The aim of the present study was to test the hypothesis that low concentrations of hydrogen peroxide (H2O2) have a beneficial effect on post-ischaemic myocardial recovery. Functional and metabolic measurements were performed in isolated buffer-perfused rat hearts exposed to 30 min perfusion with 0 (control group A), 25, 50, 100 or 200 mu M H2O2 or 30 min global ischaemia followed by 30 min reperfusion with 0 (control group B), 25, 50 or 100 mu M H2O2. Catalase (200 U/ml) was added as scavenger during reperfusion with 25 mu M H2O2. Non-ischaemic perfusion: All concentrations of H2O2 induced an immediate vasodilatation, which was maintained in the 50 mu M group, but it was followed by vasoconstriction in the 100 and 200 mu M group. Left ventricular developed pressure (LVDP) was significantly increased at the end of perfusion in the 50 mu M group compared to the control, group. Exposure to 100 and 200 mu M H2O2 significantly decreased LVDP and increased end-diastolic pressure. ATP was reduced in the 100 mu M group. Post-ischaemic perfusion: Exposure to 25 mu M H2O2 caused improved coronary now during the first 20 min of reperfusion compared to the control group (accumulated coronary now; 235.5 +/- 10.8 v 172.7 +/- 8.6 ml). LVDP was significantly higher in the 25 mu M group compared to the control (59.8 +/- 10.2 v 22.1 +/- 7.3 mmHg), and end-diastolic pressure was significantly lower (32.1 +/- 19.6 v 78.8 +/- 2.2 mmHg) at the end of reperfusion. Improved recovery was not observed in the group exposed to 25 mu M H2O2 plus catalase. Treatment with 25 mu M H2O2 caused significantly improved recovery of tissue ATP and creatine phosphate. In conclusion, the present study showed that exposure to 25 mu M H2O2 improved post-ischaemic recovery in hearts subjected to global ischaemia. (C) 1997 Academic Press Limited.