Studies on experimental growth retardation in sheep. The effects of maternal hypoxaemia.
Intrauterine growth retardation in fetal sheep was caused by removal of endometrial caruncles prior to conception. Such fetuses are chronically hypoxaemic and to establish their ability to withstand additional episodes of hypoxia, the effects of administration of 9% O2 to the pregnant ewe was investigated. Fetuses were studied at 135-140 days. During maternal hypoxia the small fetuses showed a greater tendency to further hypoxaemia and acidaemia, but the differences compared with controls were not large. Whilst the initial response to hypoxaemia was a fall in heart rate in the small fetuses, unlike the controls, the heart rate returned to normal within 15 min. Metabolite responses to hypoxia in the small fetuses were less than normal and the changes in plasma insulin concentrations were uncommonly small. In contrast the plasma cortisol and ACTH responses to hypoxia were larger than normal in the small fetus. The results are discussed in relation to the altered physiological state of the growth-retarded fetal sheep.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004717:Endometrium / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications / Q000503:physiopathology*; D006339:Heart Rate; D006854:Hydrocortisone / Q000097:blood; D000860:Hypoxia / Q000150:complications*; D007328:Insulin / Q000097:blood; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D008431:Maternal-Fetal Exchange; D009092:Mucous Membrane / Q000502:physiology; D011247:Pregnancy; D012756:Sheep / Q000196:embryology*
D001786:Blood Glucose; D007328:Insulin; D007773:Lactates; D019344:Lactic Acid; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone