Study of indicators of endothelial dysfunction in rats with experimental peritonitis

The article presents the results of the study of the activity of endothelial and inducible NO-synthase, the level of Willebrand factor and endothelin-1 in rats with experimental peritonitis. The most likely mechanism that is damaged in the endothelium during peritonitis is the activation of the syn...

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Main Authors: V. Gutsulyuk, I. Savytskyi, S. Tsypoviaz, S. Znamerovskyi, V. Sarahan, T. Gerasymenko
Format: Article
Language:English
Published: Kazimierz Wielki University 2022-01-01
Series:Journal of Education, Health and Sport
Subjects:
Online Access:https://apcz.umk.pl/JEHS/article/view/41740
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author V. Gutsulyuk
I. Savytskyi
S. Tsypoviaz
S. Znamerovskyi
V. Sarahan
T. Gerasymenko
author_facet V. Gutsulyuk
I. Savytskyi
S. Tsypoviaz
S. Znamerovskyi
V. Sarahan
T. Gerasymenko
author_sort V. Gutsulyuk
collection DOAJ
description The article presents the results of the study of the activity of endothelial and inducible NO-synthase, the level of Willebrand factor and endothelin-1 in rats with experimental peritonitis. The most likely mechanism that is damaged in the endothelium during peritonitis is the activation of the synthesis of inducible NO-synthase by neutrophils/macrophages in response to infection. It is possible that hyperproduction of nitric oxide (NO), on the one hand, is aimed at destroying microflora and oxidizing toxins, and on the other hand, at suppressing the expression of tissue factor and cell adhesion molecules. platelet aggregation and cascade disorders in the hemostasis system. All this indicates that the hyperproduction of NO not only reflects the processes that occur in the focus of damage to the vascular endothelium, but also affects the severity of the inflammatory process and the outcome of the disease. In animals with experimental peritonitis on the background of OS, an increase in the number of circulating desquamated endothelial cells in the blood, which is a highly specific marker of endothelial dysfunction, was noted. The level of the Willebrand factor also increased, which can serve as a marker of increased risk of thrombus formation and indicate the pathogenetic dependence of the factors that damage the vascular wall endothelium on the concentration of the Willebrand factor, which contributes to the reduction of vascular permeability by adhesion of platelets to the endothelium. Confirmation of the development of endothelial dysfunction in peritonitis is an increase in the concentration of endothelin-1, which is a regulator of the process of vascular neoangiogenesis in response to endothelial damage.
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spelling doaj.art-9f511329358749ac9241a80429cb0a8f2023-01-08T11:41:22ZengKazimierz Wielki UniversityJournal of Education, Health and Sport2391-83062022-01-0112110.12775/JEHS.2022.12.01.043Study of indicators of endothelial dysfunction in rats with experimental peritonitisV. Gutsulyuk0I. Savytskyi1S. Tsypoviaz2S. Znamerovskyi3V. Sarahan4T. Gerasymenko5International Academy of Ecology and MedicineInternational Academy of Ecology and MedicineInternational Academy of Ecology and MedicineInternational Academy of Ecology and MedicineInternational Academy of Ecology and MedicineInternational Academy of Ecology and Medicine The article presents the results of the study of the activity of endothelial and inducible NO-synthase, the level of Willebrand factor and endothelin-1 in rats with experimental peritonitis. The most likely mechanism that is damaged in the endothelium during peritonitis is the activation of the synthesis of inducible NO-synthase by neutrophils/macrophages in response to infection. It is possible that hyperproduction of nitric oxide (NO), on the one hand, is aimed at destroying microflora and oxidizing toxins, and on the other hand, at suppressing the expression of tissue factor and cell adhesion molecules. platelet aggregation and cascade disorders in the hemostasis system. All this indicates that the hyperproduction of NO not only reflects the processes that occur in the focus of damage to the vascular endothelium, but also affects the severity of the inflammatory process and the outcome of the disease. In animals with experimental peritonitis on the background of OS, an increase in the number of circulating desquamated endothelial cells in the blood, which is a highly specific marker of endothelial dysfunction, was noted. The level of the Willebrand factor also increased, which can serve as a marker of increased risk of thrombus formation and indicate the pathogenetic dependence of the factors that damage the vascular wall endothelium on the concentration of the Willebrand factor, which contributes to the reduction of vascular permeability by adhesion of platelets to the endothelium. Confirmation of the development of endothelial dysfunction in peritonitis is an increase in the concentration of endothelin-1, which is a regulator of the process of vascular neoangiogenesis in response to endothelial damage. https://apcz.umk.pl/JEHS/article/view/41740peritonitisendothelial dysfunctionoxidative stressWillebrand factorpathogenesis
spellingShingle V. Gutsulyuk
I. Savytskyi
S. Tsypoviaz
S. Znamerovskyi
V. Sarahan
T. Gerasymenko
Study of indicators of endothelial dysfunction in rats with experimental peritonitis
Journal of Education, Health and Sport
peritonitis
endothelial dysfunction
oxidative stress
Willebrand factor
pathogenesis
title Study of indicators of endothelial dysfunction in rats with experimental peritonitis
title_full Study of indicators of endothelial dysfunction in rats with experimental peritonitis
title_fullStr Study of indicators of endothelial dysfunction in rats with experimental peritonitis
title_full_unstemmed Study of indicators of endothelial dysfunction in rats with experimental peritonitis
title_short Study of indicators of endothelial dysfunction in rats with experimental peritonitis
title_sort study of indicators of endothelial dysfunction in rats with experimental peritonitis
topic peritonitis
endothelial dysfunction
oxidative stress
Willebrand factor
pathogenesis
url https://apcz.umk.pl/JEHS/article/view/41740
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