Effects of PGF2α and indomethacin on ovulation and steroid production in the isolated perfused rabbit ovary
Abstract. Both ovaries of 31 rabbits were perfused with a chemically defined medium in vitro in a recirculation system. In one series of experiments, hCG (100 IU) was injected iv 5–6 h prior to anaesthesia and surgery. Approximately 1 h later the perfusion was started. One ovary was perfused as control while the other ovary was perfused with 5 μg/ml indomethacin or with indomethacin and 1 μg/ml PGF2α. In another series of experiments the rabbits received no pretreatment prior to operation. Instead, bovine LH was added to the perfusion medium of both control and experimental ovaries. The experimental side also received either indomethacin or indomethacin and PGF2α. Finally, the effect of PGF2α in the absence of LH was compared to the control ovary receiving only LH. After injection of hCG in vivo, ovulations occurred in 4 of 5 control ovaries. Indomethacin completely blocked ovulation in 4 of the 5 ovaries treated, while PGF2α restored ovulations in all the experimental ovaries. In the group of experiments where LH was added in vitro, ovulations were induced in all ovaries treated with varying LH doses. Furthermore, indomethacin blocked ovulation in 5 out of 7 ovaries, and PGF2α restored ovulation in all ovaries. Fifty per cent of the ovaries treated only with PGF2α (in the absence of LH) also ovulated. The pattern of steroid release did not differ between control ovaries, indomethacin treated ovaries, and indomethacin + PGF2α treated ovaries. Ovaries treated in perfusion with PGF2α alone had very low steroid levels compared to the ovaries treated with LH. This study confirms that indomethacin blocks ovulation in the perfused rabbit ovary and that this blockade can be overcome by exogenous PGF2α. Indomethacin and PG-treatments after ovulation induction did not affect ovarian steroidogenesis. Furthermore, while PGF2α was able to induce ovulations in these perfused oestrous ovaries in the absence of LH, it did not stimulate steroidogenesis.