Abstract

THE first gonadotropic principle to be demonstrated clearly was that derived from human chorionic elements and present in the urine of pregnant women. Since its demonstration in 1927, innumerable studies have catalogued its effects in laboratory animals. There have been few well-controlled studies, however, in the normal human female. Browne and Venning (1) reported increased excretion of pregnandiol and delay of menstruation with relatively small doses of chorionic gonadotropin, although these observations were not confirmed by Brown and associates (2) when they used the same dosage of hormone. Brown and Bradbury (3) later demonstrated unequivocally the luteotropic effect of chorionic gonadotropin in the human. Using relatively large doses of the substance (made possible by more highly purified preparations), they induced pseudopregnancy in women, as evidenced by persistence of the corpus luteum, delay of menstruation, decidual changes in the endometrium and prolonged excretion of pregnandiol. Their results paralleled those of Hisaw (4) in the monkey. Since in the rat prolactin is known to function as luteotropin and is, indeed, necessary for the physiologic activity of corpora lutea, it is logical to ask whether the luteotropic action of chorionic gonadotropin in the human is in any way related to prolactin.

This content is only available as a PDF.
You do not currently have access to this article.