Preconditioning with hydrogen peroxide (H₂O₂) or ischemia in H₂O₂-induced cardiac dysfunction

Abstract

The possible cardioprotective effects of preconditioning by ischaemia (IPC) or a low dose of H₂O₂ (HPC) prior to a high dose of H₂O₂ was investigated. Langendorff-perfused rat hearts (n = 10 in each group) were subjected to 10 min of 140 μmol/L H₂O₂ and 30 min recovery after either (1) control perfusion, (2) 20 μmol/L H₂O₂ for 10 min, recovery 10 min, or (3) 2 × 2 min global ischaemia and 5 min reperfusion. 140 μmol/L H₂O₂ increased left ventricular end-diastolic pressure from 0 to 68±8 mmHg in controls (mean±SEM), which was attenuated by IPC (46±9 mmHg, p < 0.001) and HPC (18±4 mmHg, p < 0.001 compared to controls, p < 0.01 compared to IPC). HPC, but not IPC, improved coronary flow (p < 0.02) and left ventricular developed pressure (p < 0.001) during recovery. Troponin T release was similar in all groups. Tissue thiobarbituric acid reactive substances, antioxidant capacity, catalase, and glutathione peroxidase were not influenced by 140 μmol/L H₂O₂. H₂O₂ decreased the level of tissue glutathione. This reduction was augmented by HPC (p < 0.02) and attenuated by IPC (p < 0.02). H₂O₂ increased superoxide dismutase (p < 0.04). The increase was attenuated by IPC (p < 0.05), but not influenced by HPC. HPC efficiently protected cardiac function in H₂O₂-induced cardiac injury, while IPC had only a small protective effect. The functional protection cannot be explained by reduction of irreversible injury, attenuation of lipid peroxidation, or modification of tissue antioxidant parameters.

Keywords:

• Catalase
• glutathione
• glutathione peroxidase
• ischaemic preconditioning
• superoxide dismutase
• rat
• thiobarbituric acid reactive substances