title: Single-ventricle physiology reduces cerebral oxygen delivery in a piglet model.
abstract: BACKGROUND
  In single-ventricle physiology, cerebral blood flow and oxygen (O2) delivery may be inadequate. This study tests the hypotheses that in acute univentricular physiology (1) cerebral blood flow increases inadequately to maintain O2 delivery, (2) the brain is incapable of increasing O2 extraction due to hypoxemia, and (3) cerebral O2 delivery diminishes selectively in different brain regions.
  
  
  METHODS
  Univentricular physiology was created in 8 piglets, while 8 animals were sham controls. Aortopulmonary shunt, echocardiography-guided atrial septostomy, tricuspid valve avulsion, and pulmonary artery occlusion were performed to allow the left ventricle to support systemic and pulmonary circulations. Cerebral blood flow (microspheres), cerebral O2 and lactate metabolism, and cerebral O2 saturation were measured at baseline, 30 minutes, and 120 minutes after conversion to univentricular physiology.
  
  
  RESULTS
  Cerebral blood flow increased in the cerebrum and subtentorium in controls (p < 0.05), whereas it remained unchanged in univentricular piglets. Cerebral O2 delivery at 30 and 120 minutes was lower in univentricular physiology than in controls (p = 0.05). Fractional oxygen extraction was unchanged in both groups. Cerebral O2 consumption trended lower in univentricular physiology (p = not significant), while it was unchanged in controls. Lactate cerebral metabolic rate (CMRLactate) increased at 30 and 120 minutes in both groups. The decline in O2 delivery was variable, but present in nearly all brain regions.
  
  
  CONCLUSIONS
  This study confirms the hypothesis that, in univentricular physiology, hypoxemia and limited cerebral blood flow reduce cerebral O2 availability in nearly all regions. These findings contribute to the understanding of brain abnormalities in infants with univentricular physiology.
authors.affiliation: Division of Cardiothoracic Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA. mricci@med.miami.edu
authors.forename: Marco
authors.initials: M
authors.lastname: Ricci
authors.forename: Pierluca
authors.initials: P
authors.lastname: Lombardi
authors.forename: Alvaro
authors.initials: A
authors.lastname: Galindo
authors.forename: Ernesto
authors.initials: E
authors.lastname: Coscarella
authors.forename: Amelia
authors.initials: A
authors.lastname: Vasquez
authors.forename: Eliot
authors.initials: E
authors.lastname: Rosenkranz
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D006330:Heart Defects, Congenital / Q000150:complications / Q000503:physiopathology*; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood* / Q000378:metabolism; D013552:Swine
chemical_list: D010100:Oxygen