Intraperitoneal injection of 50 IU PMS on Days 1–3 after mating resulted in the early transport of ova from the rat tube into the uterus. This effect was less markedly shown in the hamster but retardation of cleavage was observed in a few cases. When 100 IU HCG was injected, tubal transport was not markedly accelerated in either the rat or the hamster. Following treatment with 50 IU PMS on Days 1–3, no living embryos were found in rats and hamsters killed on Days 16 and 13, respectively. Implantation was inhibited in the rat, though not in the hamster. It also failed when normal blastocysts were transferred synchronously into the PMS-treated rats. Implantation did occur in rats treated with various doses of PMS on Days 5–7, but fetal mortality (54–100%) increased proportionately with the dose. A single dose of 100 IU PMS on one of Days 5, 7, 9 and 11 in the rat induced 67, 92, 75 and 56% fetal mortality, respectively. Administration of 100 IU HCG on Days 1–3 had a slight effect on preand post-implantation losses in the rat. The same treatment in the hamster reduced the number of implantation sites and provoked considerable embryonic mortality (73%). Although rats proved relatively more sensitive to PMS than HCG given during implantation, the effects of HCG given at this time are seen more readily in the hamster than in the rat. A single dose of 100 IU HCG given to the hamster on one of Days 4, 6, 8 and 10 induced 13, 92, 39 and 24% embryonic mortality, respectively. Supplemental treatment with progesterone in the rat and hamster did not reduce the adverse effect on pregnancy in the PMS-treated females, but was beneficial in animals ovariectomized at the time of blastocyst formation. It thus seems likely that antifertility effects of PMS may have been due to abnormal steroid production in the ovary. (Endocrinology83: 217, 1968)
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Yang et al. (1968) studied this question.