A Model of Hyperhomocysteine-Induced Endothelial Dysfunction in Rats

Корокин, М В; Pokrovsky, M. V.; Новиков, О О; Гудырев, О. С.; Гуреев, В. В.; Denisyuk, T. A.; Корокина, Л. В.; Даниленко, Л. М.; Рагулина, В. А.; Konovalova, E.S.; Белоус, А. С.

doi:10.1007/s10517-011-1491-9

Cited by 7 publications

(2 citation statements)

References 1 publication

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“…2. Test for endotheliumindependent vascular relaxation (intravenous solution of sodium nitroprusside (NP) at a dose of 30 mg/kg at the rate of 0.1 ml per 100 g) [4,5,6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Endothelio- and cardioprotective effects of vitamin в6 and folic acid in modelling methionine-induced hyperhomocysteinemia

Provotorov

Корокин

Покровский

et al. 2023

RRP

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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.

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“…2. Test for endotheliumindependent vascular relaxation (intravenous solution of sodium nitroprusside (NP) at a dose of 30 mg/kg at the rate of 0.1 ml per 100 g) [4,5,6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Endothelio- and cardioprotective effects of vitamin в6 and folic acid in modelling methionine-induced hyperhomocysteinemia

Provotorov

Корокин

Покровский

et al. 2023

RRP

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“…The leading role in the pathogenesis of these pathologies is played by endothelial dysfunction, which is manifested in a decrease in the bioavailability of nitric oxide (Durante et al 2007). This causes research interest in the pathophysiological mechanisms of the occurrence and development of the endothelial component of these diseases (Korokin et al 2011;Pokrovskii et al 2012;Danilenko et al 2017).…”

Section: Introductionmentioning

confidence: 99%

Role of Arginase 2 as a potential pharmacological target for the creation of new drugs to correct cardiovascular diseases

Demchenko¹,

Koklin²,

Koklina³

2020

RRP

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Introduction: The review provides relevant information about arginase 2, the role of this enzyme in the formation of endothelial dysfunction and, as a consequence, the development of cardiovascular diseases. History of the discovery of arginase and its functions: The discovery of arginase took place long before its active study as a substance that affects the formation of endothelial dysfunction. Role of arginase 2 in the development of a number of cardiovascular diseases: The role of NO synthase and arginase 2 in the formation of oxidative stress is determined. The pathophysiological mechanisms of the development of a number of cardiovascular diseases, such as coronary heart disease, atherosclerosis, and aortic aneurysm, are described. The modern possibilities of treatment of endothelial dysfunction in the pathology of the cardiovascular system and the possibility of creation of new drugs are considered. An increase in the activity of arginase 2 was proven to occur in the case of the development of coronary heart disease (CHD), hypertension, type II diabetes mellitus, hypercholesterolemia, as well as in the process of aging. According to the WHO, coronary heart disease and apoplectic attack have topped the list of causes of death worldwide over the past 15 years. Arginase 2 as a potential pharmacological target: The purpose of this literature review is to determine the possibilities of use of arginase 2 as a new target for the pharmacological correction of cardiovascular diseases.

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GABA Derivatives Citrocard and Salifen Reduce the Intensity of Experimental Gestosis

et al. 2014

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Substitution of drinking water with 1.8 % NaCl solution in pregnant female rats from day 1 of gestation until parturitions was followed by the development of experimental gestosis. Gestosis manifested in an increase in BP by 18.2 %, protein concentration in the urine by 6.2 times, and edema severity in muscles, brain, and omentum in comparison with the initial level. The concentration of homocysteine in blood plasma of rats with complicated pregnancy 4.4-fold surpassed that in pregnant rats without gestosis, which can probably in a cause for gestosis development. GABA derivatives citrocard (50 mg/kg) and salifen (15 mg/kg), and the reference substance sulodexide (30 U/kg) reduced the severity of gestosis manifestations, which was seen from the absence of BP rise, decrease in urinary protein concentration by 1.9, 2.0, and 1.3 times and blood level of homocysteine by 1.7, 1.5, and 2.6 times, respectively, and a decrease in edema degree in comparison with female rats with experimental gestosis receiving physiological saline.

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A Model of Hyperhomocysteine-Induced Endothelial Dysfunction in Rats

Cited by 7 publications

References 1 publication

Endothelio- and cardioprotective effects of vitamin в6 and folic acid in modelling methionine-induced hyperhomocysteinemia

Endothelio- and cardioprotective effects of vitamin в6 and folic acid in modelling methionine-induced hyperhomocysteinemia

Role of Arginase 2 as a potential pharmacological target for the creation of new drugs to correct cardiovascular diseases

GABA Derivatives Citrocard and Salifen Reduce the Intensity of Experimental Gestosis

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