Summary. This study examined the effects of varying treatment durations and doses of adrenocorticotrophin (ACTH) as well as restraint stress on the LH response to exogenous LHRH. Injection of 80 i.u. of a concentrated ACTH preparation at 11, 6, 3 or 1·5 h before LHRH administration was effective in suppressing the LH response. Injection of 40, but not 20 or 10, i.u. ACTH 3 h before an LHRH challenge inhibited the magnitude of the LH response, while cortisol values did not vary between ACTH doses. Injection of 200 μg of synthetic ACTH1–24 also resulted in a reduced LH response when given 3 h before LHRH. Restraint stress caused elevated corticosteroid levels and reduced LHRH responsiveness. The results of this study suggest that stress may cause an inhibition of pituitary gland ability to respond to LHRH by way of an hormonal component of the adrenocortical axis. A glucocorticoid-independent mechanism may be involved.
R. L. Matteri, J. G. Watson, and G. P. Moberg
A. Krishna, P. F. Terranova, R. L. Matteri, and H. Papkoff
Summary. Constant infusion of LH (400 μg NIH-S24) through an osmotic minipump inserted on Day 1 (oestrus) of the cycle in the hamster resulted in spontaneous superovulation (≃ 29 ova) at the next expected oestrus, increased blood flow (P<0·001) to the ovary on Day 3, and slight depletion (0·1 >P>0·05) of histamine in the ovary. Treatment with antihistamine (alpha-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, or cimetidine, an H2 blocker) by injections or by infusion using separate osmotic minipumps significantly (P<0·01) reduced the number of ova shed in the LH-treated hamsters. Infusion of LH with alpha-fluoromethylhistidine in the same osmotic minipump reduced the bioactivity of the LH. Infusion of antihistamine alone did not alter the normal number of ova shed. The results suggest that the LH-induced superovulation involves stimulation of histamine release; the histamine then may increase ovarian blood flow thus allowing more gonadotrophins to reach the ovary.
G. P. Adams, R. L. Matteri, and O. J. Ginther
Summary. The hypothesis was tested that greater growth of the dominant follicle of wave 1 (first follicular wave of an interovulatory interval), compared with that of subsequent anovulatory waves, is due to lower circulating concentrations of progesterone during the growing phase of the follicle. Control heifers (n = 6) were compared with heifers (n = 6) treated with a decreasing dose of progesterone from day 0 to day 5 (ovulation = day 0). Maximum diameter (12·7 ± 0·9 versus 15·3 ± 0·7 mm) and mean diameter of the dominant follicle of wave 1, averaged over days, were smaller (P < 0·05) in the progesterone-treated than in the control group. Progesterone treatment did not suppress circulating follicle-stimulating hormone (FSH); but the second FSH surge was earlier, resulting in earlier emergence of wave 2 as indicated by a tendency (P ≤ 0·1) for group × day interactions attributed to earlier detection of the dominant follicle and an earlier rise in the total number of follicles detected. The stated hypothesis was supported.
We also tested the hypothesis that exposure to low circulating concentrations of progesterone at the end of the growing phase of the anovulatory dominant follicle of wave 1 results in continued growth and prolonged maintenance of the dominant follicle. Heifers (n = 6 per group) were given a luteolytic dose of prostaglandin F2α (PGF2α) on day 6 and treated with a low (30 mg day−1), physiological (150 mg day−1), or high (300 mg day−1) dose of progesterone on days 6 to 20. Continued periodic emergence of anovulatory follicular waves occurred (2·1 ± 0·0 waves, 2·8 ± 0·2 waves, 3·8 ± 0·3 waves, respectively; P < 0·05) until treatment was stopped (interovulatory intervals: 26·2 ± 1·0, 30·8 ± 0·6 and 40·3 ± 1·7 days, respectively; P < 0·05). Compared with the physiological dose group, the growth of the dominant follicle was inhibited to a lesser degree in the low-dose group since it grew for longer (P < 0·05) and to a larger diameter (P < 0·05), and persisted for longer (P < 0·05). Prolonged dominance of this oversized (> 20 mm) follicle was associated with delayed emergence of wave 2. The hypothesis was supported. Results also showed that the high dose of progesterone suppressed the dominant follicle more than the physiological dose when given during the growing phase, but not when given after the growing phase. The suppressive effects of progesterone were not mediated by decreased circulating FSH, since progesterone treatment did not suppress FSH. Collectively, the results demonstrated that progesterone inhibited the dominant follicle in a dose-dependent manner when the follicle was exposed during its growing phase.
Keywords: progesterone; follicle-stimulating hormone; follicles; follicular waves; ultrasound; cow
G. P. Adams, R. L. Matteri, J. P. Kastelic, J. C. H. Ko, and O. J. Ginther
Summary. The effects of ablation of a dominant follicle and treatment with follicular fluid on circulating concentrations of follicle-stimulating hormone (FSH) were studied and the temporal relationships between surges of FSH and follicular waves were studied in heifers with two or three follicular waves/interovulatory interval. Cauterization of the dominant follicle on Day 3 or Day 5 (ovulation on Day 0) (six control and six treated heifers/day) resulted in a surge (P < 0·05) in FSH beginning the day after cautery. The FSH surge prior to wave 2 (first post-treatment follicular wave) occurred 4 days (Day 3 cautery) and 2 days (Day 5 cautery) before the surge in control groups, corresponding to a 4-day and a 2-day advance in emergence of wave 2 compared with controls. It was concluded that the dominant follicle on Day 3 and Day 5 was associated with the suppression of circulating FSH concentrations. Heifers (n = 4/group) were untreated or treated intravenously with a proteinaceous fraction of bovine follicular fluid on Days 0–3, 3–6, or 6–11. Concentrations of FSH were suppressed (P < 0·05) for the duration of treatment, regardless of the days of treatment. Cessation of treatment was followed within 1 day by the start of a surge in FSH. The FSH surge prior to wave 2 occurred 2 days earlier (treatment on Days 0–3), 1 day later (treatment on Days 3–6), and 6 days later (treatment on Days 6–11) than in controls, corresponding to an equivalent advance or delay, respectively, in the emergence of wave 2 compared with controls. The results suggest that the effects of exogenous follicular fluid on follicular development were mediated, in whole or in part, by altering plasma FSH concentrations. Control heifers combined for the two experiments were separated into those with 2-wave (n = 11) or 3-wave (n = 5) interovulatory intervals. Two-wave heifers had two FSH surges and 3-wave heifers had three apparent FSH surges during the interovulatory interval. Results of the cautery and follicular fluid experiments indicated that a surge in FSH necessarily preceded the emergence of a wave. The FSH surges in treated and control heifers began 2–4 days before the detectable (ultrasound) emergence of a follicular wave (follicles of 4 and 5 mm), peaked 1 or 2 days before emergence and began to decrease approximately when the follicles of a wave begin to diverge into a dominant follicle and subordinate follicles (follicles 6–7 mm).
Keywords: FSH; follicles; follicular waves; follicular fluid; inhibin; heifer