title: Cardiac hypertrophy impairs recovery from ischaemia because there is a reduced reactive hyperaemic response.
abstract: OBJECTIVE
  The aim was to investigate whether impaired coronary flow reserve associated with cardiac hypertrophy could significantly limit the flow debt repayment following short periods of coronary occlusion and exacerbate or prolong episodes of myocardial ischaemia.
  
  
  METHODS
  Left ventricular hypertrophy was induced in guinea pigs by aortic constriction and the hearts were isolated six weeks later for Langendorff perfusion. Sham operated animals served as controls. The reactive hyperaemic response was studied following various lengths of occlusion of flow and the extent of aerobic and anaerobic metabolism was assessed in each group.
  
  
  RESULTS
  Heart weight/body weight ratio was increased by approximately 25% (P < 0.001) with aortic constriction. The reactive hyperaemic flow response in isolated hearts was impaired by hypertrophy in both magnitude (P < 0.05) and duration. The repayment of flow debt was also significantly reduced, suggesting an inadequate recovery of the myocardium following the occlusion. The total amount of O2 consumed by the heart throughout the duration of hyperaemia was less in hypertrophy than in sham operated controls, suggesting a decrease in aerobic metabolism. Total lactate discharge expressed as a ratio of O2 consumed, which provides an estimation of the degree of anaerobic in relation to aerobic metabolism, was greater in hypertrophy than in sham operated controls.
  
  
  CONCLUSIONS
  The hypertrophied heart is more vulnerable to brief periods of ischaemia because of an impaired reactive hyperaemic response which results in delayed metabolic recovery. These abnormalities may contribute to the increased morbidity associated with cardiac hypertrophy.
authors.affiliation: Academic Cardiology Unit, St. Mary's Hospital Medical School, London, UK.
authors.forename: A M
authors.initials: AM
authors.lastname: McAinsh
authors.forename: M A
authors.initials: MA
authors.lastname: Turner
authors.forename: D
authors.initials: D
authors.lastname: O'Hare
authors.forename: R
authors.initials: R
authors.lastname: Nithythyananthan
authors.forename: D G
authors.initials: DG
authors.lastname: Johnston
authors.forename: D J
authors.initials: DJ
authors.lastname: O'Gorman
authors.forename: D J
authors.initials: DJ
authors.lastname: Sheridan
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology*; D003326:Coronary Circulation; D006168:Guinea Pigs; D006940:Hyperemia / Q000378:metabolism / Q000503:physiopathology*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010477:Perfusion
chemical_list: D007773:Lactates; D019344:Lactic Acid