Incidence of atresia or of luteinization without rupture of the dominant ovarian follicle in rhesus monkeys treated with estradiol-17β on day 8 of the menstrual cycle

Previous results have established that 17β‐estradiol (E2) administered in capsules for 24 h on Day 6 of the menstrual cycle results in atresia of the dominant follicle (DF). The present experiment was designed to determine if atresia could be induced similarly as late as Day 8, when the DF is presumably larger, to facilitate biochemical analyses. On the morning of Day 8, laparoscopy was used to confirm the presence of the DF, and 4, 6, or 8 Silastic capsules containing E2 were placed s.c. for 12 or 24 h. Treatment with E2 for 12 h resulted in atresia of the dominant follicle: 2/4,4/5, and 2/5 with 4, 6, and 8 capsules, respectively. Increases in luteinizing hormone (LH) usually occurred following removal of E2 after 12 h; similar increases resulted previously from treatment on Day 6, and are interpreted as the result of removal of E2‐induced negative feedback rather than an effect of positive feedback. In contrast to the efficacy of treatment for 12 h, treatment with E2 for 24 h resulted in a lower incidence of atresia (2/5,1/6, and 1/4 with 4, 6, and 8 capsules), and premature LH surges were seen during treatment in almost all animals, especially with 6 or 8 capsules, initiating luteinization of the DF without ovulation. Regarding intrafollicular changes, E2 treatment resulted in a 10‐fold reduction in follicular fluid concentrations of estrogen, while progesterone (P) levels were augmented; the output of P by granulosa cells in culture was also enhanced by E2 treatment. We conclude that the DF in monkeys remains susceptible to the atretogenic effects of E2 as late as Day 8 of the cycle, but the amount of follicular material recoverable is not increased with the later treatment. Furthermore, the similarity between the luteinized unruptured follicles induced in this study and those occurring spontaneously in women suggests that this model may be valuable in elucidating the factors involved in this source of infertility in women. © 1994 Wiley‐Liss, Inc.