Orel K. Pathogenetic mechanisms of endothelial dysfunction in osteoarthritis and how its correct

Dissertation is devoted to the determination of the main pathophysiological endothelial dysfunction mechanisms in osteoarthritis and research correction methods efficacy. As a result of the performed research, has proven efficacy of the selected experimental osteoarthritis model. Increased level of Interleukin 1β and Interleukin 10 in the pathogenesis of the simulated osteoarthritis has been established. Content of Von Willebrand factor, endothelin-1 and asymmetric dimethylarginine increased during the study disease. Established endothelial functioning imbalance with vasoconstrictor potential predominance against the background of vasodilatory potential weakening in conditions of the simulated pathological process found increased levels of endothelin-1 on the background of S-nitrosothiols content reduction. In experimental osteoarthritis was established nitric oxide hyperproduction under the influence of significant increase in the activity of inducible NO synthase. It has been proved decreasing in endothelial NO synthase activity against the background of experimental osteoarthritis development and due to its activation and inducible NO synthase. Also, has been proved effectiveness of endothelial dysfunction correction with osteoarthritis via aminoguanidine, which is an inhibitor of inducible NO synthase. Using L-arginine was found its effectiveness as a corrective remedy for disturbance of the endothelium functioning caused by experimental osteoarthritis development. Comparative correction remedy characteristic has shown that nitric oxide donor use is more effective than inhibition of inducible NO synthase. In animals group receiving L-arginine as part of complex osteoarthritis correction, was proved normalization of endothelial function indicators.