Background. In the structure of purulent complications, peritonitis, destructive lesions of abdominal organs, and, as a rule, advanced forms of these diseases occupy one of the first places - 15-25% of urgent surgical diseases are complicated by peritonitis. It is generally known that the leading role in the triggering mechanism of the development of peritonitis belongs to the systemic inflammatory reaction, a component of which is phagocytosis, cellular and humoral immunity. However, the results of research on the state of functional activity of the endothelium in experimental peritonitis are limited.
Aim: to study the activity of NO-synthase, FV and endothelin-1 in rats with experimental peritonitis.
Materials and methods. Experimental studies were conducted on 24 non-linear laboratory rats, which were divided into 2 groups: 1 group – intact control (animals received distilled water), 2 group – animals of the control pathology group. According to the "Methodological recommendations for preclinical study of medicinal products", experimental peritonitis was studied on the model of V. A. Lazarenko. Indicators of vascular-platelet and coagulation hemostasis were determined according to generally accepted methods. Indicators characterizing endothelial dysfunction were studied according to generally accepted methods.
Results. 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 the hyperproduction of nitric oxide, 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. In animals with experimental peritonitis against the background of oxidative stress, there was an increase in the number of circulating desquamated endothelial cells in the blood, which is a highly specific marker of endothelial dysfunction. The level of the Willebrand factor also increased, which indicates the pathogenetic dependence of the factors that damage the endothelium of the vascular wall on the concentration of the Willebrand factor, which helps to reduce the permeability of blood vessels 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.
Conclusion. Hyperproduction of nitric oxide not only reflects the processes that occur in the focus of vascular endothelium damage, but also affects the severity of the inflammatory process and the consequences of the disease.
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