Abstract
The review focuses on the pathogenetic mechanisms of ethanol influence on the development of oxidative stress (OS) and endothelial dysfunction (ED). It is shown that both in acute and chronic alcohol intoxication, the intake of ethanol in the body initiates the development of OS, the formation of reactive oxygen species, causes a decrease in the content of endothelium-derived relaxing factors (nitric oxide (NO), prostacyclin, endothelium-derived hyperpolarization factor (EDHF)), an increase in the concentration of endothelium-derived constricting factors (endothelin, angiotensin-II), thereby causing the development of ED. When alcohol is consumed in small doses by healthy non-drinkers, ethanol can act as an antioxidant, cause the neutralization of reactive oxygen species, promote the formation of NO, and prevent the formation of ED. Currently used methods for evaluating ED allow us to characterize the functional state of the endothelium. Structural changes in the blood vessel wall as a manifestation of ED in alcoholic disease are not sufficiently described, which indicates the need to study them using modern histological, histochemical, immunohistochemical and electron microscopic methods.
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