title: Fetoplacental vascular tone during fetal circuit acidosis and acidosis with hypoxia in the ex vivo perfused human placental cotyledon.
abstract: OBJECTIVE
  Our purpose was to determine the effects of acidosis and acidosis-hypoxia on fetoplacental perfusion pressure and its response to angiotensin II.
  
  
  METHODS
  Perfused cotyledons from 14 placentas were studied with either an acidotic fetal circuit perfusate (n = 7) or an acidotic-hypoxic fetal circuit perfusate (n = 7). Each cotyledon's fetal vasculature was initially perfused under standard conditions and bolus injected with 1 x 10(-10) moles of angiotensin II. Fetoplacental perfusate was then replaced with either an acidotic medium (pH 6.90 to 7.00 and Po2 516 to 613 mm Hg) or an acidotic-hypoxic medium (pH 6.90 to 7.00 and Po2 20 to 25 mm Hg) followed by an angiotensin II injection. The vasculature was subsequently recovered with standard perfusate and again injected with angiotensin II. Perfusion pressures within each group were compared by one-way analysis of variance, and results were expressed as mean pressure +/- SEM.
  
  
  RESULTS
  Resting fetoplacental perfusion pressure did not change when the fetal circuit perfusate was made acidotic (28 +/- 1 mm Hg vs 25 +/- 2 mm Hg) or acidotic-hypoxic (26 +/- 2 mm Hg vs 25 +/- 2 mm Hg). The maximal fetoplacental perfusion pressure achieved in response to angiotensin II did not differ with an acidotic perfusate (41 +/- 2 mm Hg vs 38 +/- 1 mm Hg) or with an acidotic-hypoxic perfusate (39 +/- 2 mm Hg vs 36 +/- 2 mm Hg).
  
  
  CONCLUSIONS
  In the perfused placental cotyledon fetoplacental perfusion pressure and pressor response to angiotensin II are not affected by fetal circuit acidosis or acidosis-hypoxia. This suggests that neither fetal acidosis nor fetal acidosis combined with hypoxia has a direct effect on fetoplacental vascular tone.
authors.affiliation: Department of Obstetrics and Gynecology, Madigan Army Medical Center, Tacoma, Washington, USA.
authors.forename: N J
authors.initials: NJ
authors.lastname: Hoeldtke
authors.forename: P G
authors.initials: PG
authors.lastname: Napolitano
authors.forename: K H
authors.initials: KH
authors.lastname: Moore
authors.forename: B C
authors.initials: BC
authors.lastname: Calhoun
authors.forename: R F
authors.initials: RF
authors.lastname: Hume
mesh_terms: D000138:Acidosis / Q000503:physiopathology*; D000804:Angiotensin II / Q000494:pharmacology; D001794:Blood Pressure; D005260:Female; D005311:Fetal Hypoxia / Q000503:physiopathology*; D005333:Fetus / Q000098:blood supply*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009569:Nitric Oxide / Q000502:physiology; D010477:Perfusion; D010920:Placenta / Q000098:blood supply* / Q000187:drug effects; D011247:Pregnancy
chemical_list: D000804:Angiotensin II; D009569:Nitric Oxide