Abstract

Plasma LH concentrations were monitored in post-partum beef cows treated with the GnRH agonist Buserelin, administered via biodegradable implants. Animals were given either untreated Buserelin implants (Group 1, n = 6) or implants that had been preincubated for 7 (Group 2, n = 6) or 14 (Group 3, n = 6) days. Control cows were sham-implanted (Group 4, n = 3). The implants were inserted subcutaneously at a mean time of 25 ± 2.8 days after caiving, and LH concentrations were monitored over 8 h periods of blood sampling (samples taken at 10 min intervals) undertaken on Days — 2, 1, 2, 3, 7, 14, 21 and 28 (Day 1 was the day of implantation). In all animals treated with Buserelin, plasma LH concentrations increased within 1 h of implantation to reach a maximum concentration (mean 35.4 ± 2.86 ng ml −1) within 4 h. In all three Buserelin-treated groups, mean LH concentrations were higher on Day 1 ( P < 0.001) and on Days 2 and 3 ( P < 0.05) than on Day — 2, before the start of treatment. On subsequent sampling days (Days 7, 14, 21 and 28), mean LH concentrations did not differ significantly from pretreatment values, but on Days 14, 21 and 28, mean LH concentrations were lower ( P < 0.05) in Buserelin-treated than in control cows. There were no significant differences in either the magnitude or the duration of the LH response between Buserelin treatment groups. Before treatment, LH episodes occurred with a mean frequency of 1.9 ± 0.4 episodes per 8 h, and in control cows occurred at a frequency of 2.3 ± 0.2 episodes per 8 h throughout the 28-day sampling period. In contrast, LH episodes were not recorded in any of the Buserelin-treated cows on the first 3 days after implantation, and were recorded in only 1 of 18, 2 of 18, 1 of 18 and 4 of 18 animals on Days 7, 14, 21 and 28, respectively. Following luteal regression, plasma progesterone concentrations remained low for the remainder of the sampling period (mean 18.2 ± 1.2 days) in 17 of 18 Buserelin treated cows. These results demonstrate that Buserelin treatment induces a short period of increased LH secretion, after which there is a prolonged period of suppression of LH release which blocks ovulation.

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