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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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1437-4315
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Volume 389, Issue 6

Issues

Attenuation of left ventricular dysfunction by an ACE inhibitor after myocardial infarction in a kininogen-deficient rat model

Matthias Koch
  • The first two authors contributed equally to this work.
    1Department of Cardiology and Pneumology, Charité – University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
  • Other articles by this author:
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/ Klaus Bonaventura
  • 2Department of Cardiology and Pneumology, Charité – University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
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/ Frank Spillmann
  • 3Department of Cardiology and Pneumology, Charité – University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
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/ Andreas Dendorfer
  • 4Institute of Experimental and Clinical Pharmacology and Toxicology, Medical University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany
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/ Heinz-Peter Schultheiss
  • 5Department of Cardiology and Pneumology, Charité – University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
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/ Carsten Tschöpe
  • 6Department of Cardiology and Pneumology, Charité – University Medicine Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, D-12200 Berlin, Germany
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Published Online: 2008-05-15 | DOI: https://doi.org/10.1515/BC.2008.083

Abstract

Bradykinin (BK) coronary outflow and left ventricular (LV) performance of kininogen-deficient Brown Norway Katholiek (BNK) rats and Brown Norway Hannover (BNH) controls were investigated. We analyzed whether the angiotensin-converting enzyme (ACE) inhibitor ramipril is able to attenuate LV dysfunction after induction of myocardial infarction (MI) in this animal model. Ex vivo, the basal BK content in the coronary outflow of buffer-perfused, isolated hearts was measured by specific radioimmunoassay. In vivo, left ventricular pressure (LVP), the maximal rate of LVP increase, LV end-diastolic pressure, the maximal rate of LVP decrease and heart rate were determined using a tip catheter 3 weeks after induction of MI. Compared to BNK rats, basal BK outflow was increased 30-fold in controls (p<0.01). In vivo, we found no significant differences between sham-ligated BNK and BNH rats in basal LV function. After MI, the impairment of LV function was significantly worse in BNK rats when compared to BNH rats. ACE inhibition significantly attenuated this LV dysfunction in both groups, when compared to untreated animals. Reduced basal BK level resulting from kininogen deficiency has no effect on basal LV function, but remains to be a risk factor for the ischemic heart. However, ACE inhibition is sufficient to improve LV function despite kininogen deficiency.

Keywords: bradykinin; hemodynamics; ischemia; transgenic animal models

About the article

Corresponding author


Received: 2007-10-31

Accepted: 2008-02-11

Published Online: 2008-05-15

Published in Print: 2008-06-01


Citation Information: Biological Chemistry, Volume 389, Issue 6, Pages 719–723, ISSN (Online) 14374315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2008.083.

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