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Studies using in-vitro culture (Brinster, 1969; Whitten, 1970), in-vitro microsurgery (Gardner, 1968), and embryo transfer to ectopic sites (Fawcett, 1950; Kirby, 1962, 1969) have shown that before blastulation the mammalian ovum develops independently of its uterine environment. After this time the blastocyst becomes less autonomous and development depends increasingly on the local environment. Evidence for dependence upon the uterine milieu also arises from experiments on the transfer of embryos between donor and recipient animals and the transfer of blastocysts to ectopic sites, and from investigations of the phenomenon of delayed implantation. In this paper we consider the nature of the interaction between the endometrium and the blastocyst and indicate where interception may inhibit maternal or embryonic signals which are indispensible for implantation and the establishment of pregnancy.

This study examined the effects of LH and PGE2on progesterone secretion by small and large porcine luteal cells with or without low-density lipoproteins. Corpora lutea were isolated from gilts 13–14 days after administering gonadotrophins; enzymatically dissociated and small and large cells were isolated by elutriation. Culture plates, 24-well, were then seeded with 150 000 small or 30 000 large luteal cells suspended in 1 ml M199 medium supplemented with 5 μg insulin ml−1, 40 ng hydrocortisone ml−1and with or without low-density lipoproteins (50 μg cholesterol ml−1) or PGE2. Cells were cultured for up to 24 h in a humidified incubator at 37°C under 5% CO2in air. The low-density lipoproteins stimulated (P< 0.05) progesterone secretion by large, but not small, luteal cells. Prostaglandin E2 stimulated (P< 0.05) progesterone production by large luteal cells in a dose-dependent manner, and the stimulatory effects of PGE2were greater (P< 0.05) in the presence than in the absence of low-density lipoproteins. Progesterone secretion by small luteal cells was not significantly affected by PGE2. Progesterone production by small luteal cells was enhanced (P< 0.05) by LH, and the stimulatory effects of LH were greater (P< 0.05) in the presence than in the absence of low-density lipoproteins. In the absence of these lipoproteins, LH had no effect on progesterone secretion by large luteal cells; however, in the presence of low-density lipoproteins, LH increased (P< 0.05) progesterone secretion by large cells, though to a lesser (P< 0.05) extent than the effect of LH on small cells. These data demonstrate that progesterone secretion by porcine luteal cells is stimulated differentially by LH and PGE2 and that small luteal cells are more responsive to LH and PGE2 acts primarily on large luteal cells.

Summary.Oestrogen synthesis by the early embryo in vitrowas studied with tissue from pigs, sheep, cows, roe deer, ferrets, cats, rabbits and a plains viscacha. Definitive evidence for aromatase activity and oestrogen synthesis in preimplantation trophoblast was obtained for the pig with the formation of oestrone, oestradiol-17β and oestradiol-17α from3H-labelled androstenedione and dehydroepiandrosterone. Aromatase activity was appreciably lower in all other species studied, and labelled oestrogens were recovered only from incubations of allantochorionic tissue of roe deer, recovered shortly after implantation, and from pooled samples of early embryonic tissue of cows. High aromatase activity in preimplantation trophoblast of pigs was associated with the maternal recognition of pregnancy and the occurrence of superficial implantation in this species.

In these studies the beta-adrenergic receptor antagonist propranolol was administered to estrogen-treated hypophysectomized pseudopregnant rabbits in vivo, and serum progesterone concentrations were measured to monitor luteal function. In Experiment 1, which was designed to determine an effective dose of propranolol, 1 mg/(kg X h) s.c. propranolol for 3 h (integral of 80 ng/ml in serum) gave an adequate level of beta-adrenergic receptor blockade, i.e., a 1000-fold inhibition of the blood pressure/isoproterenol dose-response relationship. In Experiment 2, "acute" administration of propranolol (P; 1 mg/(kg X h) s.c.) or saline (control, C) for 24 h on Days 7-8, 10-11, and 13-14 of pseudopregnancy did not produce any marked differences in serum progesterone concentrations in P or C animals on any of the days tested, although hourly fluctuations were observed. In Experiment 3, "chronic" (4-day) treatment with propranolol was achieved by the use of propranolol-containing pellets placed s.c. (integral of 200-600 ng/ml in serum), on Days 13-17. Control animals received pellets of vehicle only. Serum progesterone concentrations were very similar in P and C animals throughout the period of treatment (Days 13-17) and on Days 18 and 20. We conclude that endogenous catecholamines play no major role in regulating luteal steroidogenesis or corpus luteum regression in the pseudopregnant rabbit.