Ischaemic contracture in isolated rat heart: reversible or irreversible myocardial injury?

An isolated rat heart preparation was reperfused at 37 degrees C for 10 min after 10, 20, 30 and 40 min of ischaemia. The left ventricular tension was measured by means of a balloon catheter filled with water and connected to a pressure recorder. The left ventricular resting tension began to increase at 9 +/- 1 min (mean +/- SEM) and was maximally developed (myocardial contracture) at 18 +/- 1 min of ischaemia. There was a striking and constant exacerbation of the resting tension during reperfusion after 30 and 40 min (but not after 10 or 20 min) of ischaemia with simultaneous acceleration of creatine phosphokinase (CK) release into the coronary effluent and with the loss of the recovery of contractile activity. Myocardial adenosine triphosphate (ATP)-content decreased during 20 min of ischaemia more in the endocardial (ENDO) (from 17.7 +/- 1.9 mumol/g to 0.7 +/- 0.1 mumol/g) than in epicardial (EPI) (from 15.5 +/- 0.9 mumol/g to 3.2 +/- 0.6 mumol/g) parts of myocardium. Reperfusion after 10 min of ischaemia resulted in a slight increase of myocardial ATP-content both in EPI (from 7.5 +/- 0.6 to 10.4 +/- 0.8 mumol/g, p less than 0.05) and ENDO (from 5.0 +/- 0.8 to 8.9 +/- 2.5 mumol/g, n.s.). Reperfusion after the completion of contracture (after 20 min) had no effect on myocardial ATP-content. The results indicate that there is a transmural ATP gradient in ischaemic isolated rat heart and that myocardial ATP net production during reperfusion (10 min) is prevented after the development of ischaemic contracture.(ABSTRACT TRUNCATED AT 250 WORDS)