title: Myocardial self-preservative effect of heat shock protein 70 on an immature lamb heart.
abstract: BACKGROUND
  Heat shock proteins have been shown to enhance myocardial tolerance of ischemia-reperfusion injury and are induced in the myocardium of many animals by various stressors.
  
  
  METHODS
  To assess the effects and time course of the inducible form of heat shock protein 70, we raised the rectal temperature of 15 neonatal lambs to 43 degrees C for 15 minutes. At 15, 30, 60, and 120 minutes and 24 hours after heat shock, hearts were subjected to immunoblot analysis for heat shock protein (hsp 72/73). Twenty-four hours after heat shock, neonatal lamb hearts (n = 8) were subjected to 2 hours of cold cardioplegic ischemia (HSP group). Eight neonatal lamb hearts without heat shock served as control. After 60 minutes of reperfusion, left ventricular systolic and diastolic function, coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and lactate levels were measured. Endothelial function was assessed by measuring in situ coronary vascular resistance response to acetylcholine and trinitroglycerine.
  
  
  RESULTS
  The HSP group showed a significantly higher recovery of systolic function as well as MVO, and a lower lactate level compared to the control group at 60 minutes after reperfusion. Recovery of coronary endothelial function was also significantly better in the HSP group than in the control group. Inducible form of HSP 70 was expressed 15 minutes after heat shock and continued to be observed at 24 hours after the stress.
  
  
  CONCLUSIONS
  Heat shock stress associated with the production of inducible heat shock proteins improved the recovery of ventricular function as well as endothelial function and aerobic metabolism after hypothermic cardioplegic ischemia. Induction of heat shock proteins by any means prior to planned hypothermic ischemia may lead to a new approach for myocardial protection.
authors.affiliation: Department of Cardiovascular Surgery, Children's Hospital, Boston, Massachusetts, USA. fnomura@kure-nh.go.jp
authors.forename: F
authors.initials: F
authors.lastname: Nomura
authors.forename: M
authors.initials: M
authors.lastname: Aoki
authors.forename: J M
authors.initials: JM
authors.lastname: Forbess
authors.forename: J E
authors.initials: JE
authors.lastname: Mayer
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D003326:Coronary Circulation / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D018840:HSP70 Heat-Shock Proteins / Q000502:physiology*; D019157:Ischemic Preconditioning, Myocardial; D019344:Lactic Acid / Q000097:blood; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology*; D010101:Oxygen Consumption / Q000502:physiology; D012756:Sheep; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D018840:HSP70 Heat-Shock Proteins; D019344:Lactic Acid