title: Relationship between flow through the fetal aortic isthmus and cerebral oxygenation during acute placental circulatory insufficiency in ovine fetuses.
abstract: OBJECTIVE
  We sought to investigate whether the reversal of blood flow through the aortic isthmus, as observed during an increase in placental vascular resistance, could be responsible for a significant fall in oxygen delivered to the fetal brain.
  
  
  METHODS
  With the appearance of reverse flow in the aortic isthmus, preplacental blood with low oxygen saturation could contaminate the ascending aorta blood destined for the brain. Stepwise compression of the umbilical veins of 8 exteriorized fetal lambs was realized at approximately 140 days of gestation. Four other animals were used as controls. Flows through the aortic isthmus and both carotid and umbilical arteries were measured by Doppler echocardiography in the basal state (hemodynamic class 1) and during moderate (class 2), severe (class 3), and extreme (class 4) increases in resistance to placental flow. Oxygen delivered to the brain was calculated from carotid blood flow and oxygen content.
  
  
  RESULTS
  In the control group no change was noted in umbilical and carotid arteries or in the aortic isthmus blood flow. Oxygen delivered to the brain remained stable. In the study group the increase in resistance to placental flow caused a significant fall in umbilical flow and carotid oxygen content, while blood flow in the carotid arteries increased slightly. The values for aortic isthmus flow and oxygen delivered to the brain during the 4 hemodynamic classes were, on average, as follows: class 1, 98.2 and 2.9 mL/(min x kg); class 2, 52.8 and 3.1 mL/(min x kg); class 3, 3.7 and 2.6 mL/(min x kg); and class 4, -29.8 and 0.7 mL/(min x kg), respectively.
  
  
  CONCLUSIONS
  During an acute increase in placental vascular resistance, delivery of oxygen to the brain is preserved despite a significant drop in arterial oxygen content as long as net flow through the isthmus is anterograde.
authors.affiliation: Fetal Cardiology Unit, Cardiology Division, Department of Pediatrics, Ste-Justine Hospital, University of Montreal, Quebec, Canada.
authors.forename: J C
authors.initials: JC
authors.lastname: Fouron
authors.forename: A
authors.initials: A
authors.lastname: Skoll
authors.forename: S E
authors.initials: SE
authors.lastname: Sonesson
authors.forename: M
authors.initials: M
authors.lastname: Pfizenmaier
authors.forename: E
authors.initials: E
authors.lastname: Jaeggi
authors.forename: M
authors.initials: M
authors.lastname: Lessard
mesh_terms: D000138:Acidosis; D000208:Acute Disease; D000818:Animals; D001011:Aorta / Q000196:embryology / Q000503:physiopathology; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply* / Q000196:embryology / Q000378:metabolism* / Q000503:physiopathology; D002245:Carbon Dioxide / Q000378:metabolism; D002339:Carotid Arteries / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D015150:Echocardiography, Doppler; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005318:Fetal Heart / Q000196:embryology / Q000503:physiopathology*; D005333:Fetus / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology; D010100:Oxygen / Q000378:metabolism*; D010927:Placental Insufficiency / Q000503:physiopathology*; D011247:Pregnancy; D012039:Regional Blood Flow; D012756:Sheep / Q000196:embryology; D014469:Umbilical Arteries / Q000378:metabolism / Q000503:physiopathology; D014471:Umbilical Veins / Q000378:metabolism / Q000503:physiopathology
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen