title: Recovery of hypoxic neonatal hearts after cardioplegic arrest.
abstract: OBJECTIVE
  Surgery for repair of congenital heart defects in the infant may be affected by hypoxia associated with the defect. The effects of chronic hypoxia on systemic ventricular function are not well characterised and few studies have considered myocardial preservation in the hypoxic neonatal heart. The aim was to determine how chronic hypoxia would affect left ventricular function in neonatal rabbit hearts subjected to global ischaemia.
  
  
  METHODS
  Hearts from rabbits one, four, and six weeks of age and raised at 9% O2 were compared with hearts from rabbits raised in ambient air. Haemodynamic variables were measured with an isolated heart preparation before and after cardioplegic arrest. Creatine kinase was measured during reperfusion and myocardial oxygen consumption (MVO2) during ischaemia.
  
  
  RESULTS
  At all ages, hypoxic hearts had significantly lower peak dP/dt and contractility index (dP/dt/left ventricular pressure (LVP)) than normoxic controls. After ischaemia and reperfusion, one week hypoxic hearts did not differ significantly in recovery from controls. Four week hypoxic hearts had significantly higher stroke volume and aortic flow, and six week hearts had significantly higher coronary flow than age matched controls. Contractility index did not show significant differences between hypoxic and control animals at any age. Hypoxic hearts released less creatine kinase in the coronary effluent during reperfusion than did control hearts of similar age. Six week hypoxic hearts had significantly higher MVO2 measured during the second administration of cardioplegia compared with six week control hearts but MVO2 did not differ significantly at one and four weeks of age.
  
  
  CONCLUSIONS
  Despite reduced baseline function, chronically hypoxic immature rabbit hearts can recover from an ischaemic insult as well as age matched controls, with less evidence of myocardial necrosis. This parallels clinical findings in cyanotic infants.
authors.affiliation: Department of Surgery, SUNY Health Science Center, Syracuse 13210.
authors.forename: D M
authors.initials: DM
authors.lastname: Feldbaum
authors.forename: L J
authors.initials: LJ
authors.lastname: Kohman
authors.forename: L J
authors.initials: LJ
authors.lastname: Veit
mesh_terms: D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D003402:Creatine Kinase / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D011817:Rabbits
chemical_list: D003402:Creatine Kinase