The aim of this study was to develop a model of myocardial infarction in rats, which would be easy to reproduce, would have low mortality and at the same time would correspond to the most common idea about the etiology of this disease in humans. In the preparatory phase, a model of cardiovasopathy was applied, which was induced by keeping rats for two months on a diet with excess fat and calcium and sodium salts. During the last week, rats were induced systemic inflammation by injecting bacterial lipopolysaccharide. The development of myocardial infarction was initiated in two ways: animals were exposed to hypoxia-hypercapnia or immobilization stress. The results of the experiments show that the use of the diet led to the development of hyperlipidemia in animals and a statistically significant increase in the atherogenic index, and both stressors used in the model were equally effective and within 1–2 days caused myocardial infarction, which was confirmed by electrocardiography, enzyme-linked immunosorbent assay and histological methods.
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