Animal model of reversible, right ventricular failure

Stephen H. McKellar, Hadi Javan, Megan E. Bowen, Xiaoquing Liu, Christin L. Schaaf, Casey M. Briggs, Huashan Zou, Arnold David Gomez, Osama Abdullah, Ed W. Hsu, Craig H. Selzman

Research output: Contribution to journalArticle

Abstract

Background Heart failure is a leading cause of death but very little is known about right ventricular (RV) failure (RVF) and right ventricular recovery (RVR). A robust animal model of reversible, RVF does not exist, which currently limits research opportunities and clinical progress. We sought to develop an animal model of reversible, pressure-overload RVF to study RVF and RVR. Materials and methods Fifteen New Zealand rabbits underwent implantation of a fully implantable, adjustable, pulmonary artery band. Animals were assigned to the control, RVF, and RVR groups (n = 5 for each). For the RVF and RVR groups, the pulmonary artery bands were serially tightened to create RVF and released for RVR. Echocardiographic, cardiac magnetic resonance imaging, and histologic analysis were performed. Results RV chamber size and wall thickness increased during RVF and regressed during RVR. RV volumes were 1023 μL ± 123 for control, 2381 μL ± 637 for RVF, and 635 μL ± 549 for RVR, and RV wall thicknesses were 0.98 mm ± 0.12 for controls (P = 0.05), 1.72 mm ± 0.60 for RVF, and 1.16 mm ± 0.03 for RVR animals (P = 0.04), respectively. Similarly, heart weight, liver weight, cardiomyocyte size, and the degree of cardiac and hepatic fibrosis increased with RVF and decreased during RVR. Conclusions We report an animal model of chronic, reversible, pressure-overload RVF to study RVF and RVR. This model will be used for preclinical studies that improve our understanding of the mechanisms of RVF and that develop and test RV protective and RVR strategies to be studied later in humans.

Original languageEnglish (US)
Pages (from-to)327-333
Number of pages7
JournalJournal of Surgical Research
Volume194
Issue number2
DOIs
StatePublished - Jan 1 2015

Fingerprint

Animal Models
Pulmonary Artery
Pressure
Weights and Measures
Liver
Cardiac Myocytes
Cause of Death
Fibrosis
Heart Failure
Magnetic Resonance Imaging
Rabbits
Research

ASJC Scopus subject areas

  • Surgery

Cite this

McKellar, S. H., Javan, H., Bowen, M. E., Liu, X., Schaaf, C. L., Briggs, C. M., ... Selzman, C. H. (2015). Animal model of reversible, right ventricular failure. Journal of Surgical Research, 194(2), 327-333. https://doi.org/10.1016/j.jss.2014.11.006

Animal model of reversible, right ventricular failure. / McKellar, Stephen H.; Javan, Hadi; Bowen, Megan E.; Liu, Xiaoquing; Schaaf, Christin L.; Briggs, Casey M.; Zou, Huashan; Gomez, Arnold David; Abdullah, Osama; Hsu, Ed W.; Selzman, Craig H.

In: Journal of Surgical Research, Vol. 194, No. 2, 01.01.2015, p. 327-333.

Research output: Contribution to journalArticle

McKellar, SH, Javan, H, Bowen, ME, Liu, X, Schaaf, CL, Briggs, CM, Zou, H, Gomez, AD, Abdullah, O, Hsu, EW & Selzman, CH 2015, 'Animal model of reversible, right ventricular failure', Journal of Surgical Research, vol. 194, no. 2, pp. 327-333. https://doi.org/10.1016/j.jss.2014.11.006
McKellar SH, Javan H, Bowen ME, Liu X, Schaaf CL, Briggs CM et al. Animal model of reversible, right ventricular failure. Journal of Surgical Research. 2015 Jan 1;194(2):327-333. https://doi.org/10.1016/j.jss.2014.11.006
McKellar, Stephen H. ; Javan, Hadi ; Bowen, Megan E. ; Liu, Xiaoquing ; Schaaf, Christin L. ; Briggs, Casey M. ; Zou, Huashan ; Gomez, Arnold David ; Abdullah, Osama ; Hsu, Ed W. ; Selzman, Craig H. / Animal model of reversible, right ventricular failure. In: Journal of Surgical Research. 2015 ; Vol. 194, No. 2. pp. 327-333.
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abstract = "Background Heart failure is a leading cause of death but very little is known about right ventricular (RV) failure (RVF) and right ventricular recovery (RVR). A robust animal model of reversible, RVF does not exist, which currently limits research opportunities and clinical progress. We sought to develop an animal model of reversible, pressure-overload RVF to study RVF and RVR. Materials and methods Fifteen New Zealand rabbits underwent implantation of a fully implantable, adjustable, pulmonary artery band. Animals were assigned to the control, RVF, and RVR groups (n = 5 for each). For the RVF and RVR groups, the pulmonary artery bands were serially tightened to create RVF and released for RVR. Echocardiographic, cardiac magnetic resonance imaging, and histologic analysis were performed. Results RV chamber size and wall thickness increased during RVF and regressed during RVR. RV volumes were 1023 μL ± 123 for control, 2381 μL ± 637 for RVF, and 635 μL ± 549 for RVR, and RV wall thicknesses were 0.98 mm ± 0.12 for controls (P = 0.05), 1.72 mm ± 0.60 for RVF, and 1.16 mm ± 0.03 for RVR animals (P = 0.04), respectively. Similarly, heart weight, liver weight, cardiomyocyte size, and the degree of cardiac and hepatic fibrosis increased with RVF and decreased during RVR. Conclusions We report an animal model of chronic, reversible, pressure-overload RVF to study RVF and RVR. This model will be used for preclinical studies that improve our understanding of the mechanisms of RVF and that develop and test RV protective and RVR strategies to be studied later in humans.",
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T1 - Animal model of reversible, right ventricular failure

AU - McKellar, Stephen H.

AU - Javan, Hadi

AU - Bowen, Megan E.

AU - Liu, Xiaoquing

AU - Schaaf, Christin L.

AU - Briggs, Casey M.

AU - Zou, Huashan

AU - Gomez, Arnold David

AU - Abdullah, Osama

AU - Hsu, Ed W.

AU - Selzman, Craig H.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Background Heart failure is a leading cause of death but very little is known about right ventricular (RV) failure (RVF) and right ventricular recovery (RVR). A robust animal model of reversible, RVF does not exist, which currently limits research opportunities and clinical progress. We sought to develop an animal model of reversible, pressure-overload RVF to study RVF and RVR. Materials and methods Fifteen New Zealand rabbits underwent implantation of a fully implantable, adjustable, pulmonary artery band. Animals were assigned to the control, RVF, and RVR groups (n = 5 for each). For the RVF and RVR groups, the pulmonary artery bands were serially tightened to create RVF and released for RVR. Echocardiographic, cardiac magnetic resonance imaging, and histologic analysis were performed. Results RV chamber size and wall thickness increased during RVF and regressed during RVR. RV volumes were 1023 μL ± 123 for control, 2381 μL ± 637 for RVF, and 635 μL ± 549 for RVR, and RV wall thicknesses were 0.98 mm ± 0.12 for controls (P = 0.05), 1.72 mm ± 0.60 for RVF, and 1.16 mm ± 0.03 for RVR animals (P = 0.04), respectively. Similarly, heart weight, liver weight, cardiomyocyte size, and the degree of cardiac and hepatic fibrosis increased with RVF and decreased during RVR. Conclusions We report an animal model of chronic, reversible, pressure-overload RVF to study RVF and RVR. This model will be used for preclinical studies that improve our understanding of the mechanisms of RVF and that develop and test RV protective and RVR strategies to be studied later in humans.

AB - Background Heart failure is a leading cause of death but very little is known about right ventricular (RV) failure (RVF) and right ventricular recovery (RVR). A robust animal model of reversible, RVF does not exist, which currently limits research opportunities and clinical progress. We sought to develop an animal model of reversible, pressure-overload RVF to study RVF and RVR. Materials and methods Fifteen New Zealand rabbits underwent implantation of a fully implantable, adjustable, pulmonary artery band. Animals were assigned to the control, RVF, and RVR groups (n = 5 for each). For the RVF and RVR groups, the pulmonary artery bands were serially tightened to create RVF and released for RVR. Echocardiographic, cardiac magnetic resonance imaging, and histologic analysis were performed. Results RV chamber size and wall thickness increased during RVF and regressed during RVR. RV volumes were 1023 μL ± 123 for control, 2381 μL ± 637 for RVF, and 635 μL ± 549 for RVR, and RV wall thicknesses were 0.98 mm ± 0.12 for controls (P = 0.05), 1.72 mm ± 0.60 for RVF, and 1.16 mm ± 0.03 for RVR animals (P = 0.04), respectively. Similarly, heart weight, liver weight, cardiomyocyte size, and the degree of cardiac and hepatic fibrosis increased with RVF and decreased during RVR. Conclusions We report an animal model of chronic, reversible, pressure-overload RVF to study RVF and RVR. This model will be used for preclinical studies that improve our understanding of the mechanisms of RVF and that develop and test RV protective and RVR strategies to be studied later in humans.

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