Mechanisms of Endothelial Dysfunction in Pathologies of Various Genesis

DOI

10.2991/ichw-19.2019.23How to use a DOI?

Keywords

endothelial dysfunction, pathologies, biomedicine, vascular endoteleum

Abstract

Studies in the experiment and the clinic demonstrated the nature of changes in the system of POL - AOC, nitric oxide homeostasis and cholesterol as factors contributing to dysfunction of the vascular endothelium. In metabolic syndrome in pregnant women and in patients with myocardial ischemia, as well as in intoxication syndrome (cobalt chloride), the induction of the lipid peroxidation process according to malonic aldehyde and impaired AODS cells was detected. A deficit of nitric oxide (NO), a violation of its bioavailability and vasoconstriction develops. Consequently, lipid peroxidation-triggering factors: elevated blood glucose, impaired oxygen supply to the myocardium (ischemia), and exposure to cobalt chloride play an important role in disrupting the formation of nitric oxide and adaptive mechanisms from reactive oxygen species (ROS). Disruption of nitric oxide homeostasis (eNOS/NO) plays a decisive role in the genesis of vascular complications and can be considered a biochemical marker for the development and progression of various pathologies. Based on these data, it is possible to develop a methodology for correcting the pathogenetic orientation.

Copyright

© 2019, the Authors. Published by Atlantis Press.

Open Access

This is an open access article distributed under the CC BY-NC license (http://creativecommons.org/licenses/by-nc/4.0/).

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TY  - CONF
AU  - S. G. Dzugkoev
AU  - I. V. Mozhaeva
AU  - F. S. Dzugkoeva
AU  - A. I. Tedtoeva
AU  - O. I. Margieva
AU  - O.Yu. Garmash
AU  - N.M. Karchaidze
PY  - 2019/10
DA  - 2019/10
TI  - Mechanisms of Endothelial Dysfunction in Pathologies of Various Genesis
BT  - Proceedings of the International Conference on Health and Well-Being in Modern Society (ICHW 2019)
PB  - Atlantis Press
SP  - 92
EP  - 95
SN  - 2468-5739
UR  - https://doi.org/10.2991/ichw-19.2019.23
DO  - 10.2991/ichw-19.2019.23
ID  - Dzugkoev2019/10
ER  -