Decreased defence against free radicals in rat heart during normal reperfusion after hypoxic, ischemic and calcium-free perfusion.

Excessive formation of free radicals possibly plays an important role in the origin of irreversible damage of the heart after hypoxic, ischemic or Ca2+-free treatment. The effect of these treatments on the activity of superoxide dismutase and the glutathione system was studied on isolated rat heart. These activities reflect the protective capacity of the heart against reactive substances. In addition the peroxidation of lipids is determined in the treated hearts using malondialdehyde formation as an indicator. All experiments were performed using a Langendorff-apparatus with recirculating perfusion. The observed changes in the components of the glutathione system and superoxide dismutase activity both after hypoxic, ischemic and Ca2+-free perfusion, as measured upon reperfusion, indicate a decrease in cellular defense mechanisms in the heart against free radicals. The effect was most pronounced upon Ca2+-repletion after a period of Ca2+-free perfusion. No malondialdehyde could however be detected either in the tissue of the treated hearts or in the perfusate. Our data give reason to expect beneficial effects of an adequate pharmacological treatment, which replenishes the cellular defence systems.