Hegstad A C, Antonsen O H, Ytrehus K
Department of Morphology, Institute of Medical Biology, University of Tromso, Norway.
J Mol Cell Cardiol. 1997 Oct;29(10):2779-87. doi: 10.1006/jmcc.1997.0513.
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 microM H2O2 or 30 min global ischaemia followed by 30 min reperfusion with 0 (control group B), 25, 50 or 100 microM H2O2. Catalase (200 U/ml) was added as scavenger during reperfusion with 25 microM H2O2. Non-ischaemic perfusion: All concentrations of H2O2 induced an immediate vasodilatation, which was maintained in the 50 microM group, but it was followed by vasoconstriction in the 100 and 200 microM group. Left ventricular developed pressure (LVDP) was significantly increased at the end of perfusion in the 50 microM group compared to the control group. Exposure to 100 and 200 microM H2O2 significantly decreased LVDP and increased end-diastolic pressure. ATP was reduced in the 100 microM group. Post-ischaemic perfusion: Exposure to 25 microM H2O2 caused improved coronary flow during the first 20 min of reperfusion compared to the control group (accumulated coronary flow; 235.5 +/- 10.8 v 172.7 +/- 8.6 ml). LVDP was significantly higher in the 25 microM 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 microM H2O2 plus catalase. Treatment with 25 microM H2O2 caused significantly improved recovery of tissue ATP and creatine phosphate. In conclusion, the present study showed that exposure to 25 microM H2O2 improved post-ischaemic recovery in hearts subjected to global ischaemia.