ISSN 2149-2263 | E-ISSN 2149-2271
The Anatolian Journal of Cardiology
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
Manuscript Language: English


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