Abstract
Aim. To investigate the effect of perfluoroorganic compounds and poloxamer 188 on liver regeneration and the severity of systemic inflammatory response in an experimental model of sepsis.Materials and methods. Sepsis was induced in 52 male Wistar rats. Rats in experimental group 1 (n = 16) received a single intravenous injection of Oxiftem, rats in experimental group 2 (n = 15) were injected with Myotiv, and rats in the control group (n = 21) received a 0.9% NaCl solution. An intact group of rats (n = 11) was not subjected to sepsis modeling and received no treatment. Daily observations were conducted for 14 days. On the 15th day, rats were euthanized under light ether anesthesia. Biochemical serum parameters and the results of histological examination of liver tissue with immunohistochemical assessment of CD68 expression were studied.Results. No abnormalities were observed in the liver parenchyma of the intact group of rats. In the liver of the control group during sepsis, structural alterations of hepatic plates, perinuclear edema of hepatocytes, fatty degeneration of the liver, and congestion of portal tract vessels were noted, indicating morphological manifestations of liver necrosis, as well as proliferation of bile ducts, which is a histological consequence of cholestasis. In the experimental group, preservation of hepatic plate structure, an increase in the total number of nuclei, and binucleated hepatocytes were observed; sinusoids were not dilated. Hepatocyte proliferation and an increase in the number of binucleated liver cells indicated a regenerative response to systemic inflammatory damage and metabolic demand. A reduction in CD68-positive cell content in the liver following administration of both perfluoroorganic compounds and poloxamer 188 may be attributed to the suppression of macrophage activity and phagocytosis. This indicates a blockade of the immune functions of Kupffer cells in the experimental model of sepsis.Conclusion. The application of perfluoroorganic compounds and poloxamer 188 enhances liver regeneration and reduces the amplitude of systemic inflammatory response reactions in an experimental model of sepsis.
Published Version
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