Bovine model of doxorubicin-induced cardiomyopathy.

Left ventricular assist devices (LVADs) constitute a recent advance in heart failure (HF) therapeutics. As the rigorous experimental assessment of LVADs in HF requires large animal models, our objective was to develop a bovine model of cardiomyopathy. Male calves (n = 8) were used. Four animals rece...

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Published in:Journal of Biomedicine & Biotechnology pp. 758736 - 758737
Main Authors: Bartoli, Carlo R, Brittian, Kenneth R, Giridharan, Guruprasad A, Koenig, Steven C, Hamid, Tariq, Prabhu, Sumanth D
Format: research Journal Article
Published: Wiley-Blackwell 2011
Online Access:View this record in EBSCOhost
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        atl: Bovine model of doxorubicin-induced cardiomyopathy.
      aug:
        au:
          Bartoli, Carlo R
          Brittian, Kenneth R
          Giridharan, Guruprasad A
          Koenig, Steven C
          Hamid, Tariq
          Prabhu, Sumanth D
        affil: Department of Physiology and Biophysics, University of Louisville, Louisville, KY 40202, USA.
      sug:
        subj:
          Myocardial Diseases Chemically Induced
          Myocardial Diseases Pathology
          Models, Biological
          Animals
          Apoptosis
          Myocardial Diseases Physiopathology
          Myocardial Diseases Ultrasonography
          Cattle
          Coronary Circulation Physiology
          Doxorubicin
          Epinephrine Blood
          Fibrosis
          Genes
          Hemodynamics Physiology
          Male
          Myocardium Metabolism
          Myocardium Pathology
          Cells Pathology
          Norepinephrine Blood
          RNA
          RNA Metabolism
          Male
      ab: Left ventricular assist devices (LVADs) constitute a recent advance in heart failure (HF) therapeutics. As the rigorous experimental assessment of LVADs in HF requires large animal models, our objective was to develop a bovine model of cardiomyopathy. Male calves (n = 8) were used. Four animals received 1.2 mg/kg intravenous doxorubicin weekly for seven weeks and four separate animals were studied as controls. Doxorubicin-treated animals were followed with weekly echocardiography. Target LV dysfunction was defined as an ejection fraction <= 35%. Sixty days after initiating doxorubicin, a terminal study was performed to determine hemodynamic, histological, biochemical, and molecular parameters. All four doxorubicin-treated animals exhibited significant (P < 0.05) contractile dysfunction, with target LV dysfunction achieved in three animals. Doxorubicin-treated hearts exhibited significantly reduced coronary blood flow and interstitial fibrosis and significantly increased apoptosis and myocyte size. Gene expression of atrial natriuretic factor increased more than 3-fold. Plasma norepinephrine and epinephrine levels were significantly increased early and late during the development of cardiomyopathy, respectively. We conclude that sequential administration of intravenous doxorubicin in calves induces a cardiomyopathy with many phenotypic hallmarks of the failing human heart. This clinically-relevant model may be useful for testing pathophysiologic responses to LVADs in the context of HF.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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