ULTRASTRUCTURAL CHANGES AND MYOFIBROBLAST BEHAVIOR IN EXPERIMENTALLY INDUCED ACUTE MYOCARDIAL INFARCTION AND THE POSSIBLE ANTIOXIDANT DEFENSE
Ibrahim Labib Abdalla, Sherif Mohamed Zaki, Abir Oueida El Sadik, Enas Ahmad Mohamed, Sarah Mahmoud Kaooh.
Anatomy department, Faculty of medicine, Cairo University.
Background: After necrotizing injuries, like an acute myocardial infarction (MI), the myocardial tissue responds by inflammation and repair to form the final scar. These events accompanied by increased production of reactive oxygen species that attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Aim of the work: to investigate the ultrastructural changes and the healing process of the myocardium in experimentally induced acute myocardial infarction with the possible antioxidant (AO) defense. Material and methods: Ninety adult male albino rats were used in the present study and divided randomly into four groups: Group I (normal control) included 40 rats. Group II (MI group) 20 rats which received a daily dose (200 mg/kg/day) of Isoprenaline (ISP) for 2 consecutive days. Group III (AO before MI): 20 rats which received a daily dose of N-acetylcysteine (100mg/kg/day) for 16 consecutive days and a concomitant dose of ISP on the 15th and 16th days. Group IV (AO before and after MI): 10 rats which received a daily dose of N-acetylcysteine (100mg/kg/day) for 28 consecutive days and a concomitant dose of ISP on the 15th and 16th. Myocardial sections were stained with immunohistochemichal stains for α-SMA and PCNA and the myocardial tissue was prepared for electron microscopic examination. The mean area % of immunopositive cells were measured. Result: Electron microscopic examination of myocardial sections revealed disrupted myofibrils with nuclear and mitochondrial degeneration in group II with significant increase in the mean area % of α-SMA and PCNA immunoreactivity compered to those of the control rats. The difference in the mean area % of α-SMA and PCNA immunoreactivity in groups III and IV was non-significant as compared to those of the control group with few morphological ultrastructural changes. Conclusion: acute myocardial infarction has an inflammatory proliferative changes with cardiac muscle fiber necrosis followed by repair which is dependent on myofibroblst action with many ultrastructural changes. These changes where markedly prevented with the use of the antioxidant.