1.
An experiment was designed to evaluate the effects of estradiol‐17β (E17β) on follicular wave dynamics and ovulatory response in Holstein heifers receiving either a progestogen ear‐implant (Crestar
®; Intervet International b.v. Boxmeer, The Netherlands) or an intravaginal progesterone‐releasing device [controlled internal drug release‐bovine device (Eazibreed, CIDR‐B
®; Bodinco BV, Alkmaar, The Netherlands)]. For comparison, another group of heifers was also synchronized using Crestar plus an injection of estradiol valerate (EV) and norgestomet as recommended by the pharmaceutical company. Twenty 20–22‐month‐old cycling Holstein heifers were allocated to one of the following treatment groups at random stages of the oestrous cycle: (I) simultaneous insertion of Crestar and intramuscular injection of 3 mg norgestomet and 5 mg EV (Crestar 9 + EV 9); (II) simultaneous insertion of Crestar and intramuscular injection of 5 mg E17β (Crestar 9 + E17β 9); (III) insertion of Crestar followed 2 days later by intramuscular injection of 5 mg E17β (Crestar 9 + E17β 7); or (IV) insertion of CIDR‐B device followed 2 days later by intramuscular injection of 5 mg E17β (CIDR 9 + E17β 7). The CIDR‐B or Crestar implants were removed after 9 days and all heifers received 500
μg Cloprostenol (Estrumate
®, Pitman‐Moore Nederland BV, Houten, The Netherlands). Ovarian ultrasonographic examinations were performed once daily during the synchronization period using a B‐mode scanner equipped with a 7.5 MHz linear‐array transrectal transducer. In addition, heifers were scanned every 12 h after implant/device withdrawal until 3 days after ovulation in order to monitor follicular activity, detect ovulation and subsequent early luteal formation. Detection of oestrus was performed every 6 h for 4 days after device/implant removal. Oestrus was observed 24–32 h before ovulation in all heifers. The mean hours interval from treatment withdrawal to ovulation was not significantly different (84.0 ± 16.5, 77.6 ± 4.1, 73.6 ± 4.1 and 64.0 ± 4.4 h for treatments I, II, III and IV, respectively; p > 0.1). However, the variance for heifers treated with EV + norgestomet was significantly larger (Levene’s Test; p < 0.01) than those treated with E17β. All E17β treatments resulted in dominant follicle suppression and a new wave emerged 4.1 days after treatment compared with 6.6 days for the EV + norgestomet treatment (p < 0.05). The time from emergence of the new ovulatory wave to ovulation was longer for the new wave that emerged after E17β treatment (9.2 ± 0.3 days) than after EV + norgestomet treatment (6.9 ± 0.4 days; p < 0.05). The results of this study suggest that the four treatments used were effective in inducing synchronous behavioural oestrus and ovulation. However, a higher degree of oestrus and ovulation synchrony was observed in heifers treated with E17β than in heifers treated with EV + norgestomet. Synchronization treatments with exogenous E17β or EV + norgestomet at the time of progestin device insertion (Crestar or CIDR‐B) or 2 days later in heifers can regulate a different emergence pattern of ovarian follicular development in randomly cyclic heifers. The E17β was effective in inducing follicular suppression and resulted in the consistent emergence of a new follicular wave.
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