Proapoptotic and antiapoptotic stimuli alternation in myocardial infarction experimental model.

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Myocardial infarction is a life-threatening complication of the coronary artery disease - the leading cause of premature death worldwide. The severity of this condition is the result of cellular death following the myocardial ischaemia, which occurs via several mechanism including apoptosis. For the research of this condition, animal models are often employed. We established isoprenaline-induced rat model of myocardial infarction, focusing on the immunohistochemical analysis of the expression of antiapoptotic and proapoptotic proteins BCL-2 and BAX, respectively. Apoptosis (based on BAX-positivity) was activated in cardiac muscle cells within the first day, later on day 8 also in fibroblasts of the forming scar tissue. Antiapoptosis in cardiac muscle cells was weak to moderate on the day 1 and 2, on the day 8 macrophages were strongly positive for BCL-2. The results confirmed that programmed cell death as well as mechanisms of antiapoptosis contribute to the pathogenesis of myocardial infarction. Previous research demonstrated that by experimentally affecting proapoptotic and antiapoptotic signals, it is possible to influence various aspects of myocardial infarction including: infarction size, cardiac remodelling and prognosis of the heart failure. Future research is warranted to fully elucidate the role of this process during myocardial infarction, which will result in refined diagnostic and therapeutic strategies (Tab. 1, Fig. 1, Ref. 21). Keywords: myocardial infarction, isoprenaline, apoptosis, necrosis, BCL-2, BAX.