Late luteal rescue in the baboon (Papio cynocephalus)

Numerous studies have used human chorionic gonadotrophin (HCG) administration to study the response of the primate ovary to gonadotrophin stimulation. These studies are generally performed in the luteal phase with very few studies of the follicular phase. We have studied the effect of both HCG and gonadotrophin releasing hormone (GnRH) agonist administered at the early follicular phase in normally cycling baboons (Papio cynocephalus). Five baboons mere treated with increasing doses of HCG for 5 consecutive days starting on day 1 of the cycle and three untreated baboons served as controls. Follicular and luteal phase lengths were determined and serum samples were assayed for progesterone, oestradiol and 17 alpha-OH progesterone. In a separate study, six baboons were treated with GnRH agonist (WY-40972) on days 2-6 of the cycle and saline-treated baboons served as controls (n = 5). Mean peak progesterone concentrations (+/- SE) during the treatment interval were 3.88 +/- 0.56 ng/ml in HCG-treated baboons compared to 0.19 +/- 0.07 ng/ml in controls (P < 0.001). A similar significant increase (P < 0.001) in serum 17 alpha-OH progesterone concentrations was also observed (6.13 +/- 1.12 ng/ml versus 1.13 +/- 0.49 ng/ml). In association with the increase in luteal steroids there was also a significant prolongation of menstrual cycle length from 32.7 +/- 1.2 days in controls to 46.8 +/- 4.9 days in HCG-treated baboons (P < 0.05), which involved prolongation of the follicular phase (16.7 +/- 1.2 days to 29.0 +/- 4.6 days; P < 0.05) with no difference in luteal phase length or progesterone concentrations. In GnRH agonist-treated baboons, mean (I SE) cycle length was prolonged to 46.3 +/- 1.6 days and in saline-treated controls was 32.8 +/- 0.8 days (P < 0.001), again this was completely represented by the change in follicular phase length, from 13.4 +/- 0.7 days in controls to 27.2 +/- 2.1 days in agonist-treated baboons (P < 0.001). In contrast, there was no significant difference in luteal phase length between these two groups (19.4 +/- 0.7 versus 19.2 +/- 1.0 days). The prolongation of the follicular phase was accompanied by significant increases in both progesterone (P < 0.01) and oestradiol (P < 0.01) during GnRH agonist treatment above control concentrations. Luteal phase concentrations of these hormones were not different from controls. These results demonstrate the previously unreported finding that gonadotropin stimulation will rescue the corpus luteum in the next follicular phase.