serum prolactin concentration was increased (P < 0.01) by MC administration. Therefore, MC did not have adverse effect on LH secretion in postpartum cows.

A study was conducted to test the hypothesis that high cortisol concentrations associated with products of infections (endotoxin) cause derangement in the neuroendocrine mechanism controlling ovulation in heifers. Eight Holstein heifers were given 2 injections of prostagladin (PG), 11 days apart, to synchronize estrus. Starting from 25 hours after the second injection of PG (PG-2), the uterus of each heifer was infused with 5 ml of pyrogen-free water (control, n =3) or Escherichia coli endotoxin (5 microgram/kg of body weight) in 5 ml of pyrogen-free water (treated, n = 5), once every 6 hours for 10 treatments. Blood samples were obtained every 15 minutes via indwelling jugular catheter for an hour before and 2 hour after each infusion, then hourly until an hour before the next infusion. Ultrasonography of the ovaries was performed every 12 hours, starting 24 hours after PG-2 injection until 96 hours after PG-2 injection. Serum concentrations of luteinizing hormone and cortisol were determined by validated radioimmunoassays. Changes in cortisol concentrations were not detected in control heifers with preovulatory luteinizing hormone surges at 60 to 66 hours after PG-2 injection, followed by ovulations 72 to 96 hours after PG-2 was injected. None of the treated heifers ovulated, and the resulting follicular cysts (14 to 18 mm diameter) persisted for 7 to 21 days. In all treated heifers, serum cortisol concentrations increased (4- to 10-fold) during the first 2 hours after each infusion and then decreased gradually until the next infusion. Luteinizing hormone concentrations remained at baseline values throughout the treatment period in all treated heifers. These findings suggested that endotoxin-induced increases in cortisol concentrations during the preovulatory period of the estrous cycle prevented ovulations by blunting the preovulatory luteinzing hormone surges.