The influence of the fetal hypothalamus and pituitary on the onset and course of parturition.
The possibility that the fetal brain or pituitary either initiates parturition or influences the course of labour was studied in human and rat. The results when corticotropin or neurohypophysial hormones were injected directly into human anencephalic fetuses in utero, and data obtained from 147 clinical records of such fetuses, seemed to show that the fetal brain does not trigger the onset of parturition. On the other hand, the course of labour was seriously protracted in anencephalic fetuses. Gestation length of brain-aspirated rat fetuses was not significantly longer than in sham-operated controls. However, the course of labour was protracted in the brain-aspirated fetuses. A similarly protracted expulsion pattern was observed in Brattleboro rats homozygous for a hypothalamic form of diabetes insipidus. These data all pointed to the likelihood that fetal neurohypophysial hormones stimulate the course of labour. Neither oxytocin nor vasopressin could be demonstrated in the rat fetus on the last day of pregnancy, when specific immunofluorescence was used. However, a closely related compound was found that was identified as most probably being vasotocin. The hypothesis is put forward that this fetal hormone normally stimulates the course of labour.
D000757:Anencephaly / Q000196:embryology; D000818:Animals; D001921:Brain / Q000196:embryology; D005260:Female; D005333:Fetus / Q000502:physiology*; D006801:Humans; D007745:Labor Onset; D007743:Labor, Obstetric; D010902:Pituitary Gland / Q000196:embryology*; D011247:Pregnancy; D051381:Rats; D014668:Vasotocin / Q000502:physiology
D014668:Vasotocin