Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure

Aim. To study the role of plasma redox potential reduction in the development of endothelial dysfunction (ED) among patients with chronic heart failure (CHF) and to investigate the potential of its pharmacological correction. Material and methods. This randomised cohort study included 73 patients wi...

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Main Authors: O. P. Donetskaya, V. A. Tulupova, N. V. Shuldeshova, M. M. Fedorova
Format: Article
Language:Russian
Published: «SILICEA-POLIGRAF» LLC 2012-02-01
Series:Кардиоваскулярная терапия и профилактика
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Online Access:https://cardiovascular.elpub.ru/jour/article/view/1699
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author O. P. Donetskaya
V. A. Tulupova
N. V. Shuldeshova
M. M. Fedorova
author_facet O. P. Donetskaya
V. A. Tulupova
N. V. Shuldeshova
M. M. Fedorova
author_sort O. P. Donetskaya
collection DOAJ
description Aim. To study the role of plasma redox potential reduction in the development of endothelial dysfunction (ED) among patients with chronic heart failure (CHF) and to investigate the potential of its pharmacological correction. Material and methods. This randomised cohort study included 73 patients with CHF, due to coronary heart disease (CHD) and arterial hypertension. Mean age of the participants was 59,2±5,9 years. Functional Class (FC) I CHF was registered in 9 patients, FC II CHF in 21, FC III CHF in 23, and FC IV CHF in 11. After the baseline examination, all participants were randomised into two groups. The main group (MG) received standard therapy plus adenocin (2 ampoules in 70 ml 5% glucose, intravenously) for 10 days. Results. For the first time, the dynamics of redox potential and total pyridine nucleotide levels was assessed in relation to the FC of ischemic CHF. Redox potential reduction preceded the changes in the total pyridine nucleotide levels. In contrast to standard therapy, adenocin increased plasma redox potential and endothelial growth factor levels, while reducing endothelin-1 concentrations and NADPH oxidase activity. Conclusion. Combination therapy with adenocin – a unique medication of reduced NAD form, cardiac glycoside, and inosine, in contrast to standard treatment, significantly increased cellular redox potential in CHF, which could play an important role in angiogenesis stimulation and reverse endothelial remodelling.
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institution Kabale University
issn 1728-8800
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language Russian
publishDate 2012-02-01
publisher «SILICEA-POLIGRAF» LLC
record_format Article
series Кардиоваскулярная терапия и профилактика
spelling doaj-art-cf72dd3620d5481aa91f2d9bc86ffedb2025-08-20T03:35:47Zrus«SILICEA-POLIGRAF» LLCКардиоваскулярная терапия и профилактика1728-88002619-01252012-02-01111545810.15829/1728-8800-2012-1-54-581417Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failureO. P. Donetskaya0V. A. Tulupova1N. V. Shuldeshova2M. M. Fedorova3Clinical Hospital No. 1, Russian Federation President’s Administration, MoscowClinical Hospital No. 1, Russian Federation President’s Administration, MoscowClinical Hospital No. 1, Russian Federation President’s Administration, MoscowRussian Medical Academy of Post-Diploma Education, MoscowAim. To study the role of plasma redox potential reduction in the development of endothelial dysfunction (ED) among patients with chronic heart failure (CHF) and to investigate the potential of its pharmacological correction. Material and methods. This randomised cohort study included 73 patients with CHF, due to coronary heart disease (CHD) and arterial hypertension. Mean age of the participants was 59,2±5,9 years. Functional Class (FC) I CHF was registered in 9 patients, FC II CHF in 21, FC III CHF in 23, and FC IV CHF in 11. After the baseline examination, all participants were randomised into two groups. The main group (MG) received standard therapy plus adenocin (2 ampoules in 70 ml 5% glucose, intravenously) for 10 days. Results. For the first time, the dynamics of redox potential and total pyridine nucleotide levels was assessed in relation to the FC of ischemic CHF. Redox potential reduction preceded the changes in the total pyridine nucleotide levels. In contrast to standard therapy, adenocin increased plasma redox potential and endothelial growth factor levels, while reducing endothelin-1 concentrations and NADPH oxidase activity. Conclusion. Combination therapy with adenocin – a unique medication of reduced NAD form, cardiac glycoside, and inosine, in contrast to standard treatment, significantly increased cellular redox potential in CHF, which could play an important role in angiogenesis stimulation and reverse endothelial remodelling.https://cardiovascular.elpub.ru/jour/article/view/1699coronary heart diseaseheart failureredox potentialendothelial dysfunctionadenocinnicotinamide adenine dinucleotide
spellingShingle O. P. Donetskaya
V. A. Tulupova
N. V. Shuldeshova
M. M. Fedorova
Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
Кардиоваскулярная терапия и профилактика
coronary heart disease
heart failure
redox potential
endothelial dysfunction
adenocin
nicotinamide adenine dinucleotide
title Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
title_full Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
title_fullStr Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
title_full_unstemmed Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
title_short Pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
title_sort pharmacological correction of plasma redox potential and endothelial dysfunction in ischemic heart failure
topic coronary heart disease
heart failure
redox potential
endothelial dysfunction
adenocin
nicotinamide adenine dinucleotide
url https://cardiovascular.elpub.ru/jour/article/view/1699
work_keys_str_mv AT opdonetskaya pharmacologicalcorrectionofplasmaredoxpotentialandendothelialdysfunctioninischemicheartfailure
AT vatulupova pharmacologicalcorrectionofplasmaredoxpotentialandendothelialdysfunctioninischemicheartfailure
AT nvshuldeshova pharmacologicalcorrectionofplasmaredoxpotentialandendothelialdysfunctioninischemicheartfailure
AT mmfedorova pharmacologicalcorrectionofplasmaredoxpotentialandendothelialdysfunctioninischemicheartfailure