Effect of L-arginine on endothelial dysfunction in patients with congenital mitral valve prolapse
- Authors: Shodikulova GZ1
-
Affiliations:
- Samarkand State Medical Institute, Samarkand, Uzbekistan
- Issue: Vol 95, No 3 (2014)
- Pages: 326-331
- Section: Theoretical and clinical medicine
- URL: https://journals.rcsi.science/kazanmedj/article/view/1506
- DOI: https://doi.org/10.17816/KMJ1506
- ID: 1506
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Abstract
АIM. To study the effect of L-arginine on endothelium-dependent vasodilatation in patients with congenital mitral valve prolapse and different degrees of regurgitation. Methods. The study included 86 patients [36 (41.9%) males and 50 (58.1%) females aged 15-25 (mean age 19.9±1.42) years] with signs of congenital mitral valve prolapse. The first group included 41 patients were L-arginine (Tivortin) as a prophylaxis medication. The second group included 45 patients who were not taking L-arginine. Subgroup A of each group included 20 and 22 patients with stage I of mitral regurgitation, accordingly; subgroup B of each group included 21 and 23 patients with stage II of mitral regurgitation, accordingly. Results. In patients of the first group with mitral valve prolapse and stages I and II of mitral regurgitation, distinct positive changes were observed after 6 months of treatment with L-arginine. Compared to baseline data, in patients of the first group with stage I of mitral regurgitation brachial artery diameter increased by 1,44 times (р <0.001), resistance index - by 1.5 times (р <0.001); in patients with stage II of mitral regurgitation the following parameters increased by 1.65 and 1.39 times (р <0.001 and р <0.01) accordingly. At the same time, parameters of NO-system also improved in patients of the first group with stages I and II of mitral regurgitation after 6 months of treatment: endothelial NO synthase activity increased by 1.18 and 1.29 times (р <0.05 and р <0.02) accordingly, NO level decreased by 1.17 and 1.18 times (р <0.05), inducible NO synthase activity - by 1.17 and 1.29 times (р <0.05 and р <0.02), and there was a reduction of peroxynitrite levels by 1.23 and 1.34 times (р <0.02 and р <0.01), endotheline-1 - by 1.07 and 1.26 times (р <0.05 and р <0.02), vascular endothelial growth factor - by 1.08 and 1.24 times (р <0.05 and р <0.01) accordingly. Conclusion. Recommended doses of L-arginine restores the stream-dependent vasodilation, activity of the NO-system and process of angiogenesis after 6 months of treatment.
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##article.viewOnOriginalSite##About the authors
G Z Shodikulova
Samarkand State Medical Institute, Samarkand, Uzbekistan
Email: shodikulovagulandom@mail.ru
References
- Байрамгулов Ф.М., Булганова А.Д., Курсанкова М.Е. и др. Тканевая инсулин-резистентность и функциональное состояние эндотелия крупных сосудов у больных артериальной гипертонией // Тер. арх. - 2002. - №12. - С. 24-26.
- Голиков П.П., Николаева Н.Ю., Гаврилинко И.А. и др. Оксид азота и перекисное окисление липидов как факторы эндогенной интоксикации при неотложные состояниях // Пат. физиол. и эксп. тер. - 2000. - №1. - С. 6-9.
- Земцовский Э.В. Недифференцированные дисплазии соединительной ткани. «Карфаген должен быть разрушен?» // Кардиоваск. тер. и проф. - 2008. - №6. - С. 73-76.
- Кадурина Т.И., Горбунова В.Н. Дисплазия соединительной ткани. - СПб.: ЭЛБИ, 2009. - 722 с.
- Комарин А.С., Азимов Р.К. Патофизиология обмена монооксида азота: метод. рекомендации. - Ташкент, 2005. - 29 с.
- Коромок М.А., Иванова Л.И., Майорова И.Г., Токарев В.Е. Метод определения каталазы // Лаб. дело. - 1988 - №1. - С. 16-19.
- Ольбинская Л.И., Сизова Ж.М., Колбая А.Г. Коррекция изосорбит-5-мононитратами эндотелиальной дисфункции у больных хронической сердечной недостаточностью // Клин. мед. - 2007. - №1. - С. 27-31.
- Степанов Ю.М., Колонов И.Н., Журбина А.И., Филиппова А.Ю. Аргинин в медицинской практике // Ж. АМН Украины. - 2004. - Т. 10, №1. - С. 340-352.
- Сумбаев В.В., Ясинская И.М. Влияние ДДТ на активность синтазы оксида азота в печени, лёгких и головном мозге // Соврем. проб. токсикол. - 2000. - №3. - С. 3-7.
- Филиппов А.Е., Ханджян А.М., Солодухин К.А. и др. Дисфункция эндотелия и факторы риска при ишемической болезни сердца // Клин. мед. - 2006. - №2. - С. 28-32.
- Celerman D.S., Sovengen K.E., Yooch V.M. et al. Noninvagive defection of endothelial dysfunction in children and adults at risk of atherosis // Lancet. - 1992. - Vol. 340. - P. 1111-1115.
- Habid S., Ali A. Biochemistry of nitric oxide // Ind. J. Clin. Biochem. - 2011. - Vol. 26, N 1. - P. 3-17.
- Robinson C.J., Stringer S.E. The splicavariants of vascular endothelial growth factor (VEGF) and their receptors // J. Cell Sci. - 2011. - Vol. 114, N 5. - P. 853-865.
- Shibuga M. Vascular endothelial growth factor receptor-1 (VEGFR)/Fl+1 a dual regulator for angiogenesis // Angeogenesis. - 2006. - Vol. 9, N 4. - P. 225-230.
- Siraik D.A., Chang D.L., Colucci W.S. Interleukin-1β and tumor necrosis factor α decrease collagen synthesis and increase matrix metalloproteinase activity in cardiac fibroblasts in vitro // Circ. Res. - 2000. - Vol. 86, N 3. - P. 1259-1265.
- Sugimoto H., Hamano Y., Charytan D. et al. Neutralization of circulating vascular endothelial growth factor (VEGF) by anti-VEGF antibodies and soluble VEGF receptor 1(sFlt1) in duced proteinuria // J. Biol. Chem. - 2003. - Vol. 278. - P. 12 605-12 608.
- Tsuruda T., Boerrigter G., Huntley B.K. Brain natriuretic peptide is produced in cardiac fibroblasts and induces matrix metalloproteinase // Circ. Res. - 2002. - Vol. 91, N 2. - P. 1127-1134.
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