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Merits of Non-Invasive Rat Models of Left Ventricular Heart Failure

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Abstract

Heart failure (HF) is characterized as a limitation to cardiac output that prevents the heart from supplying tissues with adequate oxygen and predisposes individuals to pulmonary edema. Impaired cardiac function is secondary to either decreased contractility reducing ejection (systolic failure), diminished ventricular compliance preventing filling (diastolic failure), or both. To study HF etiology, many different techniques have been developed to elicit this condition in experimental animals, with varying degrees of success. Among rats, surgically induced HF models are the most prevalent, but they bear several shortcomings, including high mortality rates and limited recapitulation of the pathophysiology, etiology, and progression of human HF. Alternatively, a number of non-invasive HF induction methods avoid many of these pitfalls, and their merits in technical simplicity, reliability, survivability, and comparability to the pathophysiologic and pathogenic characteristics of HF are reviewed herein. In particular, this review focuses on the primary pathogenic mechanisms common to genetic strains (spontaneously hypertensive and spontaneously hypertensive heart failure), pharmacological models of toxic cardiomyopathy (doxorubicin and isoproterenol), and dietary salt models, all of which have been shown to induce left ventricular HF in the rat. Additional non-invasive techniques that may potentially enable the development of new HF models are also discussed.

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Abbreviations

ACE:

Angiotensin-converting enzyme

ANG II:

Angiotensin II

βAR:

Beta adrenergic receptor

CO:

Cardiac output

DM:

Diabetes mellitus

DOX:

Doxorubicin

dP/dt max :

Peak rate of increase in LV pressure

dP/dt min :

Peak rate of decrease in LV pressure

DOCA:

Deoxycorticosterone acetate

DS:

Dahl salt sensitive

E/A:

Ratio of early-to-late inflow velocities

EF:

Ejection fraction

ESV:

End-systolic volume

FS:

Fractional shortening

HF:

Heart failure

HR:

Heart rate

i.v. :

Intravenous

ISO:

Isoproterenol

LAD:

Left anterior descending coronary artery

LV:

Left ventricular

LVP:

LV pressure

LVEDP:

LV end-diastolic pressure

LVESP:

LV end-systolic pressure

LVOT:

LV outflow tract

MAP:

Mean arterial pressure

MHC:

Myosin heavy chain

MI:

Myocardial infarction

PO:

Pressure overload

PTU:

Propylthiouracil

s.c. :

Subcutaneous

SD:

Sprauge Dawley

SERCA:

Sarcoplasmic reticulum Ca2+ ATPase pump

SERCA2a:

SERCA type “2”, isoform ‘a’

SH:

Spontaneously hypertensive

SHHF:

Spontaneously hypertensive heart failure

SHR:

Spontaneously hypertensive rat

SV:

Stroke volume

T3 :

Triiodothyronine

T4 :

Thyroxine

TAC:

Transverse aortic constriction

TNF-α:

Tumor necrosis factor-α

UPS:

Ubiquitin–proteasome system

VO:

Volume overload

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Acknowledgments

The authors thank and acknowledge Drs. Urmila Kodavanti of the U.S. EPA and David Kurtz of Experimental Pathology Laboratories for their reviews of this manuscript.

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This paper has been reviewed and approved for release by the National Health and Environmental Effects Research Laboratory, U.S. EPA. Approval does not signify that the contents necessarily reflect the views and policies of the U.S. EPA, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

Declaration of interest

Alex Carll is supported by UNC/EPA CR83323601.

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Authors and Affiliations

  1. Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, 148 Rosenau Hall, CB# 7431, Chapel Hill, NC, 27599, USA

    Alex P. Carll

  2. McAllister Heart Institute & Department of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina, Chapel Hill, NC, 27599, USA

    Monte S. Willis

  3. Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, 27834, USA

    Robert M. Lust

  4. Office of Research and Development, U. S. Environmental Protection Agency, Research Triangle Park, NC, 27709, USA

    Daniel L. Costa

  5. Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Lab, Office of Research and Development, U. S. Environmental Protection Agency, Research Triangle Park, NC, 27709, USA

    Aimen K. Farraj

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Carll, A.P., Willis, M.S., Lust, R.M. et al. Merits of Non-Invasive Rat Models of Left Ventricular Heart Failure. Cardiovasc Toxicol 11, 91–112 (2011). https://doi.org/10.1007/s12012-011-9103-5

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