Abstract
During the experiment, the modeling of endothelial dysfunction of male rats was performed by intraperitoneal administration of L-NAME at a dose of 25 mg/kg for 7 days, and the same of female rats was performed by bilateral ovarioectomy and further intraperitoneal administration of L-NAME at a dose of 25 mg/kg for 7. The deficiency of nitric oxide as a result of the NO-synthase blockade was accompanied by the impairment of the endotheliumdependent and independent vasodilatation estimated in the pharmacological tests, which was expressed in the increasing coefficient of endothelial dysfunction. As a result of the research it was discovered that the combined application of thioctic acid at a dose of 50 mg/kg/day with antioxidant features and rosuvastatin at a dose of 0.85 mg/kg/day, which is a lipid-lowering drug, has endothelioprotective effect on the models of L-NAME-induced and hypoestrogen-LNAME-induced deficiency of nitric oxide, which is expressed in prevalence of endotheliumdependent relaxations of vessels and decreasing coefficient of endothelial dysfunction, as well as prevention of increase in nitric oxide production.
Highlights
According to statistics, the incidence of and mortality from complications of cardiovascular diseases, arterial hypertension (AH) and coronary heart disease (CHD) has been steadily increasing, which is evidence of the need to study the development mechanisms of this disease and possibilities of its correction capacity exposure to certain pathogenetic links [1]
Models of L-NAME- and hypoestrogen-L-NAME-induced nitrogen oxide deficiency realize the antioxidant properties of thioctic acid, as according to the literature, inhibition of nitrogen oxide production upon L-NAME use is accompanied by a significant increase in the spontaneous production of a superoxide-anion radical [5, 16, 20]
Vol 2, No1 (2): P. 9-15 antioxidant protection and increased formation of oxidation products, which is a factor for the formation of endothelial dysfunction [20, 21, 24]
Summary
The incidence of and mortality from complications of cardiovascular diseases, arterial hypertension (AH) and coronary heart disease (CHD) has been steadily increasing, which is evidence of the need to study the development mechanisms of this disease and possibilities of its correction capacity exposure to certain pathogenetic links [1]. The role of endothelial cells in the development of cardiovascular diseases was an important discovery for understanding the pathogenesis of hypertension, atherosclerosis, ischemic heart disease, cardiomyopathy, congestive heart failure, and metabolic disorders such as hyperlipidemia, hyperhomocysteinemia, diabetic vascular lesions, and venous transformation [2, 3, 4, 5]. This factor is called endothelial dysfunction (ED). The endothelium lines all vessels, regardless of their organ localization, endothelial dysfunction, which is based on the decrease in nitric oxide (NO) synthesis by endothelial cells, is a predictor of both arterial and venous diseases, and diseases of the microvasculature components [11, 12, 13].
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