title: Effects of heat stress on metabolism of high-energy phosphates. Comparison of normothermic and hypothermic ischemia.
abstract: BACKGROUND
  Alterations in metabolic pathways may contribute to the cardioprotective effects of heat stress (HS). We investigated the effects of HS on ATP and phosphocreatine (PCr) levels in the ischemic rat myocardium, after both normothermic and hypothermic ischemia.
  
  
  METHODS
  Two protocols were used: (1) normothermic ischemia (20 min at 37 degrees C) with no myocardial protection (n=6 HS; n=6 control); (2) hypothermic ischemia (4 hrs at 4 degrees C) after cardioplegic arrest (n=6 HS; n=6 control). ATP and PCr levels in the heart were measured using 31P nuclear magnetic resonance spectroscopy.
  
  
  RESULTS
  At the end of normothermic ischemia, ATP levels were better maintained in HS hearts (C vs HS: 4.51+/-0.66 vs 7.81+/-1.06 micromol/g dry wt+/-SEM, p=0.04). A trend for higher ATP content in HS hearts was observed after 40 min of reperfusion (C vs HS: 11.7+/-1.5 vs 16.9+/-2.0 micromol/g dry wt+/-SEM, p=0.09). PCr content was also higher at the end of 40 minutes of reperfusion in HS hearts (C vs HS: 46.4+/-2.9 vs 56.9+/-3.0 micromol/g dry wt+/-SEM, p=0.03). After prolonged hypothermic ischemia under cardioplegic arrest, heat stress again led to better preservation of ATP levels at the end of ischemia (C vs HS: 5.71+/-0.88 vs 9.23+/-1.38 micromol/g dry wt+/-SEM, p=0.05) and after 40 minutes of reperfusion (C vs HS: 16.8+/-1.4 vs 24.6+/-2.8 micromol/g dry wt+/-SEM, p=0.03). PCr levels were also better maintained at the end of ischemia (C vs HS: 4.87+/-0.77 vs 12.4+/-3.0 micromol/g dry wt+/-SEM, p=0.03) and after 40 minutes of reperfusion in HS hearts (C vs HS: 55.1+/-7.0.vs 79.8+/-7.3 micromol/g dry wt+/-SEM, p=0.03).
  
  
  CONCLUSIONS
  Heat stress induces changes in the energy profile of the heart which results in better preservation of ATP and phosphocreatine levels. These changes could be observed after brief normothermic ischemia and also after prolonged hypothermic ischemia under cardioplegic arrest, mimicking conditions of preservation for cardiac transplantation.
authors.affiliation: Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College School of Medicine, Harefield Hospital, Middlesex, UK.
authors.forename: J
authors.initials: J
authors.lastname: Jayakumar
authors.forename: R T
authors.initials: RT
authors.lastname: Smolenski
authors.forename: C C
authors.initials: CC
authors.lastname: Gray
authors.forename: A T
authors.initials: AT
authors.lastname: Goodwin
authors.forename: M
authors.initials: M
authors.lastname: Amrani
authors.forename: M H
authors.initials: MH
authors.lastname: Yacoub
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001831:Body Temperature / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D006324:Heart Arrest, Induced; D016027:Heart Transplantation / Q000502:physiology*; D007036:Hypothermia, Induced; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D010725:Phosphocreatine / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate