title: Effects of positive inotropic stimulation on postischemic myocardium with graded dysfunction.
abstract: OBJECTIVE
  To investigate the effects of moderate prolonged and of maximum short-term positive inotropic stimulation of postischemic myocardium as a function of the severity of stunning.
  
  
  METHODS
  Stunned isolated rat hearts (n = 116) after 30 min and 45 min of ischemia were stimulated with dopamine to raise systolic function (double product) back to control levels. In the isovolumetrically beating hearts, left ventricular developed pressure, double product, dp/dtmax, coronary flow, and myocardial oxygen consumption were determined during steady-state conditions. After maximum stimulation the contractile reserve was examined. Measurements of adenine nucleotides (n = 47) and electron microscopy (n = 9) were made.
  
  
  RESULTS
  30 min ischemia resulted in moderate postischemic dysfunction (LVP 81 +/- 3%; P < 0.05). After 45 min ischemia, function was more severely reduced (LVP 66 +/- 5%; P < 0.01). Coronary flow tended to be lower after ischemia. Myocardial oxygen consumption was not reduced in parallel with the dysfunction. Adenine nucleotides were gradually reduced after ischemia (ATP: 2.5 +/- 0.2 and 1.2 +/- 0.1 vs. 4.2 +/- 0.2 mumol/gww; P < 0.01). Contractile reserve also decreased in relation to the previous ischemic injury (after 45 min ischemia max. LVP 105 +/- 10% vs. max. LVP 152 +/- 8% in controls, P < 0.01). Prolonged stimulation did not result in further reduction in adenine nucleotides and function.
  
  
  CONCLUSIONS
  Contractile reserve is decreased in postischemic myocardium in parallel with the previous ischemic burden. Depending on the degree of contractile dysfunction a disturbed function-flow-oxygen consumption relation is present. Prolonged stimulation of stunned myocardium with dopamine back to the control level of function has no harmful short-term effects, indicating sufficient mitochondrial energy generation.
authors.affiliation: Medizinische Universitätsklinik, Abt. III, Eberhard-Karls-Universität, Tübingen, Germany.
authors.forename: H M
authors.initials: HM
authors.lastname: Hoffmeister
authors.forename: J
authors.initials: J
authors.lastname: Schaper
authors.forename: M E
authors.initials: ME
authors.lastname: Beyer
authors.forename: S
authors.initials: S
authors.lastname: Kazmaier
authors.forename: L
authors.initials: L
authors.lastname: Seipel
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation; D004298:Dopamine / Q000494:pharmacology*; D006352:Heart Ventricles / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects*; D017682:Myocardial Stunning / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D010101:Oxygen Consumption / Q000187:drug effects*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D013997:Time Factors
chemical_list: D000255:Adenosine Triphosphate; D004298:Dopamine