title: Fetal sheep left ventricle is more sensitive than right ventricle to progressively worsening hypoxemia and acidemia.
abstract: OBJECTIVE
  In a sheep model we tested the hypothesis that the fetal left ventricle is less tolerant to worsening acidemia than the right ventricle.
  
  
  METHODS
  At 106-124/145 days of gestation, 12 fetuses were instrumented. After a 4-day recovery, placental vascular resistance was increased by fetal angiotensin (AT) II infusion. After a 2h ATII infusion, to further deteriorate fetal oxygenation, maternal hypoxemia was induced. Fetal cardiac function and hemodynamics were assessed by tissue Doppler imaging (TDI) and pulsed Doppler imaging. Ultrasonography was performed at baseline, at 1 and 2h after the beginning of ATII infusion and during the ATII+hypoxemia phase.
  
  
  RESULTS
  Fetal pH and pO₂ decreased significantly and progressively during the experiment. Left ventricular TDI-derived isovolumic relaxation velocity (IVRV) was lower during ATII 2h and ATII+hypoxemia phases than at baseline. The IVRV deceleration was significantly less during the ATII+hypoxemia phase than at baseline. Right ventricular IVRV was significantly lower during the ATII+hypoxemia phase than at baseline. IVRV deceleration did not change. Only left ventricular IVRV deceleration correlated with fetal pO₂ (R=0.36, p<0.05). Fetal right and left ventricular cardiac outputs, as well as umbilical artery, aortic isthmus and ductus venosus pulsatility indices remained unchanged during the experiment.
  
  
  CONCLUSIONS
  Our results show that signs of cardiac dysfunction develop earlier in the left ventricle than in the right ventricle. The fetal left ventricle seems to be more sensitive to progressively worsening hypoxemia and acidemia than the right ventricle.
authors.affiliation: Department of Obstetrics and Gynecology, University of Oulu, Oulu, Finland.
authors.forename: Juulia
authors.initials: J
authors.lastname: Junno
authors.forename: Ella
authors.initials: E
authors.lastname: Bruun
authors.forename: Jorge H
authors.initials: JH
authors.lastname: Gutierrez
authors.forename: Tiina
authors.initials: T
authors.lastname: Erkinaro
authors.forename: Mervi
authors.initials: M
authors.lastname: Haapsamo
authors.forename: Ganesh
authors.initials: G
authors.lastname: Acharya
authors.forename: Juha
authors.initials: J
authors.lastname: Räsänen
mesh_terms: D000138:Acidosis / Q000196:embryology* / Q000209:etiology; D000818:Animals; D017849:Animals, Inbred Strains; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D005387:Finland; D006352:Heart Ventricles / Q000196:embryology* / Q000503:physiopathology; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000196:embryology* / Q000209:etiology; D019344:Lactic Acid / Q000097:blood; D010100:Oxygen / Q000097:blood; D021041:Placental Circulation; D010927:Placental Insufficiency / Q000503:physiopathology*; D011247:Pregnancy; D034561:Sheep, Domestic; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000196:embryology* / Q000209:etiology; D018497:Ventricular Dysfunction, Right / Q000097:blood / Q000196:embryology / Q000209:etiology
chemical_list: D019344:Lactic Acid; D010100:Oxygen