Steroids and cAMP in follicles of postpartum beef cows treated with norgestomet.

To determine time of occurrence of follicular changes that may be associated with the length of the subsequent luteal phase, follicles were collected at different times before ovulation from cows expected to have corpora lutea of short (control) or normal (norgestomet-treated) life span. Beginning on d 20 to 23 postpartum (d 0 of study), 34 crossbred beef cows received either a 6-mg implant of norgestomet for 9 d or served as untreated controls. Ovaries were removed from norgestomet-treated cows on d 6 (N6; n = 9), d 8 (N8; n = 8), or the day after implant removal (N10; n = 8). Control cows were ovariectomized on d 6 (C6; n = 4) or d 10 (CIO; n = 5). The largest and second largest follicles > 8 mm (F1 and F2, respectively) were dissected from the ovaries. Granulosal and thecal layers and follicular fluid were separated and assayed for estradiol-17 beta, progesterone, androstenedione, and testosterone. Cyclic 3'5'adenosine monophosphate (cAMP) was determined in thecal and granulosal tissue. Diameters of the F1 (14.6 +/- 0.4 mm) and F2 (10.6 +/- 0.4 mm) did not differ due to treatment. A greater proportion (P < 0.05) of the F1 (20/33) than of the F2 (4/27) had estradiol:progesterone ratios of > 1 in follicular fluid. Contents of estradiol, androstenedione, and testosterone in theca and granulosa and estradiol in follicular fluid were greater in the F1 than in the F2. An interaction of duration of norgestomet treatment with follicle occurred for contents of estradiol in granulosa and follicular fluid, androstenedione in theca, and testosterone in theca and follicular fluid (all P < 0.05). In each case, steroid content in the F1 was higher for N8 and N10 than for N6, but content in the F2 was lower for N8 and N10 than for N6. Neither thecal nor granulosal contents of cAMP differed due to treatment. Follicular changes associated with normal luteal function, expected after norgestomet treatment, would seem to include a divergence in steroidogenic activity of the F1 and F2 between d 6 and 8 of treatment.