Abstract
The endotelio- and cardioprotective effects of vitamin B6 (2 mg/kg) and folic acid (0.2 mg/kg) upon modeling of methionine-induced hyperhomocysteinemia via methionine intragastric administration at a dose of 3 g/kg were studied. It was shown that the combined use of vitamin B6 and folic acid allows on the background of a significant reduction in homocysteine concentrations normalizing the endothelial dysfunction coefficient and the parameters of maximum left ventricular pressure in response to intravenous administration of adrenaline. The research was partially supported by the grant of the President of the Russian Federation №MD-4711.2015.7.
Highlights
A number of factors of different nature has been determined [1], contributing to the development and progression of cardiovascular disease such as dyslipidemia, hypertension, overweight, smoking, physical inactivity, and diabetes
According to the study design, a hyperhomocysteinemia-induced endothelial dysfunction was simulated by daily intragastric administration of methionine at a dose of 3 g/kg for Intragastric administration of the stated dose of methionine resulted in a significant increase in the endothelial dysfunction coefficient up to 3.3 ± 0.3, while the EDC in the control group was 0.9 ± 0.2
Systolic and diastolic blood pressure values remained within physiological limits in all series of the experiments (Table 1)
Summary
A number of factors of different nature has been determined [1], contributing to the development and progression of cardiovascular disease such as dyslipidemia, hypertension, overweight, smoking, physical inactivity, and diabetes. A group of so-called "new" risks can be distinguished, which primarily includes an increase in homocysteine levels in the blood. More than 80 clinical and epidemiological studies have confirmed that hyperhomocysteinemia is a significant, independent risk factors for early development and rapid progression of atherosclerosis, and thrombosis of the coronary, cerebral and peripheral arteries, and may be a predictor of death [2]. S.H.Mudd, T.Gerritsen, H.A.Waismann et al demonstrated that high concentration of homocysteine in the blood and, in urine, resulting in homocystinuria is a consequence of deficiency of the cystathionine-beta-synthase enzyme
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