title: Heat stress attenuates ATP-depletion and pH-decrease during cardioplegic arrest.
abstract: BACKGROUND
  The capacity of heat stress induction to improve myocardial tolerance against ischemia is well known. We investigated cardiac energy metabolism after hsp 72(+)/73(+) induction in isolated perfused neonatal rabbit hearts subjected to prolonged cold cardioplegic ischemia.
  
  
  METHODS
  Hearts from neonatal rabbits were excised, isolated perfused and arrested by 2-h cold cardioplegic ischemia. Rectal temperature of eight neonatal rabbits was raised to 42.0 to 42.5 degrees C for heat shock protein expression in a whole body water bath for 15 min before the onset of arrest. Another set of eight rabbits without hyperthermia pretreatment served as control. Recovery of left ventricle function was assessed by aortic flow, cardiac output, and max dP/dt. Status of high-energy phosphates was measured by (31)phosphorus nuclear magnetic resonance-spectroscopy.
  
  
  RESULTS
  Immunoblot analysis revealed clear hsp 72+/73+ induction after a brief period of systemic hyperthermia. Heat stress pretreatment resulted in a better recovery of left ventricular function (aortic flow and cardiac output improvement P < 0.05, max dP/dt P < 0.01) than in controls at 60 min after reperfusion. During ischemia and reperfusion, myocardial energy metabolism was better preserved in hearts after hsp induction as a consequence of increased gamma-, alpha-, and beta-ATP as well as phosphocreatine-values over controls. The ischemia-induced pH-decrease was attenuated.
  
  
  CONCLUSIONS
  These data contribute to the evidence of heat stress mediated beneficial effects on functional myocardial recovery and improved cardiac energy metabolism after prolonged cold cardioplegic ischemia. More importantly, the attenuation of ischemic pH reduction and better restoration suggest an involvement of mitochondrial membrane potential alterations.
authors.affiliation: Biomedical Research Center, Cardiovascular Research Lab and Heart Surgery, University Hospital, Philipps-University Marburg, Marburg, Germany. vogts@med.uni-marburg.de
authors.forename: Sebastian
authors.initials: S
authors.lastname: Vogt
authors.forename: Dirk
authors.initials: D
authors.lastname: Troitzsch
authors.forename: Hashim
authors.initials: H
authors.lastname: Abdul-Khaliq
authors.forename: Rainer
authors.initials: R
authors.lastname: Moosdorf
mesh_terms: D000255:Adenosine Triphosphate / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D000818:Animals; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003080:Cold Temperature; D004734:Energy Metabolism; D050883:HSC70 Heat-Shock Proteins / Q000096:biosynthesis; D050884:HSP72 Heat-Shock Proteins / Q000096:biosynthesis; D006324:Heart Arrest, Induced; D006863:Hydrogen-Ion Concentration; D006979:Hyperthermia, Induced; D066298:In Vitro Techniques; D009682:Magnetic Resonance Spectroscopy; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011522:Protons; D011817:Rabbits; D020127:Recovery of Function; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D002314:Cardioplegic Solutions; D050883:HSC70 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D011522:Protons; D010725:Phosphocreatine; D000255:Adenosine Triphosphate