The Effect of Mexidol on Brain Natriuretic Peptide of Cardiomyocytes in a Post-Reperfusion Period in Experiment
Brain natriuretic peptide (BNP) participates in electrolyte balance maintenance in the body playing a critical part in the pathogenesis of cardiovascular diseases, and has the prognostic value in clinical presentation. It is of interest to analyze the peculiarities of BNP interaction with medicinal drugs, e.g. Mexidol, an antihypoxic agent of metabolic type that has a cardioprotective effect and is widely used in cardiology. The effect of Mexidol on BNP in a post-reperfusion period was studied for the first time.
The aim of the investigation was to estimate the effect of Mexidol on BNP accumulation and release intensity in cardiomyocyte granules in rats in a post-reperfusion period.
Materials and Methods. The experiments were carried out on 25 outbred male rats weighing 220–250 g. Total ischemia (10 min) was modeled by cardiovascular bundle compression according to Korpachev. Mexidol was administered intermittently, it being injected intraperitoneally after resuscitation, every 20 min within the first hour. BNP accumulation and release intensity was assessed by a quantitative analysis of immunolabeled granules of atrial myocytes under a transmission electron microscope.
Results. Mexidol administered at a dose of 25 mg/kg body mass within the first hour reperfusion after 10 min of total ischemia has a positive prolonged effect on BNP: after 60 days of a postperfusion period the processes of peptide accumulation and release in atrial myocytes of rats enhance resulting in an additional cardioprotective effect. The increase of BNP release against high synthetic and proliferative activity of fibroblasts contributes to the reduction of cardiosclerosis development in a long-term post-reperfusion period.
The study of immunolabeled granules of BNP myocytes in rat right atrium enabled to discover a new mechanism of a cardioprotective effect of Mexidol in a long-term post-reperfusion period.
Conclusion. Mexidol has a prolonged effect on brain natriuretic peptide and significantly enhances its accumulation and release in atrial cardiomyocytes of rats in a long-term post-reperfusion period having an additional cardioprotective effect and reducing cardiosclerosis development.
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