Fetal and maternal adaptations to chronic hypoxia: prevention of premature labor in response to chronic stress.
Both mother and fetus have the remarkable ability to adapt to conditions of chronic hypoxia during the course of gestation. One of these adaptations appears to be mechanisms that prevent premature delivery despite the chronic stress of hypoxia. Our studies in the chronically hypoxic sheep revealed that the fetal adrenal is less responsive to ACTH stimulation. This in turn may prevent a premature rise in cortisol that would normally trigger labor and delivery. In the rat, the myometrium is affected with a decrease in contractile sensitivity to oxytocin following chronic hypoxia. This response is mediated by a significant reduction in myometrial oxytocin receptors. Our preliminary studies have also suggested that this blunting of myometrial responsiveness also occurs in the chronically hypoxic sheep. Taken together, these data indicate an adaptive response by both mother and fetus to prevent preterm delivery in the face of a chronic stress.
Department of Physiology, Loma Linda University School of Medicine, California 92350, USA. cducsay@ccmail.llu.edu
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D000222:Adaptation, Physiological; D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000818:Animals; D005260:Female; D005311:Fetal Hypoxia / Q000503:physiopathology*; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008431:Maternal-Fetal Exchange; D007752:Obstetric Labor, Premature / Q000517:prevention & control*; D010121:Oxytocin / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000502:physiology; D011247:Pregnancy; D051381:Rats; D012756:Sheep; D013312:Stress, Physiological / Q000503:physiopathology; D014590:Uterine Contraction / Q000502:physiology
D010121:Oxytocin; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone