Method of Correction of Endothelial Dysfunction With Combination of Ademetionine and Taurine

Khadieva, T.A.; Dovgan, A. P.; Pokroskaya, T.G.

doi:10.18413/2313-8971-2016-2-2-36-40

Cited by 1 publication

(1 citation statement)

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“…In the walls of the vessels involved in the pathological process, there is an increased production of proinflammatory cytokines: IL-6, IL-8, MMP-31 and proteolytic enzymes, adhesion molecules, and accumulation of lipid peroxidation products (Lattimer et al 2016, Denisiuk 2017. In addition, there is an increase in the adhesive properties of platelets and leukocytes to the endothelium, with the latter further migrating the into the vessel wall (Khadieva et al 2016). The resulting vein-specific inflammation leads to a violation of endothelial function and permeability of the vascular wall (Aliev et al 2008, Kudryavtsev et al 2017.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of pharmacological correction of L-name-induced endothelial dysfunction, platelet aggregation and venous tone with diosmin Detralex 1000 mg

Lukyanova¹,

Kolesnichenko²,

Гуреев³

et al. 2018

RRP

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Introduction. Chronic venous diseases are one of the urgent problems of modern medicine. Recent studies have shown high significance of endothelial dysfunction (ED) and oxidative stress in their pathogenesis. For the correction of the occurring changes, drugs of the flavonoid group, particularly diosmin and hesperidin, are currently used. Numerous studies have confirmed a vast range of biological effects of diosmin; however, there are only sporadic data on its endothelium protective effects. Materials and methods. The study was performed in 70 white mature male rats of Wistar line, weighing 180-220 g. ED simulation was performed using non-selective blocker of NO-synthase N-nitro-L-arginine methyl ester (L-NAME). Functional vascular tests and biochemical markers were used to determine a degree of correction of functional disorders. An anti-inflammatory effect of Detralex 1000 mg was estimated in 10 mature albino rabbits weighing 2800 - 3200 g by using o-xylene. The study of the venotonic property of the drug was carried out in the experiment in an isolated segment of the rats’ portal vein with Ca2+ solutions at a concentration of 0.08-1.75 mcM. The histologic specimens were prepared in accordance with the generally accepted methods. Results and discussion. The administration of the test drug did not lead to a statistically significant decrease in blood pressure in the conditions of L-NAME-induced ED. However, there was a dose-dependent statistically significant decrease in the coefficient of ED (CED), which indicates a positive endothelium protective effect. Course administration of Detralex 1000 mg leads to a significant dose-dependent correction of platelet aggregation disorders, which is manifested in the extended aggregation time. The results of studying an anti-inflammatory activity of the drug showed a decrease in the size of spots caused by the application of o-xylene, and the extention of the time interval before their onset. Studying a Ca2+-mediated smooth muscle response showed that the vein contractile force reaches its maximum at a higher dosage of the drug with a lower concentration of Ca2+. In the morphological study of the stomach wall, small and large intestine of the intact rats and rats receiving a course of Detralex 1000 mg, there were no inflammatory changes in the mucosa of the comparison group. Conclusions. The study found that Detralex 1000 mg significantly reduces the ED coefficient and slows platelet aggregation against the background of L-NAME-induced ED; the efficacy is dose-dependent. Detralex 1000 mg dose-dependently reduces vascular permeability disorders caused by the application of o-xylene. The test drug has a Ca2+-mediated mechanism of increasing the contractile activity of the venous wall. It was found that the course administration of the drug per os has no local irritative effect.

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Section: Introductionmentioning

confidence: 99%