Follicle deviation is characterized by continued growth of the largest (developing dominant) follicle and reduced growth of the smaller (subordinate) follicles. The aim of the present study was to test the following hypotheses: (1). oestradiol contributes to the depression of circulating FSH encompassing follicle deviation and (2). oestradiol plays a role in the initiation of deviation. Heifers were treated with progesterone (n = 5) or antiserum against oestradiol (n = 7) or given no treatment (control; n = 6). On the basis of previous studies, progesterone treatment would decrease LH and thereby the circulatory and intrafollicular concentrations of oestradiol and the antiserum would reduce the availability of oestradiol. Progesterone was given in six 75 mg injections at 12 h intervals beginning when the largest follicle of wave 1 first reached >or=5.7 mm (t = 0 h). Oestradiol antiserum (100 ml) was given in a single injection at t = 12 h. Follicles of the wave were defined as F1 (largest) and F2, according to the diameter at each examination. Blood samples were collected at 12 h intervals during t = 0-72 h. Treatment with progesterone lowered the circulatory concentrations of LH by 12 h after the start of treatment (P < 0.05), and concentrations remained low compared with those of controls during the treatment period. Treatment with oestradiol antiserum had no effect on LH. Both progesterone and the antiserum treatments increased the FSH concentrations compared with controls (P < 0.05), which supports the first hypothesis. The interval from t = 0 h to the beginning of deviation was longer in the progesterone- (51.0 +/- 7.6 h; P < 0.06) and antiserum (51.4 +/- 6.3 h; P < 0.05)-treated groups than in the controls (38.0 +/- 3.7 h), which supports the second hypothesis. There was no difference among groups in the diameters of F1 and F2 at deviation. Reduced diameter (P < 0.05 or P < 0.06) of both F1 and F2 occurred in both the progesterone- and antiserum-treated groups at t = 36 h and 48 h, compared with controls. Follicle retardation occurred in both the progesterone- and antiserum-treated groups despite the high FSH concentrations, whereas LH was altered only in the progesterone-treated group. Therefore, the follicle effect can be attributed to inadequate intrafollicular oestradiol. This interpretation implies a functional local role for oestradiol in the deviation process, independent of the systemic negative effect on FSH.
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