After synchronization of oestrus, normally cyclic heifers (n = 31) received 2500 iu pregnant mares' serum gonadotrophin (PMSG) i.m. and had a progesterone-releasing intravaginal device (PRID) without the oestradiol capsule inserted on day 10 of the oestrous cycle and received 15 mg prostaglandin (PG) i.m. 48 h later. PRIDs were removed 96 h after insertion and 16 heifers received 1.0 mg GnRH i.m. while the controls (n = 15) received 10 ml saline i.m. All heifers were injected with anti-PMSG i.v. 10 h later. Peripheral blood concentrations of PMSG, progesterone, oestradiol and LH were compared. Ovaries were collected on death 7 days after the GnRH or saline injection and the number of corpora lutea counted. Heifers were considered to have responded well (> 60 pmol l⁻¹) or poorly (< 60 pmol l⁻¹) to superovulation on the basis of the oestradiol concentration 24 h after PG administration. During PRID treatment, LH concentrations remained at basal values. In the heifers treated with GnRH, a single LH surge occurred 2.3 ± 0.1 h (sd) after the GnRH injection with a maximum concentration of 14.6 ± 2.3 (sem) μg l⁻¹ and a duration of 6–8 h. In 12 of the 15 control heifers, LH concentrations remained low (range 0.10–1.94 μg l⁻¹) during the 72 h following the saline injection; three controls showed a spontaneous LH surge at 18, 23 and 23 h after the saline injection, respectively, with a maximum concentration of 6.0–12.5 μg l⁻¹ and a duration of 10–12 h. The oestradiol concentration increased continuously during PRID treatment until the injection of GnRH or saline, when it was four times higher in the heifers that responded well than in the heifers that responded poorly. It decreased sharply 6 h after GnRH indicating that the follicles still responded normally to a preovulatory LH signal, whereas in control heifers a similar decrease took place 4 h later following anti-PMSG treatment. In the GnRH-treated heifers, the heifers responding well showed a significantly higher number of corpora lutea than did the animals showing a poor response, 16.4 ± 2.2 (n = 9) and 5.4 ± 1.4 (n = 7), respectively. Five of the 12 control heifers without an immediate LH surge showed a single corpus luteum, and seven heifers did not have a corpus luteum. For the three controls with an LH surge, 33.0 ± 8.5 corpora lutea were observed. In conclusion, the preovulatory LH signal can be effectively postponed in PMSG/PG-superovulated heifers using a PRID. However, the PRID treatment has to be followed by GnRH to obtain the LH surge at a defined time of preovulatory follicular development. Follicular function with regard to oestradiol secretion and the potential to ovulate remains unchanged.

Normally cyclic heifers (n = 34) received 2500 iu pregnant mares' serum gonadotrophin (PMSG) i.m. at day 10 of oestrus, and 15 mg prostaglandin (PG) i.m. at day 12. Thereafter, a monoclonal antibody against PMSG was administered i.v. before (n = 24), at (n = 6) or shortly after (n = 4) the preovulatory LH surge. Peripheral blood concentrations of LH and oestradiol were compared; follicular development was monitored by daily ultrasound scanning; and the numbers of preovulatory-sized follicles and ovulations were counted 96 h after injection of PG following death. Anti-PMSG treatment before the LH surge inhibited the LH surge in 16 heifers (67%). In these heifers, the initial increase in oestradiol concentration upon PMSG stimulation to 167.5 ± 35.0 pmol l⁻¹ was terminated immediately after anti-PMSG treatment and decreased rapidly to basal values, while the number of preovulatory-sized follicles remained constant until 68 h after PG injection; on average 0.4 ± 0.1 ovulations were counted. In the remaining eight heifers, five animals showed an immediate, but temporary, 20–60% drop in oestradiol concentration after anti-PMSG treatment. In all eight heifers 25% of the preovulatory-sized follicles ovulated. Treatment with anti-PMSG at or shortly after the LH surge did not affect the pattern of oestradiol concentration, but a significantly higher ovulation rate was observed in the animals treated shortly after the LH surge: 20.3 ± 2.6 versus 6.3 ± 2.3 in animals treated at the LH surge, which corresponded to 76% and 24% of the preovulatory-sized follicles monitored shortly before the period of multiple ovulations. Thus, neutralization of PMSG at any time before the maximum concentration of the preovulatory LH surge severely suppresses the functionality of the majority or all of the stimulated follicles, which is dependent on the time of injection of anti-PMSG. Although the follicles retain their size, they lose the potential to ovulate. It is concluded that interfollicular asynchrony of development is present at the time the LH surge occurs.

Summary. Five dogs were hypophysectomized on Day 4 and 9 on Day 18. Prolactin and LH stimulation tests showed that hypophysectomy was complete in 6 dogs only. In these dogs, the progesterone concentration was measured in the peripheral blood; it decreased sharply immediately after surgery. It regained normal values in 3 of the 4 dogs hypophysectomized on Day 4, and remained low in the 2 dogs hypophysectomized on Day 18. This indicates that, in the dog, luteal function is autonomous during a certain period. The luteal period of the 3 dogs hypophysectomized on Day 4 was shorter than that of control animals, although the time of onset of luteal regression appeared to be similar. This indicates that pituitary luteotrophic support is required during the second part of the oestrous cycle of the dog.

The sensitivity of the pituitary to GnRH in early and late anoestrus and the indirect response of the ovary were investigated in six adult beagle bitches. Plasma concentrations of LH and oestradiol were determined after i.v. injection of graded doses of GnRH (0, 0.01, 0.1, 1, 10 and 100 μg kg⁻¹). The responses were measured by the LH and oestradiol concentration profiles over time. The responses of LH and oestradiol were significantly dose dependent (P = 0.002 and P < 0.001, respectively). The responses of LH and oestradiol were significantly higher (P = 0.02 and P = 0.001, respectively) in late anoestrus than in early anoestrus. The responses of LH and the responses of oestradiol were positively correlated (r = 0.97, P = 0.001). It is concluded that during the course of anoestrus in the bitch pituitary sensitivity to GnRH increases while the ovary responds accordingly.

Summary. Pregnant gilts (3/group) were given no treatment, 10 mg bromocriptine twice daily by mouth, from Day 111 of pregnancy to 1 day post partum, 25 mg progesterone s.c. at 6-h intervals from Days 111 to 116 inclusive or 400 mg indomethacin by mouth at 6-h intervals from Day 111 to 116 inclusive. Before spontaneous delivery maternal plasma prolactin and relaxin concentrations started to rise almost simultaneously between 57 and 47 h before the first piglet and both hormones reached peak values when the plasma progesterone concentration had started to decline rapidly (~21–23 h). Suppression of prolactin levels by bromocriptine prevented the onset of lactation completely but had no obvious influence on changes of the other hormone concentrations and the course of parturition. Progesterone treatment delayed the onset of expulsion of the piglets but did not delay the simultaneous increase in prolactin and relaxin concentrations. These changes in hormone levels were prevented by indomethacin treatment but occurred essentially unchanged when the treatment was ended. The results support the concept that parturition in the pig is preceded by a biphasic increase of plasma prostaglandin levels.