title: Fetal endocrine responses to chronic placental embolization in the late-gestation ovine fetus.
abstract: OBJECTIVE
  The purpose of this study was to examine the effect of chronic fetal placental embolization on the fetal corticotropin, cortisol, and catecholamines concentrations and on myometrial contractility pattern.
  
  
  METHODS
  Fourteen fetal sheep were studied (seven embolized, seven controls) for 10 days between 0.84 and 0.91 of gestation. Daily injections of nonradioactive microspheres were performed to decrease fetal arterial oxygen content by 30% to 35% of the preembolization value. Umbilical artery Doppler flow velocity waveforms were measured daily.
  
  
  RESULTS
  Chronic fetal placental embolization produced progressive fetal hypoxemia (p < 0.001) with changes in umbilical artery Doppler flow velocity waveforms indicative of a 25% increase in placental vascular resistance (p < 0.01). In response to chronic fetal hypoxemia there was a progressive increase in baseline fetal plasma norepinephrine concentration (p < 0.001). There was a transient fourfold to fivefold increase in baseline fetal plasma cortisol levels concomitant with a significant decrease in baseline immunoreactive corticotropin between days 7 and 9 of embolization (both p < 0.05), with a return to control values by day 10. There was a 57% increase in myometrial contracture frequency in the embolized group when compared with controls (p = 0.001).
  
  
  CONCLUSIONS
  During repetitive chronic placental damage that led to fetal hypoxemia, the fetal endocrine environment changed with time in a direction that would prevent the onset of premature activation of the hypothalamic-pituitary-adrenal axis and premature delivery.
authors.affiliation: Department of Obstetrics/Gynaecology, St. Joseph's Health Centre, Lawson Research Institute, London, Ontario, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Gagnon
authors.forename: J
authors.initials: J
authors.lastname: Challis
authors.forename: L
authors.initials: L
authors.lastname: Johnston
authors.forename: L
authors.initials: L
authors.lastname: Fraher
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002395:Catecholamines / Q000097:blood*; D002908:Chronic Disease; D004617:Embolism / Q000503:physiopathology; D005260:Female; D005312:Fetal Blood / Q000737:chemistry*; D005311:Fetal Hypoxia / Q000097:blood / Q000503:physiopathology; D005333:Fetus / Q000503:physiopathology*; D005865:Gestational Age; D006854:Hydrocortisone / Q000097:blood; D000860:Hypoxia / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D012756:Sheep; D014463:Ultrasonography; D014469:Umbilical Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology; D014590:Uterine Contraction / Q000097:blood / Q000502:physiology*
chemical_list: D002395:Catecholamines; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone