title: Ischaemic preconditioning limits infarct size in the rat heart.
abstract: OBJECTIVE
  One of the mechanisms by which ischaemic preconditioning is thought to protect against later prolonged ischaemia is via a reduction in ATP utilisation during ischaemia. The ATP "wastage" that occurs during ischaemia is thought to be due to mitochondrial ATPase activity, which may be prevented in ischaemic preconditioning by the binding of a specific inhibitor protein. As the rat is known to have less inhibitor protein than other species, this study was designed to determine whether the rat heart could be ischaemically preconditioned.
  
  
  METHODS
  Rats were anaesthetised with pentobarbitone, the chest opened and the hearts ischaemically preconditioned with a 5 min occlusion of the left main coronary artery followed by 10 min reperfusion. The hearts were then subjected to a 45 min occlusion followed by 3 h reperfusion. Control hearts were treated identically but without ischaemic preconditioning. Infarct size was measured using triphenyl tetrazolium and expressed as a percentage of the region at risk, measured with fluorescent particles.
  
  
  RESULTS
  Infarct size as a percent of the risk area in the ischaemically preconditioned group (n = 8) was 31.4(SEM 6.1)%, versus 61.0(4.8)% in control hearts (n = 8) (p < 0.005).
  
  
  CONCLUSIONS
  These results show that rat hearts can be ischaemically preconditioned and suggest that the protective mechanism involved in this phenomenon is not mediated through the endogenous inhibition of mitochondrial ATPase. An overall reduction in mitochondrial ATP "wastage" may not be the sole mechanism in the protection seen in ischaemic preconditioning.
authors: Hatter Institute for Cardiovascular Studies, Department of Academic Cardiology, University College and Middlesex Hospital, London, United Kingdom.
authors: D M
authors: DM
authors: Yellon
authors: A M
authors: AM
authors: Alkhulaifi
authors: E E
authors: EE
authors: Browne
authors: W B
authors: WB
authors: Pugsley
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D008297:Male; D008929:Mitochondria, Heart / Q000201:enzymology; D009203:Myocardial Infarction / Q000473:pathology / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000251:Adenosine Triphosphatases