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Objectives: Ascent to high altitude may result in a hypobaric hypoxic brain injury. The development of acute mountain sickness (AMS) is considered a multifactorial process with hypoxia-induced blood-brain barrier (BBB) dysfunction and resultant vasogenic oedema cited as one potential mechanism. Peripheral S100B is considered a biomarker of BBB dysfunction. This study aims to investigate the S100B release profile secondary to hypoxic brain injury and comment on BBB disturbance and AMS., Methods: A prospective field study of 12 subjects who ascended Mt Fuji (3700 m) was undertaken., Results: The mean baseline plasma S100B level was 0·11 μg/l (95% CI 0·09-0·12), which increased to 0·22 μg/l (95% CI 0·17-0·27) at the average of three high altitude levels (2590, 3700, and 2590 m on descent) (P < 0·001). The mean level for the seven subjects who experienced AMS rose from 0·10 to 0·19 μg/l compared to 0·12 to 0·25 μg/l for the five subjects who did not develop AMS (P  =  0·33)., Conclusion: Ascending to 3700 m resulted in elevated plasma S100B levels but this was not associated with AMS.

The ability of gonadotrophin releasing hormone (GnRH) agonist implants to suppress ovarian activity and prevent pregnancies, long-term, was examined in heifers and cows maintained under extensive management. At three cattle stations, heifers (2-year-old) and older cows (3- to 16-year-old) were assigned to a control group that received no treatment, or were treated with high-dose (12 mg, Station A) or low-dose (8 mg, Station B and Station C) GnRH agonist implants. The respective numbers of control and GnRH agonist-treated animals (heifers + cows) at each station were: Station A, 20 and 99; Station B, 19 and 89; Station C, 20 and 76. Animals were maintained with 4% bulls and monitored for pregnancy at 2-monthly intervals for approximately 12 months. Pregnancy rates for control heifers and control cows ranged from 60-90% and 80-100%, respectively, depending on the study site. The respective number of animals (heifers + cows) treated with GnRH agonist that conceived, and days to first conception, were: Station A, 9 (9%) and 336 +/- 3 days; Station B, 8 (10%) and 244 +/- 13 days; Station C, 20 (26%) and 231 +/- 3 days. Treatment with high-dose GnRH agonist prevented pregnancies for longer (approximately 300 days) than treatment with low-dose GnRH agonist (approximately 200 days). In the majority of heifers and cows treated with GnRH agonist, ovarian follicular growth was restricted to early antral follicles (2-4mm). The findings indicate that GnRH agonist implants have considerable potential as a practical technology to suppress ovarian activity and control reproduction in female cattle maintained in extensive rangelands environments. The technology also has broader applications in diverse cattle production systems., (Copyright 2002 Elsevier Science B.V.)

The requirement for pulsatile LH and the LH surge for the acquisition of oocyte fertilizing potential and embryo developmental competency was examined in Zebu heifers. Follicular growth was superstimulated using the GnRH agonist-LH protocol in which pulsatile LH and the preovulatory LH surge are blocked. In experiment 1, heifers were assigned on Day 7 of the estrous cycle to receive: group 1A (n = 5), 1.5 mg norgestomet (NOR) implant; group 1B (n = 5), GnRH agonist implant. Follicular growth was superstimulated with 2x daily injections of FSH from Day 10 (a.m.) to Day 13 (p.m.), with PGF2alpha injection on Day 12 (a.m.). Heifers were ovariectomized on Day 15 (a.m.) and oocytes were placed immediately into fertilization, without 24 h maturation. Respective cleavage and blastocyst development rates were: group 1A, 0/64 oocytes (0%) and 0/64 (0%); group 1B, 34/70 oocytes (48.6%) and 2/70 (2.9%). In experiment 2, heifers were assigned on Day 7 of the estrous cycle to receive: group 2A (n = 10), 1.5 mg NOR implant; group 2B (n = 10), GnRH agonist implant; group 2C (n = 10), GnRH agonist implant. Follicular growth was superstimulated as in experiment 1 above. Heifers in groups 2A and 2B received an injection of 25 mg LH on Day 14 (p.m.) and all heifers were ovariectomized on Day 15 (a.m.); oocytes were placed immediately into fertilization without 24 h maturation. Cleavage rates were similar for heifers in group 2A (84/175 oocytes, 48.0%), group 2B (61/112 oocytes, 54.5%) and group 2C (69/163, 42.3%). Blastocyst development rates were similar for heifers in group 2A (22/175 oocytes, 12.6%) and group 2B (25/112 oocytes, 22.3%) and lower (P < 0.05) for heifers in group 2C (9/163 oocytes, 5.5%). Oocytes obtained from heifers treated with GnRH agonist, without injection of exogenous LH, underwent cleavage indicating that neither pulsatile LH nor the preovulatory LH surge are obligatory for nuclear maturation in cattle oocytes. Exposure to a surge-like increase in plasma LH increased embryo developmental competency indicating that the preovulatory LH surge promotes cytoplasmic maturation. The findings have important implications for controlling the in vivo maturation of oocytes before in vitro procedures including nuclear transfer.

The contraceptive efficacy of an intra-uterine device was evaluated using 218 heifers and 212 cows on three north Australian cattle stations. The heifers were aged approximately 2 years and weighed 250-378 kg; the cows were aged 3-16 years and weighed 256-540 kg. All cattle were non-pregnant, non-lactating Brahmans. At the end of the monsoon (wet) season (April-June 1997), the cattle were allocated by stratified randomisation to the three treatments which were untreated controls (n=59), surgical ovariectomy (n=105), or implantation with a bovine intra-uterine device (BIUD; n=266). All cattle grazed and were managed as one group within each station. They were exposed to bulls (4 per 100 females) from soon after treatment until slaughter approximately 12 months later. The BIUD could not be implanted in 25% of heifers and 8% of cows due to narrow or twisted cervices. Correct placement of the BIUDs appeared to be achieved in 57% of heifers and 72% of cows. At slaughter, the devices were incorrectly positioned in 73% of heifers and 49% of cows into which BIUDs had been inserted and that remained non-pregnant. Uterine perforations by the BIUD were observed in 35 and 45% of these heifers and cows, respectively; most perforations appeared to occur during implantation. Low-grade endometritis was observed at slaughter in most BIUD-implanted animals; 2% had pyometra.BIUD animals did not have significantly different growth to that of control or ovariectomised animals, other than when ovariectomy suppressed growth following surgery. Most animals implanted with BIUDs appeared to have normal ovarian function and animals were observed mating. All ovariectomised animals remained non-pregnant. Over 80% of controls were pregnant within 8 months of exposure to bulls, except heifers at one station where pregnancy rate was restricted to 25% as a result of severe nutritional conditions. Pregnancy was diagnosed in 21% of heifers and 33% of cows with implanted BIUDs. The device remained correctly positioned and with no pregnancy diagnosed in the year following implantation in only 2% of heifers and 14% of cows originally allocated. Because of the difficulties of implanting BIUDs, the high frequency of associated uterine injury, the high pregnancy rate in implanted animals, and that growth was unaffected by the presence of a BIUD, it was concluded that the device had poor contraception efficacy and no growth-promotant effect in Brahman cattle.

The response in cattle to treatment with gonadotrophin releasing hormone (GnRH) agonist includes downregulation of GnRH receptors on gonadotrophe cells, desensitisation of the anterior pituitary gland to endogenous GnRH, and the abolition of pulsatile release of LH. In bulls, a tonic pattern of LH release is associated with increased secretion of testosterone, which persists for the duration of treatment with GnRH agonist. The mechanism for this response in bulls has not been elucidated, but clearly pulsatile release of LH is not required to stimulate the synthesis of steroidogenic enzymes that sustain elevated secretion of testosterone. In heifers, desensitisation to endogenous GnRH prevents the occurrence of the pre-ovulatory surge release of LH, thus blocking ovulation. The latter provided the opportunity to evaluate the potential of a GnRH agonist bioimplant to control fertility in heifers under extensive management. Bioimplants that contained graded amounts of GnRH agonist prevented pregnancies in heifers for periods of 3 to 12 months. Zebu crossbred heifers treated with GnRH agonist from 14 to 23 months of age failed to conceive, but showed normal conception patterns when introduced into mating herds at around 26 months of age. After treatment with GnRH agonist for 4 to 6 weeks, ovarian follicular growth in heifers is restricted to relatively small (2-4 mm) antral follicles. Suppressed follicular growth in heifers treated long-term with GnRH agonist is due to a lack of gonadotrophin support, rather than a direct action of agonist at the ovaries. This was demonstrated by the ability to induce apparently normal follicular growth and ovulation by acute treatment with FSH for 4 days, followed by an injection of LH, in heifers that had been exposed to GnRH agonist for around 6 months, and which had only small (2-4 mm) antral follicles at the start of FSH treatment. GnRH agonist bioimplants have been incorporated into new multiple ovulation and embryo transfer protocols that allow control of the time of ovulation subsequent to superstimulation of ovarian follicular growth with FSH. In these protocols, the endogenous surge release of LH is blocked by treatment with agonist and ovulation is timed by injection of exogenous LH, allowing fixed-time AI. It can be concluded from recent studies that GnRH agonist bioimplants have considerable potential for both pro-fertility and anti-fertility applications in cattle. It is likely that commercial bioimplants will be available within the next 3 to 5 years.

The capacity of heifer calves of a late sexually maturing Zebu (Bos indicus) genotype to respond to superstimulation with FSH at a young age and in vitro oocyte development were examined. Some calves were treated with a GnRH agonist (deslorelin) or antagonist (cetrorelix) to determine whether altering plasma concentrations of LH would influence follicular responses to FSH and oocyte developmental competency. Brahman calves (3-mo-old; 140 +/- 3 kg) were randomly assigned to 3 groups: control (n = 10); deslorelin treatment from Day -8 to 3 (n = 10); and cetrorelix treatment from Day -3 to 2 (n = 10). All calves were stimulated with FSH from Day 0 to 2, and were ovariectomized on Day 3 to determine follicular responses to FSH and to recover oocytes for in vitro procedures. Before treatment with FSH, heifers receiving deslorelin had greater (P < 0.001) plasma LH (0.30 +/- 0.01 ng/ml) than control heifers (0.17 +/- 0.02 ng/ml), while plasma LH was reduced (P < 0.05) in heifers treated with cetrorelix (0.13 +/- 0.01 ng/ml). Control heifers had a surge release of LH during treatment with FSH, but this did not occur in heifers treated with deslorelin or cetrorelix. All heifers had large numbers of follicles > or = 2 mm (approximately 60 follicles) after superstimulation with FSH, and there were no differences (P > 0.10) between groups. Total numbers of oocytes recovered and cultured also did not differ (P > 0.05) for control heifers and heifers treated with deslorelin or cetrorelix. Fertilization and cleavage rates were similar for the 3 groups, and developmental rates to blastocysts were also similar. Zebu heifers respond well to superstimulation with FSH at a young age, and their oocytes are developmentally competent.

The aim of this study was to determine the effect on ovarian follicular growth and atresia, of acute treatment with either 100 mg of progesterone (n = 10), 200 mg of progesterone (n = 10), 10 mg of oestradiol + 100 mg of progesterone (n = 10), 10 mg of oestradiol (n = 10) or no treatment (n = 10), given on Day 10 of a 17-day treatment with a norgestomet implant in randomly cycling Bos indicus heifers. The fate of the dominant follicle on Day 10, emergence of the new cohort of follicles and the intervals from implant removal to ovulation were recorded by ultrasonography. Plasma concentrations of Luteinizing hormone (LH), progesterone and oestradiol were determined during the time when the norgestomet implant was in place. All treatments resulted in the emergence of a new cohort of follicles within 5 days of administration. The day of emergence of the ovulatory follicle tended to be delayed after treatment with 100 mg of progesterone (2.7 +/- 0.3 days after treatment), 200 mg of progesterone (3.7 +/- 0.5 days after treatment), 10 mg of oestradiol + 100 mg of progesterone (4.4 +/- 0.2 days after treatment) and 10 mg of oestradiol (4.6 +/- 0.4 days after treatment) compared to control heifers (1.4 +/- 1.4 days after time of treatment). The mean interval from implant removal to onset of oestrus was significantly shorter after treatment with 100 mg of progesterone (38.4 +/- 2.6 h) than after treatment with 200 mg of progesterone (61.5 +/- 3.9 h) but otherwise, the mean interval from implant removal to onset of oestrus did not differ. Oestrus synchrony, measured by the sample standard deviation of oestrus onset, was tighter in all treatment groups compared to untreated control heifers. The mean interval from implant removal to ovulation did not differ significantly between groups. The synchrony of ovulation, measured by the sample standard deviation of the interval from implant removal to ovulation, was significantly tighter after treatment with 100 mg of progesterone, 200 mg of progesterone and 10 mg of oestradiol compared to control heifers. Treatment with 10 mg of oestradiol resulted in ovulation in seven of 10 heifers before implant removal, three of which failed to ovulate after implant removal. Progesterone administered on Day 10 lowered plasma LH concentrations (P < 0.05), whereas treatment with oestradiol caused a surge of LH and ovulation. Progesterone administered with oestradiol prevented the LH surge. A combination treatment of oestradiol and progesterone given on Day 10 of a 17-day norgestomet treatment in a range of follicular states resulted in the consistent emergence of a new cohort of follicles which included the eventual ovulatory follicle.

The effects of day length and grazing intensity on seasonal fluctuations in plasma concentrations of luteinizing hormone (LH) and cyclic ovarian activity were determined in Brahman (Bos indicus) and Hereford-Shorthorn (Bos taurus) cows maintained at two stocking rates in a subtropical environment. Contemporary groups of ovariectomised cows were monitored for fluctuations in plasma concentrations of LH. Equal numbers (n = 5) of entire and ovariectomised Brahman and Hereford-Shorthorn cows were assigned to a pasture with a greater or lesser stocking rate. Over a 15-month period, live weight was recorded weekly, and a blood sample was taken at the same time for measurement of plasma LH in entire and ovariectomised cows, and plasma progesterone in entire cows. Plasma concentrations of progesterone were used as an index of cyclic luteal function (time of cessation or onset of oestrous cycles). Regression coefficients were calculated to determine the least-order regression coefficient (LORC; range 1st to 10 order) for which time of year explained at least 50% (r2 > 0.05) of changes in live weight, plasma LH, or plasma progesterone; regression coefficients of 4th and 5th order indicated seasonally-related changes in these variables. For all cows, live weight was greatest in late summer to early autumn and lowest in winter. Changes in live weight were more closely related to seasonal changes in pasture availability for cows on pastures at a greater stocking rate (LORC 4th-5th) than for cows on pastures at a lesser stocking rate (LORC 1st-3rd). Cyclic ovarian activity ceased in four Hereford-Shorthorn cows on pastures at a greater stocking rate in late autumn to early winter, and onset of oestrous cycles did not occur in all of these cows until late spring. Oestrous cycles were not detected in one of five cows in the other groups during different periods of the study; however, there were no apparent patterns to cessation of oestrous cycles in these groups. There were no seasonally-related changes in plasma LH in entire cows, at either stocking rate (LORC 10th; r2 = 0.16 to 0.41). In contrast, distinct seasonal fluctuations in plasma LH occurred in ovariectomised cows, with increases in spring and winter. Environmental cues induced greater fluctuations in plasma LH in ovariectomised cows at a greater stocking rate (LORC 3rd-5th; r2 = 0.71 to 0.72) compared with ovariectomised cows at a lesser stocking rate (LORC 3rd-5th; r2 = 0.53 to 0.58). The findings demonstrated that marked seasonal changes in reproductive activity of the hypothalamic pituitary axis can occur in cows with B. indicus and B. taurus genotypes in a subtropical environment; however, changes in plasma concentrations of LH are only apparent in ovariectomised cows. Concentrations of plasma LH in ovariectomised Brahman and Hereford-Shorthorn cows increased during winter, when pasture availability was limiting and cyclic luteal function ceased in four of five Hereford-Shorthorn cows.

The requirement for endogenous LHRH and LH action in the maintenance of elevated plasma concentrations of testosterone in bulls receiving the LHRH agonist deslorelin was examined. In Experiment 1, bulls were either (i) left untreated (control); (ii) implanted with deslorelin; (iii) actively immunized against LHRH; or (iv) implanted with deslorelin and immunized against LHRH. Experiment 2 was of similar design to Experiment 1, except that bulls were immunized against LH in place of LHRH. In Experiment 1, plasma LH declined in bulls immunized against LHRH, but not in the bulls immunized against LHRH and implanted with deslorelin. Also in Experiment 1, plasma testosterone declined in bulls immunized against LHRH but was elevated in bulls treated with deslorelin and bulls treated with deslorelin and immunized against LHRH. In Experiment 2, bulls immunized against LH and treated with deslorelin had plasma concentrations of testosterone similar to controls, whereas bulls treated only with deslorelin had elevated plasma testosterone. It was concluded from these experiments that endogenous LHRH action was not required for increased steroidogenic activity in bulls treated with a LHRH agonist. However, circulating LH was necessary for increased plasma testosterone in bulls implanted with deslorelin. LH is therefore involved in mediating the response of bulls to treatment with deslorelin, either by acting directly at the testes or through a permissive role that allows a direct action of deslorelin at the testes.

Agonists of GnRH were examined for their potential to achieve controlled, reversible suppression of estrous cycles in beef cattle. In Exp. 1, cyclic heifers received two (Group B2) or four (Group B4) buserelin (D-Ser[Bu(t)]6-Pro9-LHRH[1-9] nonapeptide ethylamide) implants and degree of cessation of estrous cycles was monitored. Treatment with buserelin caused estrous cycles to cease, as indicated by basal (.2 ng/mL) concentrations of progesterone, for 48.4 +/- 3.8 d (mean +/- SEM) in Group B2, which was less (P = .6) than the 87.4 +/- 17.4 d in Group B4. In Exp. 2, heifers treated with one (Group D1) or two (Group D2) implants of deslorelin (D-Trp6-Pro9-des-Gly10-LHRH ethylamide) had basal progesterone concentrations for 203 +/- 26 d (Group D1) and 170 +/- 28 d (Group D2; P > .05). In Exp. 3, stage of the estrous cycle was synchronized in cows, and, on d 7 of the ensuing cycle, cows received four deslorelin implants for 28 (Group D28) or 56 d (Group D56). Treatment with deslorelin induced an acute increase in plasma concentrations of immunoactive and bioactive LH, which remained increased over 7 d of observation. Based on profiles of progesterone, cows did not develop a functional corpus luteum during deslorelin treatment. Days to first and second estrus after implant removal were similar for cows in Group D28 (23.6 +/- 2.1 and 40.2 +/- 4.2 d, respectively) and Group D56 (21.5 +/- 3.3 and 44.3 +/- 2.9 d). The findings indicated that GnRH agonists block estrous cycles in cattle. Also, estrous cycles returned after discontinuation of treatment. Furthermore, the consistent and predictable responses detected in cows after implant removal indicated that agonists should be suitable for achieving a controlled, reversible suppression of estrous cycles in cattle.