title: Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization.
abstract: The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Western Ontario, London, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Gagnon
authors.forename: J
authors.initials: J
authors.lastname: Murotsuki
authors.forename: J R
authors.initials: JR
authors.lastname: Challis
authors.forename: L
authors.initials: L
authors.lastname: Fraher
authors.forename: B S
authors.initials: BS
authors.lastname: Richardson
mesh_terms: D000208:Acute Disease; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D002908:Chronic Disease; D015232:Dinoprostone / Q000032:analysis; D004617:Embolism / Q000196:embryology*; D004702:Endocrine Glands / Q000196:embryology*; D005260:Female; D005312:Fetal Blood; D005333:Fetus / Q000098:blood supply / Q000502:physiology*; D005740:Gases / Q000097:blood; D006340:Heart Rate, Fetal; D000860:Hypoxia / Q000196:embryology*; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D012039:Regional Blood Flow; D012756:Sheep / Q000196:embryology; D013312:Stress, Physiological / Q000196:embryology*; D014470:Umbilical Cord / Q000098:blood supply
chemical_list: D005740:Gases; D000324:Adrenocorticotropic Hormone; D015232:Dinoprostone