Heart disease is one of the major health problems of advanced as well as developing countries of the world. Extensive research through the last decade has shown beyond doubt that free radicals, particularly, reactive oxygen species play a cardinal role in the pathogenesis of oxidative myocardial damage with consequential cardiac malfunction. In the present study, the effect on oxidative stress associated with IR injury was investigated in a rat heart model. Twelve rats of 200-250g body weight were divided into sham-operated control group (I) (n=6) and ischemia and reperfusion group (II) (n=6) used for induction of ischemia-reperfusion injury. Hearts from all the groups were then processed for biochemical and histopathological studies. One way ANOVA followed by Bonferroni test was applied to test for significance and values are expressed as mean±SEM (p<0.05). There was a significant decrease in myocardial catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) & activities of these enzymes in mitochondria in I/R group. Ischemia and reperfusion induced toxicity reduced remarkable amount of RNA content as compared to sham operated control rat. Histopathology studies showed degree of myocardial damage in ischemia and reperfusion group. The study strongly suggests oxidative stress and associated ultra structural changes induced by myocardial ischemic-reperfusion injury.
