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

STUDY OBJECTIVE

The aim of the study was to assess the contribution of adenine nucleotide depletion to postischaemic myocardial dysfunction ("stunned" myocardium).

DESIGN

Isolated perfused hearts release purine catabolites even in the absence of ischaemia, and undergo spontaneous reduction of adenine nucleotide pool. A comparison was therefore made between mechanical function, purine release and tissue adenine nucleotides in working rat hearts reperfused after short term ischaemia or subjected to prolonged perfusion (up to 180 min).

EXPERIMENTAL MATERIAL

49 Sprague-Dawley rats of 250-300 g body weight were used. The animals were anaesthetised and the hearts quickly excised and perfused with the working heart technique.

MEASUREMENTS AND MAIN RESULTS

Reperfusion after 10 min ischaemia provided a good model of "stunned" myocardium: aortic flow and minute work decreased by 15(SEM 2)% and 20(3)%, no enzyme leakage was observed, and the adenine nucleotide pool decreased by 3.5(0.4) mumols.g-1. During prolonged perfusion no change was observed in any haemodynamic variable until the adenine nucleotide pool was depleted by over 8.5 mumols.g-1. Adenylate energy charge and the phosphocreatine-creatine pool were unchanged in all cases.

CONCLUSIONS

Depletion of adenine nucleotides does not account for contractile dysfunction in our model of "stunned" myocardium.