title: Development of the ovine fetal cardiovascular defense to hypoxemia towards full term.
abstract: We tested the hypothesis that fetal cardiovascular responses to hypoxemia change close to full term in relation to the prepartum increase in fetal basal cortisol and investigated, in vivo, the neural and endocrine mechanisms underlying these changes. Fetal heart rate and peripheral hemodynamic responses to 1 h of hypoxemia were studied in 25 chronically instrumented sheep within three narrow gestational age ranges: 125-130 (n = 13), 135-140 (n = 6), and >140 (n = 6) days (full term approximately 145 days). Chemoreflex function and plasma concentrations of vasoconstrictor hormones were measured. Reductions in fetal arterial Po(2) during hypoxemia were similar at all ages. At 125-130 days, hypoxemia elicited transient bradycardia, femoral vasoconstriction, and increases in plasma concentrations of catecholamines, neuropeptide Y (NPY), AVP, ACTH, and cortisol. Close to full term, in association with the prepartum increase in fetal basal cortisol, there was a developmental increase in the magnitude and persistence of fetal bradycardia and in the magnitude of the femoral constrictor response to hypoxemia. The mechanisms mediating these changes close to full term included increases in the gain of chemoreflex function and in the magnitudes of the fetal NPY and AVP responses to hypoxemia. Data combined irrespective of gestational age revealed significant correlations between fetal basal cortisol and fetal bradycardia, femoral resistance, chemoreflex function, and plasma AVP concentrations. The data show that the fetal cardiovascular defense to hypoxemia changes in pattern and magnitude just before full term because of alterations in the gain of the neural and endocrine mechanisms mediating them, in parallel with the prepartum increase in fetal basal cortisol.
authors.affiliation: Dept. of Physiology, Development & Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
authors.forename: Andrew J W
authors.initials: AJ
authors.lastname: Fletcher
authors.forename: David S
authors.initials: DS
authors.lastname: Gardner
authors.forename: C Mark B
authors.initials: CM
authors.lastname: Edwards
authors.forename: Abigail L
authors.initials: AL
authors.lastname: Fowden
authors.forename: Dino A
authors.initials: DA
authors.lastname: Giussani
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D001784:Blood Gas Analysis; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000196:embryology*; D005260:Female; D047109:Fetal Development; D005311:Fetal Hypoxia / Q000503:physiopathology*; D005333:Fetus / Q000098:blood supply* / Q000378:metabolism; D006340:Heart Rate, Fetal / Q000502:physiology; D006854:Hydrocortisone / Q000097:blood; D000860:Hypoxia / Q000097:blood / Q000503:physiopathology*; D008297:Male; D009478:Neuropeptide Y / Q000097:blood; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000097:blood / Q000502:physiology*; D012756:Sheep; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D009478:Neuropeptide Y; D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone