Objective: The aim was to examine electrical and metabolic responses of myocardium to ischaemia after recovery from preceding ischaemia. Methods: In 23 open chest dogs (5 min occlusion group), the left anterior descending coronary artery was occluded three times in the following order: 2 min occlusion (Trial 1) followed by 15 min reperfusion; then 5 min occlusion followed by 90 min reperfusion and 2 min occlusion (Trial 2). In 15 control dogs, the 2 min occlusion was performed twice at a 110 min reperfusion interval; the former occlusion was also referred to as Trial 1 and the latter as Trial 2. The dogs were monitored by epicardial surface ECG, while regional myocardial function was estimated by sonomicrometry. Continuous measurements of myocardial tissue PCO2, pH, and extracellular K+ concentration were made concurrently. Results: Both trial occlusions produced a biphasic change in R wave amplitude characterised by a transient initial decrease succeeded by an increase with ST elevation. This biphasic change in R wave amplitude was indistinguishable between Trial 1 and Trial 2 in the control group. By contrast, in the 5 min group, the R wave amplitude initially decreased to a greater degree in Trial 2 than in Trial 1. More rapid contractile failure was also noticed in Trial 2, suggesting the possible involvement of mechanically induced electrical changes in the genesis of decreased R wave amplitude. After 45-60 s of occlusion, however, the R wave amplitude increased to a level much beyond the initial amplitude in Trial 1 [124.9(SEM 8.4)% at 120 s], whereas this level of increase was not observed in Trial 2 [106.5(7.8)%, p<0.05 v Trial 1]. There was also reduced elevation of the ST segment in Trial 2: 3.6(0.8) mV v 6.5(0.8) mV in Trial 1 at 120 s (p<0.05). This reduction in ST elevation was concomitant with decreased changes in PCO2, pH, and extracellular K+ concentration in Trial 2. These reduced changes in the ST segment and the metabolic variables were absent in the control group. Conclusions: These altered electrical responses of the myocardium may be the result of more rapid early contractile failure and attenuated metabolic changes during ischaemia occurring after recovery from preceding ischaemia.