Abstrakt: |
The aim of this study was to determine whether daily increasing doses of hCG could overcome luteal regression induced by PGF2αin rhesus monkeys. Prostaglandin F2α(10 ng μl−1h−1) or vehicle (tham buffer; 1 μl h−1) was infused directly into the corpus luteum for 7 days, beginning 7 days after the preovulatory oestradiol surge. hCG was injected i.m. in increasing doses (15, 30, 60, 90, 180, 360 and 720 iu) for 7 days, starting on the eighth day after the preovulatory oestradiol surge, or 1 day after the initiation of luteal infusion of PGF2αor vehicle. Monkeys receiving vehicle plus hCG on the same days served as controls. Daily progesterone, oestradiol and hCG concentrations were determined from blood drawn from the saphenous or femoral vein, and the duration of the luteal phases were recorded. Where intraluteally infused PGF2αresulted in premature, functional luteolysis, hCG always inhibited the luteolytic effect of PGF2α; the secretory patterns of progesterone and oestradiol were augmented, and peak values were reached in concert with the highest concentration of hCG in the blood, and the luteal phase was significantly increased compared with those of untreated monkeys or with monkeys treated with PGF2αalone or vehicle. Treatment with hCG alone or with PGF2αvehicle also resulted in maintained luteal function and a significantly longer luteal phase, but both progesterone and oestradiol concentrations began to decline before hCG reached peak values in the circulation. Once the hCG regimen was concluded, luteal regression ensued and menses occurred at a time coincident with decreased steroid endometrial support. These results are the first to show that hCG can inhibit luteal regression induced by PGF2αin vivo, and are contrary to results obtained in vitrousing minced or sliced luteal cells, which indicates that PGF2αinhibits the trophic action of LH or hCG on progesterone secretion. We conclude that in the rhesus monkey, hCG can completely abolish the luteolytic effect of PGF2αthrough an unknown mechanism. |