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Background: Recently years, increasing coronary artery disease in the worldwide. An estimated 17.9 million people died from cardiovascular disease(CVD) in 2016, representing 31% of all global deaths. Of these deaths, 85% are due to heart attack and stroke, reported WHO. Myocardial infarction is invariably followed by numerous pathophysiological and biochemical alterations including hyperlipidemia, thrombosis, lipid peroxidation and free radical damage etc., leading to qualitative and quantitative changes of myocardium. Determination of in blood serum and cardiac tissue homogenate levels of cardiac biomarker cardiac specific troponin I and estimation of some antioxidants enzymes of experimental acute infarction model induced by coronary artery occlusion in rats. Materials and methods: Adult male Wistar rats, weighting approximately 180 to 200±20 gram, used for the experiment. We did coronary occlusion induced myocardial ischemia by Kogan A.K., Ambaga M /1979/‘s method. The experiment is 1st, 3rd, 7th, 14th 21st days blood samples were collected and used to determine in blood serum and cardiac tissue homogenate levels of cardiac biomarker cardiac specific troponin I (CTn-I) and estimation of some antioxidants enzymes (SOD, GSH, GSH-px) were estimated using standard rat ELISA KIT by enzyme-linked immunesorbent assay. Result: Determination of cardiac troponin-I levels in blood serum of experimental acute infarction model induced by coronary artery occlusion in rats increased by 31.9-58.4% in the 1st, 3rd, 7th, 14th 21st days of the test compared to healthy groups. The cardiac biomarker cardiac specific troponin I is indicative for cardiomyocyte damage and is currently used in the diagnosis and prognosis of myocardial ischemia. It is also shown that substances such as endogen and antioxidant decreases in heart ischemia. Conclusion: Determination of decreased level are antioxidants (SOD, GSH, GSH-px) in blood serum of experimental acute infarction model induced by coronary artery occlusion in rats, it seems to induced of pathogenesis of coronary disease and infarction myocardium while the accumulation of lipid product cause to damage the cell membrane. |
