Intraperitoneal injections in the rat of 12 IU ACTH on Days 1, 2 and 3 after mating resulted in a marked inhibition of both implantation and fetal development to 57 and 29%, respectively, of control values, but did not alter the rate of tubal transport or development of the ova. Following similar treatment with 3, 6 or 12 IU ACTH on Days 5, 6 and 7, both implantation and fetal development were reduced (to 80, 74 and 57% and 75, 61 and 39%, respectively). About 52% of the blastocysts transferred from donors receiving 12 IU ACTH on Days 1, 2 and 3, and 56% of the blastocysts from untreated donors developed into normal fetuses when transferred to the left or right uterine horns of recipients. Daily injections of 12 IU ACTH on Days 5, 6 and 7 with implants of 10 mg cortisone pellet on Day 5 resulted in a significantly high fetal mortality in intact females but not in females adrenalectomized on Day 5. In pregnant rats adrenalectomized on Day 5, a 10 mg corsisone pellet maintained pregnancy, whereas smaller (5 mg) or larger doses (20 or 40 mg) we re less effective. It thus seems likely that the effect of ACTH on the embryos was chiefly an indirt ct effect mediated through the adrenal gland, a:id that the antifertility effect of ACTH was {attributable to excessive production of corticosseroids by the adrenal. (Endocrinology84: 1282, 1969)
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Yang et al. (1969) studied this question.