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Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload

OBJECTIVE: The molecular pathway leading to myocardial cellular destruction after acute volume overload (AVO) may include monoamine oxidases. The aim of the present study was to investigate whether moclobemide (Mo), a monoamine oxidase inhibitor, protects the myocardium after AVO. METHODS: Sixty syn...

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Autores principales: Huuskonen, Christa, Hämäläinen, Mari, Paavonen, Timo, Moilanen, Eeva, Mennander, Ari
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Kare Publishing 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382901/
https://www.ncbi.nlm.nih.gov/pubmed/30587705
http://dx.doi.org/10.14744/AnatolJCardiol.2018.37336
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author Huuskonen, Christa
Hämäläinen, Mari
Paavonen, Timo
Moilanen, Eeva
Mennander, Ari
author_facet Huuskonen, Christa
Hämäläinen, Mari
Paavonen, Timo
Moilanen, Eeva
Mennander, Ari
author_sort Huuskonen, Christa
collection PubMed
description OBJECTIVE: The molecular pathway leading to myocardial cellular destruction after acute volume overload (AVO) may include monoamine oxidases. The aim of the present study was to investigate whether moclobemide (Mo), a monoamine oxidase inhibitor, protects the myocardium after AVO. METHODS: Sixty syngeneic Fischer rats underwent surgical abdominal aortocaval fistula to induce AVO. Eighteen rats were treated with Mo 10 mg/kg/day and were compared with 42 untreated rats with AVO without treatment. Myocardial recovery was analyzed using quantitative reverse transcription polymerase chain reaction for hypoxia-inducible factor 1-alpha, inducible nitric oxide synthase, interleukin 6, E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide, vascular endothelial growth factor-alpha, matrix metalloproteinase 9, chitinase 3-like protein (YKL-40), and transforming growth factor-beta. RESULTS: After 3 days, the relative number of ischemic intramyocardial arteries in the left ventricle was lower in AVO treated with Mo than in without [0.04 (0.02–0.07) vs. 0.09 (0.07–0.14), point score unit]. After 1 day, ANP was lower in AVO treated with Mo than in without [0.95 (0.37–1.84) vs. 2.40 (1.33–3.09), fold changes from the baseline (FC), p=0.044], whereas after 1 and 3 days, YKL-40 was higher in AVO treated with Mo than in without [22.66 (14.05–28.83) vs. 10.06 (6.23–15.02), FC, p=0.006 and 6.03 (4.72–7.18) vs. 3.70 (2.62–5.35), FC, p=0.025]. CONCLUSION: Mo decreases intramyocardial arterial ischemia of the left ventricle after AVO while increases YKL-40, reflecting cellular protection during early cardiac remodeling. In the future, adding Mo may be a simple means for myocardial protection after AVO. (Anatol J Cardiol 2019; 21: 39-45)
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spelling pubmed-63829012019-02-27 Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload Huuskonen, Christa Hämäläinen, Mari Paavonen, Timo Moilanen, Eeva Mennander, Ari Anatol J Cardiol Original Investigation OBJECTIVE: The molecular pathway leading to myocardial cellular destruction after acute volume overload (AVO) may include monoamine oxidases. The aim of the present study was to investigate whether moclobemide (Mo), a monoamine oxidase inhibitor, protects the myocardium after AVO. METHODS: Sixty syngeneic Fischer rats underwent surgical abdominal aortocaval fistula to induce AVO. Eighteen rats were treated with Mo 10 mg/kg/day and were compared with 42 untreated rats with AVO without treatment. Myocardial recovery was analyzed using quantitative reverse transcription polymerase chain reaction for hypoxia-inducible factor 1-alpha, inducible nitric oxide synthase, interleukin 6, E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide, vascular endothelial growth factor-alpha, matrix metalloproteinase 9, chitinase 3-like protein (YKL-40), and transforming growth factor-beta. RESULTS: After 3 days, the relative number of ischemic intramyocardial arteries in the left ventricle was lower in AVO treated with Mo than in without [0.04 (0.02–0.07) vs. 0.09 (0.07–0.14), point score unit]. After 1 day, ANP was lower in AVO treated with Mo than in without [0.95 (0.37–1.84) vs. 2.40 (1.33–3.09), fold changes from the baseline (FC), p=0.044], whereas after 1 and 3 days, YKL-40 was higher in AVO treated with Mo than in without [22.66 (14.05–28.83) vs. 10.06 (6.23–15.02), FC, p=0.006 and 6.03 (4.72–7.18) vs. 3.70 (2.62–5.35), FC, p=0.025]. CONCLUSION: Mo decreases intramyocardial arterial ischemia of the left ventricle after AVO while increases YKL-40, reflecting cellular protection during early cardiac remodeling. In the future, adding Mo may be a simple means for myocardial protection after AVO. (Anatol J Cardiol 2019; 21: 39-45) Kare Publishing 2019-01 2018-12-12 /pmc/articles/PMC6382901/ /pubmed/30587705 http://dx.doi.org/10.14744/AnatolJCardiol.2018.37336 Text en Copyright: © 2018 Turkish Society of Cardiology http://creativecommons.org/licenses/by-nc-sa/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
spellingShingle Original Investigation
Huuskonen, Christa
Hämäläinen, Mari
Paavonen, Timo
Moilanen, Eeva
Mennander, Ari
Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title_full Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title_fullStr Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title_full_unstemmed Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title_short Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload
title_sort monoamine oxidase a inhibition protects the myocardium after experimental acute volume overload
topic Original Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382901/
https://www.ncbi.nlm.nih.gov/pubmed/30587705
http://dx.doi.org/10.14744/AnatolJCardiol.2018.37336
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