title: Intrauterine growth restriction impairs right ventricular response to hypoxia in adult male rats.
abstract: Intrauterine growth restriction (IUGR) predisposes to cardiovascular diseases in adulthood. The mechanisms of this phenomenon remain cryptic. We hypothesized that heart mitochondria in IUGR-born adult rats are more sensitive to acute hypoxia which translates into dysfunctional cardiac response to hypoxic stress.
  
  
  
  Adult IUGR-born male rats (the offspring of dams fed with calories-restricted diet during pregnancy) were exposed to acute hypoxic stress with echocardiographic assessment of cardiac function. In parallel, mitochondrial respiration in organelles isolated from left ventricle (LV) and right ventricle (RV) was tested in normoxic and anoxic conditions. The extent of post-anoxic inhibition of mitochondrial respiration and cardiac function was compared with controls, non-IUGR rats.
  
  
  
  Compared with controls, in the IUGR rats hypoxia significantly reduced only RV contractility, evidenced by decreased fractional shortening, functional area of contraction, and tricuspid annular plane systolic excursion. In isolated mitochondria, anoxic challenge inhibited respiratory chain in both groups of rats. However, compared with controls, the extent of anoxic mitochondrial depression was significantly greater in IUGR-born rats, but only in the organelles isolated from RV.
  
  
  
  In adult IUGR-born rats, mitochondria from RV are hypersensitive to oxygen deprivation and this translates into maladaptive RV cardiac response to acute hypoxia.
authors.affiliation: Department of Pediatrics, Kings County Hospital Center, Brooklyn, New York.|Department of Pediatrics, St. Georges University, Grenada, West Indies.
authors.forename: Michael
authors.initials: M
authors.lastname: Keenaghan
authors.affiliation: Department of Anesthesiology, Columbia University, New York, New York.|Department of Pediatrics, Columbia University, New York, New York.
authors.forename: Lena
authors.initials: L
authors.lastname: Sun
authors.affiliation: Department of Anesthesiology, Columbia University, New York, New York.
authors.forename: Aili
authors.initials: A
authors.lastname: Wang
authors.affiliation: Department of Medicine, Columbia University, New York, New York.
authors.forename: Eiichi
authors.initials: E
authors.lastname: Hyodo
authors.affiliation: Department of Medicine, Columbia University, New York, New York.
authors.forename: Sinichi
authors.initials: S
authors.lastname: Homma
authors.affiliation: Department of Pediatrics, Columbia University, New York, New York.
authors.forename: Vadim S
authors.initials: VS
authors.lastname: Ten
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D004452:Echocardiography; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D008098:Litter Size; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D010101:Oxygen Consumption; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D018497:Ventricular Dysfunction, Right