title: Maternally administered dexamethasone at 0.7 of gestation suppresses maternal and fetal pituitary and adrenal responses to hypoxemia in sheep.
abstract: Women who are at risk of preterm delivery are treated with antenatal steroids to facilitate fetal lung maturation. During this period, there is a potential for fetal or maternal hypoxemia to occur. Fetal responses to hypoxemia in sheep are well documented. However, less is known regarding maternal responses to hypoxemia. Therefore, we determined the effects of dexamethasone (DM) on maternal and fetal responses to hypoxemia in sheep. Ewes received four i.m. injections of DM or saline at 12-h intervals beginning at 103 d of gestation. Samples for ACTH, cortisol, and glucose were collected at 0900 h. At 105 d of gestation, hypoxemia was induced for 1 h by maternal nitrogen gas inhalation. Samples for ACTH, cortisol, and glucose were collected at 15-min intervals before, during, and after the hypoxemia challenge. Fluorescent microspheres were administered to the mother and the fetus before and during hypoxemia to measure organ perfusion. DM suppressed basal fetal and maternal cortisol and ACTH concentrations but increased glucose levels. DM also increased fetal but not maternal blood pressure. In control subjects, hypoxemia elevated fetal and maternal cortisol and ACTH concentrations. These responses were obliterated by DM. Hypoxemia increased blood pressure in DM-exposed fetuses but not in control subjects. In addition, hypoxemia decreased fetal adrenal vascular resistance in saline but not DM fetuses or ewes from either treatment group. In summary, maternal administration of a low dose of DM at 0.7 of gestation suppresses maternal and fetal adrenal function and changes fetal responses to hypoxemic stress to resemble those observed later in gestation.
authors.affiliation: Department of Clinical Sciences, Oregon State University, Corvallis, OR 97331, USA. michelle.kutzler@oregonstate.edu
authors.forename: Michelle A
authors.initials: MA
authors.lastname: Kutzler
authors.forename: Turhan
authors.initials: T
authors.lastname: Coksaygan
authors.forename: A Damon
authors.initials: AD
authors.lastname: Ferguson
authors.forename: Stella E
authors.initials: SE
authors.lastname: Vincent
authors.forename: Peter W
authors.initials: PW
authors.lastname: Nathanielsz
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology*; D004195:Disease Models, Animal; D005260:Female; D005333:Fetus / Q000187:drug effects; D005865:Gestational Age; D005947:Glucose / Q000378:metabolism; D006854:Hydrocortisone / Q000378:metabolism; D000860:Hypoxia; D008431:Maternal-Fetal Exchange; D008863:Microspheres; D009584:Nitrogen / Q000737:chemistry / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D010477:Perfusion; D010902:Pituitary Gland / Q000187:drug effects*; D011247:Pregnancy; D012756:Sheep; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors
chemical_list: D000893:Anti-Inflammatory Agents; D012965:Sodium Chloride; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D005947:Glucose; D009584:Nitrogen; D010100:Oxygen; D006854:Hydrocortisone