Effect of superoxide dismutase and acidified sodium nitrite on infarct size following ischemia and reperfusion in dogs.

The effects of superoxide dismutase (SOD) alone or in combination with acidified sodium nitrite (NaNO2), a liberator of nitric oxide were examined in dogs after ischemia and reperfusion. Animals were divided into five groups. Left anterior descending coronary artery was occluded for 90 min followed by 4 hours of reperfusion with or without therapeutic interventions given preceding reperfusion. Left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP) and ECG changes were monitored throughout the study. Area at risk was defined by Evans blue and area of infarction by incubation in triphenyltetrazolium. Myocardial tissue lipid peroxidation was measured in ischemic and non-ischemic zones. There was no evidence of infarction until ninety minutes of ischemia. Percentage area of necrosis vis-a-vis area at risk percentage necrosis in left vertricular mass was significantly low in animals treated with combination of SOD and NaNO2 in comparison with isolated treatment with saline, SOD or NaNO2. LVEDP increased significantly following ischemia and remained unchanged during saline reperfusion. Treatment with SOD, NaNO2 in isolation or its combination significantly lowered LVEDP. Maximum increase in tissue lipid peroxidation was observed in saline and NaNO2 treated animals. SOD alone or in combination with NaNO2 significantly lowered the lipid peroxidation. The results clearly demonstrate that reperfusion can cause necrosis in ischemic myocardium. Combined treatment with SOD and NaNO2 offers significant cardioprotection against oxidative stress.