Abstract

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 200μmH2O2or 30 min global ischaemia followed by 30 min reperfusion with 0 (control group B), 25, 50 or 100μmH2O2. Catalase (200 U/ml) was added as scavenger during reperfusion with 25μmH2O2. Non-ischaemic perfusion: All concentrations of H2O2induced an immediate vasodilatation, which was maintained in the 50μmgroup, but it was followed by vasoconstriction in the 100 and 200μmgroup. Left ventricular developed pressure (LVDP) was significantly increased at the end of perfusion in the 50μmgroup compared to the control group. Exposure to 100 and 200μm H2O2significantly decreased LVDP and increased end-diastolic pressure. ATP was reduced in the 100μmgroup. Post-ischaemic perfusion: Exposure to 25μmH2O2caused improved coronary flow during the first 20 min of reperfusion compared to the control group (accumulated coronary flow; 235.5 ± 10.8v172.7 ± 8.6 ml). LVDP was significantly higher in the 25μmgroup compared to the control (59.8 ± 10.2v22.1 ± 7.3 mmHg), and end-diastolic pressure was significantly lower (32.1 ± 19.6v78.8 ± 2.2 mmHg) at the end of reperfusion. Improved recovery was not observed in the group exposed to 25μmH2O2plus catalase. Treatment with 25μmH2O2caused significantly improved recovery of tissue ATP and creatine phosphate. In conclusion, the present study showed that exposure to 25μmH2O2improved post-ischaemic recovery in hearts subjected to global ischaemia.

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