Abstract

Introduction. The active development of agriculture with the widespread use of nitrogen-containing fertilizers, increased consumption of processed meat products containing sodium nitrite as a preservative, inevitably leads to an increase in the nitrogen load on the human body and can cause the development of cardiovascular diseases. Materials and methods. The cardiotoxic effect of sodium nitrite was evaluated on a model of an isolated rat heart with subchronic intragastric administration for 28 days at doses of 0.03; 0.3; 3.0 mg/kg. Results. The use of sodium nitrite leads to dilation of the coronary vessels and myocardium, inhibition of the contractile activity of the heart, disruption of its electrical activity in the form of a shortening of the QT interval associated with an increased risk of ventricular fibrillation, and a tendency to increase the amplitude of the T wave, which indicates myocardial ischemia. In a stress test with total ischemia, it was revealed that the magnitude of the change in the parameters characterizing the restoration of myocardial function under reperfusion conditions is inversely proportional to the dose of sodium nitrite used. Limitations. The study was performed only on male white rats more prone to the development of cardiovascular pathology. Conclusion. With subchronic administration, sodium nitrite has cardiotoxicity at a dose of 0.028 mg/kg, which is twice lower than the WHO-established permissible daily intake for humans (0.06 mg/kg).

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