Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation

Abstract Few experimental model systems are available for the rare congenital heart diseases of double inlet left ventricle (DILV), a subgroup of univentricular hearts, and excessive trabeculation (ET), or noncompaction. Here, we explore the heart of the axolotl salamander (Ambystoma mexicanum, Shaw...

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Main Authors: Sophie Meyer, Henrik Lauridsen, Kathrine Pedersen, Sofie Amalie Andersson, Pim van Ooij, Tineke Willems, Rolf M. F. Berger, Tjark Ebels, Bjarke Jensen
Format: Article
Language:English
Published: Nature Portfolio 2022-11-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-022-24442-9
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author Sophie Meyer
Henrik Lauridsen
Kathrine Pedersen
Sofie Amalie Andersson
Pim van Ooij
Tineke Willems
Rolf M. F. Berger
Tjark Ebels
Bjarke Jensen
author_facet Sophie Meyer
Henrik Lauridsen
Kathrine Pedersen
Sofie Amalie Andersson
Pim van Ooij
Tineke Willems
Rolf M. F. Berger
Tjark Ebels
Bjarke Jensen
author_sort Sophie Meyer
collection DOAJ
description Abstract Few experimental model systems are available for the rare congenital heart diseases of double inlet left ventricle (DILV), a subgroup of univentricular hearts, and excessive trabeculation (ET), or noncompaction. Here, we explore the heart of the axolotl salamander (Ambystoma mexicanum, Shaw 1789) as model system of these diseases. Using micro-echocardiography, we assessed the form and function of the heart of the axolotl, an amphibian, and compared this to human DILV (n = 3). The main finding was that both in the axolotl and DILV, blood flows of disparate oxygen saturation can stay separated in a single ventricle. In the axolotl there is a solitary ventricular inlet and outlet, whereas in DILV there are two separate inlets and outlets. Axolotls had a lower resting heart rate compared to DILV (22 vs. 72 beats per minute), lower ejection fraction (47 vs. 58%), and their oxygen consumption at rest was higher than peak oxygen consumption in DILV (30 vs. 17 ml min−1 kg−1). Concerning the ventricular myocardial organization, histology showed trabeculations in ET (n = 5) are much closer to the normal human setting than to the axolotl setting. We conclude that the axolotl heart resembles some aspects of DILV and ET albeit substantial species differences exist.
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spelling doaj.art-4462126a45294135b23845e9d0ad1bdb2022-12-22T04:37:49ZengNature PortfolioScientific Reports2045-23222022-11-0112111310.1038/s41598-022-24442-9Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculationSophie Meyer0Henrik Lauridsen1Kathrine Pedersen2Sofie Amalie Andersson3Pim van Ooij4Tineke Willems5Rolf M. F. Berger6Tjark Ebels7Bjarke Jensen8Center for Congenital Heart Diseases, Department of Cardiothoracic Surgery, University Medical Center GroningenDepartment of Clinical Medicine, Aarhus UniversityDepartment of Clinical Medicine, Aarhus UniversityDepartment of Clinical Medicine, Aarhus UniversityDepartment of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location AMCDepartment of Radiology, University Medical Center GroningenCenter for Congenital Heart Diseases, Department of Pediatric Cardiology, University Medical Center GroningenCenter for Congenital Heart Diseases, Department of Cardiothoracic Surgery, University Medical Center GroningenDepartment of Medical Biology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical CentresAbstract Few experimental model systems are available for the rare congenital heart diseases of double inlet left ventricle (DILV), a subgroup of univentricular hearts, and excessive trabeculation (ET), or noncompaction. Here, we explore the heart of the axolotl salamander (Ambystoma mexicanum, Shaw 1789) as model system of these diseases. Using micro-echocardiography, we assessed the form and function of the heart of the axolotl, an amphibian, and compared this to human DILV (n = 3). The main finding was that both in the axolotl and DILV, blood flows of disparate oxygen saturation can stay separated in a single ventricle. In the axolotl there is a solitary ventricular inlet and outlet, whereas in DILV there are two separate inlets and outlets. Axolotls had a lower resting heart rate compared to DILV (22 vs. 72 beats per minute), lower ejection fraction (47 vs. 58%), and their oxygen consumption at rest was higher than peak oxygen consumption in DILV (30 vs. 17 ml min−1 kg−1). Concerning the ventricular myocardial organization, histology showed trabeculations in ET (n = 5) are much closer to the normal human setting than to the axolotl setting. We conclude that the axolotl heart resembles some aspects of DILV and ET albeit substantial species differences exist.https://doi.org/10.1038/s41598-022-24442-9
spellingShingle Sophie Meyer
Henrik Lauridsen
Kathrine Pedersen
Sofie Amalie Andersson
Pim van Ooij
Tineke Willems
Rolf M. F. Berger
Tjark Ebels
Bjarke Jensen
Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
Scientific Reports
title Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
title_full Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
title_fullStr Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
title_full_unstemmed Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
title_short Opportunities and short-comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
title_sort opportunities and short comings of the axolotl salamander heart as a model system of human single ventricle and excessive trabeculation
url https://doi.org/10.1038/s41598-022-24442-9
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