Adenine nucleotide depletion and contractile dysfunction in the "stunned" myocardium.

摘要: Study objective – The aim of the study was to assess contribution adenine nucleotide depletion postischaemic myocardial dysfunction (“stunned” myocardium). Design Isolated perfused hearts release purine catabolites even in absence ischaemia, and undergo spontaneous reduction pool. A comparison therefore made between mechanical function, tissue nucleotides working rat reperfused after short term ischaemia or subjected prolonged perfusion (up 180 min). Experimental material 49 Sprague-Dawley rats 250-300 g body weight were used. animals anaesthetised quickly excised with heart technique. Measurements main results Reperfusion 10 min provided a good model “stunned” myocardium: aortic flow minute work decreased by 15(SEM 2)% 20(3)%, no enzyme leakage observed, pool 3.5(0.4) μmol·g−1. During change observed any haemodynamic variable until depleted over 8.5 Adenylate energy charge phospho-creatine-creatine unchanged all cases. Conclusions Depletion does not account for contractile our myocardium.