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Summary. A study was conducted to determine the timing of ovulation relative to the onset of oestrus and the preovulatory LH surge in fallow deer. Mature fallow does were randomly allocated to two treatments (N = 10 per treatment) designed to synchronize oestrus on or about 17 May. Does assigned to Group 1 (prostaglandin-induced oestrus) each initially received single intravaginal CIDR [Controlled Internal Drug Release] devices for 13 days followed by an i.m. injection of 750 mg cloprostenol on Day 12(15 May) of the subsequent luteal cycle. Does assigned to Group 2 (progesterone-induced oestrus) each received CIDR devices for 13 days, with withdrawal occurring on 15 May. All does were run with crayon-harnessed bucks (10:1 ratio) from the start of synchronization (18:00 h 15 May). Ten does (5 per group) were blood sampled via indwelling jugular cannulae every 2 h for 72 h from cloprostenol injection or CIDR device withdrawal and the plasma was analysed for concentrations of progesterone and LH by radioimmunoassay. Does within each treatment were randomly allocated to an ovarian examination time of 12, 16, 20 or 24 h after the onset of oestrus. Laparoscopy was repeated at 12-h intervals until ovulation was recorded. The ovaries of does failing to exhibit oestrus were examined 72 and 86 h after cloprostenol injection or CIDR device withdrawal. A total of 17 does were observed to exhibit oestrus at a mean (±s.e.m.) interval from treatment of 44·6 ± 3·6 h for Group 1 (N = 9) and 34·1 ± 2·5 h for Group 2 (N = 8). The incidence of ovulation from 34 laparoscopic examinations was 0% for intervals <20 h, 50% at 24 h and 100% for intervals >28 h. There was no difference between animals in Groups 1 and 2. The onset of the preovulatory LH surge (n = 8 observations) occurred at the onset of oestrus, with maximum LH surge concentrations (30 ng/ml) occurring 6 h later. Of 3 does not exhibiting oestrus, 2 (Group 2) possessed active corpora lutea at CIDR device withdrawal and 1 (Group 1) possessed a large unruptured follicle 72 and 86 h after cloprostenol injection.
The data indicate that ovulation in fallow deer occurs ∼24 h after the onset of oestrus and ∼ 18 h after the peak of the preovulatory LH surge.
Keywords: fallow deer; reproduction; oestrus; ovulation; progesterone; LH
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Summary. Eighteen ovariectomized fallow deer does and two adult bucks were used to investigate the effect of exogenous progesterone and oestradiol benzoate on oestrous behaviour and secretion of luteinizing hormone (LH). In Expts 1 and 2, conducted during the breeding season (April–September), does were treated with intravaginal Controlled Internal Drug Release (CIDR) devices (0·3 g progesterone per device) for 12 days and differing doses of oestradiol benzoate administered 24 h after removal of the CIDR device. The dose had a significant effect on the proportion of does that exhibited oestrus within the breeding season (P < 0·001), the incidence of oestrus being 100% with 1·0, 0·1 and 0·05 mg, 42% for 0·01 mg and 0% for 0·002 mg oestradiol benzoate. There was a significant log–linear effect of dose on the log duration of oestrus, which was 6–20, 2–14, 2–12 and 2 h after treatment with 1, 0·1, 0·05 and 0·01 mg of oestradiol benzoate, respectively. Dose had a significant effect on the peak plasma LH concentration (P < 0·01), mean (±s.e.m.) surge peaks of 27·7 ± 2·3, 25·9 ± 1·8 and 18·6 ± 3·4 ng/ml being observed following treatment with 1, 0·1 and 0·01 mg oestradiol benzoate respectively. In Expt 3, also conducted during the breeding season, progesterone treatment (0 vs. 6–12 days) before the administration of 0·05mg oestradiol benzoate had a significant effect on the incidence of oestrus (0/6 vs. 10/12, P < 0·05), but not on LH secretion. The duration of progesterone treatment (6 vs. 12 days) had no effect on oestrus. In Expt 4, conducted in the nonbreeding season (October–March), control does were largely unresponsive to treatment with 0·1 mg oestradiol benzoate. This was manifest in a lower proportion of does exhibiting oestrous behaviour and LH surges. Melatonin treatment, with implants administered on four occasions at intervals of 28–30 days starting from 24 October, significantly increased the proportion of does that exhibited oestrus in February, during the later phase of the nonbreeding season (7/8 vs. 1/8, P < 0·05). Melatonin-treated does also exhibited significantly higher basal plasma LH concentrations after removal of CIDR devices in February (5·8 ± 0·5 vs. 2·1 ± 0·4 ng/ml, P < 0·01). While only one control doe had an LH surge, with a peak of 13·8 ng/ml, all melatonin-treated does exhibited LH surges, with a mean peak concentration of 58·0 ± 8·4 ng/ml.
Keywords: fallow deer; progesterone; oestradiol benzoate; oestrus; luteinizing hormone
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The luteolytic effect of the prostaglandin F2α analogue, cloprostenol, was investigated in red deer by monitoring concentrations of plasma progesterone, the induction of oestrus and ovulation, and fertility. Oestrus was synchronized in 48 adult hinds by intravaginal delivery of exogenous progesterone for 12 days and i.m. injection of 250 iu pregnant mares' serum gonadotrophin at progesterone withdrawal. A single i.m. dose of 500 μg cloprostenol was administered at day 4, 6, 8, 10, 12, 14 or 16 of the subsequent oestrous cycle (n = 6 hinds per treatment; day 0 = oestrus). Six other hinds were monitored by intensive collection of blood samples between day 16 and day 19 to define changes in plasma progesterone concentrations during spontaneous luteolysis. Samples of jugular blood, collected every second day throughout the study and every 6 h for 78 h from the time of administration of cloprostenol, were analysed for plasma concentrations of progesterone and LH. Oestrus was detected by continuous observation during the period of intensive collection of blood samples and all hinds were subjected to transrectal ultrasonography to assess pregnancy status. On the basis of changes in plasma progesterone concentrations, cloprostenol induced complete luteolysis in all hinds treated on days 8–16 and in five of six hinds treated on day 6. Oestrus, ovulation and conception occurred in 25 (69%), 28 (78%) and 25 (69%), respectively, of hinds treated on days 6–16 inclusive (n = 36). Luteolysis was incomplete in all hinds treated on day 4, and none of the animals exhibited oestrus or ovulated; luteolysis was incomplete for one hind treated on day 6. Short luteal cycles (< 12 days duration) occurred in six hinds following cloprostenol treatment, but this occurred only in hinds treated on day 6 (n = 3), day 8 (n = 1) or day 10 (n = 2). The mean intervals from injection of cloprostenol to onset of oestrus and peak preovulatory LH surge values were significantly shorter for hinds treated on day 6 or day 8 (∼50 h and 52 h for oestrus and LH surges, respectively) than for those treated on days 10–16 inclusive (60 h and 65 h, respectively) (P < 0.05). It is concluded that on day 4 of the cycle, the cervine corpus luteum is refractory to a single injection of the prostaglandin analogue, whereas on day 6 the corpus luteum is responsive in most animals, and that whereas corpora lutea at days 8–10 are responsive in all animals, a high incidence of subsequent premature luteal regression may occur. Fertility to cloprostenol-induced oestrus and ovulation following natural mating was high, especially for hinds treated on days 12, 14 and 16 of the oestrous cycle (i.e., >80% conception rate).
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The effects of administration of exogenous melatonin to pregnant red deer hinds on prolactin secretion, lactogenesis and reproductive seasonality were studied. Mature hinds (n = 23) were allocated to one of four treatments. Hinds in treatment 1 (n = 6) each received two subcutaneous melatonin implants (Regulin) at monthly intervals starting on 2 October, about 80 days before expected parturition. Hinds in treatment 2 (n = 6) received similar treatment starting on 2 November, about 40 days before calving, whereas hinds in treatment 3 (n = 5) received treatment starting on the actual day of calving (about 10 December). Final implants were delivered on 1 February, with overall treatment durations of 150, 120 and 90 days for treatments 1–3, respectively. Hinds in treatment 4 (n = 6) served as controls and received no melatonin treatment. Blood samples were taken twice a week from September to May, and plasma was analysed for progesterone and prolactin. Mammary development was assessed by palpation score (0–5) twice a week from October to April inclusive, and liveweights were recorded at least every two weeks throughout the trial. Calving occurred between 28 November and 24 December, with no significant differences among treatments (P > 0.10). Hinds in treatment 1 exhibited significant retardation of mammary gland development and liveweight gain leading up to parturition (P < 0.01). Furthermore, sex-adjusted calf birth weights were on average 3 kg lighter for treatment 1 (P < 0.05), with all calves either removed for bottle-rearing or having died within a few hours of birth. Failure of lactogenesis in treatment 1 was characterized by the presence of underdeveloped, hard mammary tissue devoid of expressible milk. Hinds in treatments 2–4 all exhibited full lactation and successfully reared their calves, and there were no significant differences in calf weaning weight and growth rates. Likewise, there were no significant differences in mean liveweight or lactation score profiles. Mean plasma prolactin concentrations varied significantly between treatments (P < 0.05), and control hinds exhibited a marked seasonal pattern of secretion which reached a peak at calving. However, hinds in treatments 1 and 2 failed to show any discernible seasonal increase in mean plasma prolactin concentrations, whereas there was a marked increase in mean prolactin concentrations in hinds in treatment 3 up to parturition, but concentrations decreased rapidly thereafter relative to those of control hinds. Melatonin treatment significantly advanced the date of first oestrus and decreased the postpartum–oestrus interval (P < 0.05). It was concluded that initiation of melatonin implant treatment about 80 days before parturition compromises mammary and fetal development in red deer hinds. However, the role of prolactin was not demonstrated conclusively.
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Summary. The timing of ovulation relative to the onset of oestrus and the preovulatory surge in luteinizing hormone (LH) was studied in red deer following treatments to synchronize oestrus and induce either a monovulatory or superovulatory response. Mature hinds (n = 36) were allocated randomly to two mating groups (n = 16 + 20), with respective treatments staggered by 4 weeks during the 1990 rut (March–April). Each hind was treated with an intravaginal controlled internal drug releasing (CIDR)-type S device for 14 days. Treatments to induce a monovulatory response included CIDR device alone (treatment A; n = 4 + 8) and additional injection of 200 iu pregnant mares' serum gonadotrophin (PMSG) at device removal (treatment B; n = 4 + 4). Treatments to induce a superovulatory response included injections of 200 iu PMSG and 0·5 units ovine follicle-stimulating hormone (FSH) at about time of removal of CIDR devices (treatment C; n = 4 + 4) and further treatment with gonadotrophin-releasing hormone (GnRH) analogue 18 h after removal of CIDR devices (treatment D; n = 4 + 4). The hinds were run with crayon-harnessed stags from insertion of CIDR devices (12 March or 9 April) and blood samples were taken every second day to determine plasma progesterone. Further blood samples were collected for determination of plasma LH and progesterone via indwelling jugular cannulae every 2 h for 72 h from removal of CIDR devices. Hinds were allocated randomly to an initial ovarian examination by laparoscopy at either 16 or 20 h (A and B), or 12 or 16 h (C and D) after the onset of oestrus, with laparoscopy repeated at intervals of 8 h until either ovulation was recorded (A and B), or for four successive occasions (C and D). All hinds received cloprostenol injections 15 days after device removal.
A total of 28 hinds (78%) exhibited oestrus and a preovulatory LH surge, with mean (± sem) times to onset of oestrus of 44·6 ± 1·0 h (A; n = 7), 37·4 ± 2·0 h (B; n = 7), 16·3 ± 1·7 h (C; n = 6) or 14·0 ± 1·7 h (D; n = 8). Failure to exhibit oestrus or LH surge was most prevalent among hinds in treatment A early in the rut. For all treatments, the onset of oestrus occurred between 8 h before and 8 h after the LH peak and the mean (± sem) interval from onset of oestrus to (first) ovulation was 24·7 ± 1·0 h, 20·6 ± 1·0 h, 20·0 ± 2·9 h and 22·0 ± 3·2 h for treatments A–D, respectively. Superovulation was characterized by nonsynchronous ovulations, with no apparent differences between treatments C and D. Initial ovarian examination showed that 4·5% of total (day 15) ovulations had occurred 12–16 h after oestrus, increasing progressively to 80·7% by 36–40 h, indicating poor ovulation synchrony. The overall mean ovulation rate was 8·8 ± 1·1. Concentrations of progesterone during the luteal phase were correlated with ovulation rate. Administration of cloprostenol 15 days after removal of CIDR devices promoted luteal regression in all hinds, but return to oestrus occurred over seven days and two superovulated hinds retained multiple embryos to term despite treatment.
Keywords: red deer; oestrus; ovulation; luteinizing hormone; progesterone