ISSN 2149-2263 | E-ISSN 2149-2271 Home      
 
Volume : 21 Issue : 3
Current Issue Archive Popular Article Ahead of Print

   
Quick Search





 
Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload [Anatol J Cardiol]
Anatol J Cardiol. 2019; 21(1): 39-45 | DOI: 10.14744/AnatolJCardiol.2018.37336  

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

Christa Huuskonen1, Mari Hämäläinen2, Timo Paavonen3, Eeva Moilanen2, Ari Mennander1
1Tampere University Heart Hospital, Cardiac Research and Tampere University; Tampere-Finland
2The Immunopharmacology Research Group, University of Tampere School of Medicine; Tampere-Finland
3Department of Pathology, Fimlab Laboratories, Tampere University Hospital, University of Tampere School of Medicine; Tampere-Finland

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.

Keywords: monoamine oxide A inhibition, acute volume overload, myocardial arteries, rat, YKL-40


Christa Huuskonen, Mari Hämäläinen, Timo Paavonen, Eeva Moilanen, Ari Mennander. Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload. Anatol J Cardiol. 2019; 21(1): 39-45

Corresponding Author: Ari Mennander, Finland


TOOLS
Full Text PDF
Print
Download citation
RIS
EndNote
BibTex
Medlars
Procite
Reference Manager
Share with email
Share
Send email to author

Similar articles
PubMed
Google Scholar




 
 
KARE Publishing | Copyright © 2018 Turkish Society of Cardiology