Abstract
Functioning of visceral systems in hypercytokinemia induced, inter alia, by an increase in the systemic level of bacterial lipopolysaccharides (LPS) is an important item on the research agenda in physiology. Hypercytokinemia disrupts effective functioning of visceral systems, in particular, the circulatory system. The aim of the study was to test the hypothesis that an increase in the systemic level of the pro-inflammatory cytokine tumor necrosis factor (TNF-α) changes circulatory parameters due to an increased synthesis of the inducible isoform of the cyclooxygenase enzyme (COX-2). In experiments on male Wistar rats (n = 14) anesthetized with urethane (1.6 g/kg), we studied the effects of intravenous administration of TNF-α on mean arterial pressure (MAP) and heart rate (HR) as well as the influence of the COX blocker diclofenac (DC) on the effects in question. It was found that 40 minutes after the administration of TNF-α (45 μg/kg), the mean BP and HR in the anesthetised rat rise significantly, while the preliminary administration of DC (2.5 μg/kg) prevents the development of these effects. Thus, the proposed hypothesis was experimentally confirmed. It is assumed that the observed effects of TNF-α are induced by the influence of increased levels of prostanoids on the structures of the central nervous system regulating the activity of visceral systems.
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