Right and left ventricular function after chronic pulmonary artery banding in rats assessed with biventricular pressure-volume loops

Faber, Matthijs J.; Dalinghaus, Michiel; Lankhuizen, Inge M.; Steendijk, Paul; Hop, Wim C. J.; Schoemaker, Regien G.; Duncker, Dirk J.; Lamers, Jos M. J.; Helbing, Willem A.

doi:10.1152/ajpheart.00286.2006

Cited by 113 publications

(112 citation statements)

References 33 publications

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“…18 In that study, the Valsalva maneuver was validated against inferior vena cava occlusion in order to decrease venous return for the definition of E max by a family of pressure-volume loops. 18 These limited reports confirm the importance of systolic function adaptation to afterload previously demonstrated in various animal species 19 or experimental models of acute 15,20,21 or chronic [22][23][24][25][26] pulmonary hypertension.…”

Section: Systolic Functionsupporting

confidence: 77%

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Naeije¹,

Brimioulle²,

Dewachter³

2014

Pulm. circ.

107

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Right ventricular (RV) function is a major determinant of the symptomatology and outcome in pulmonary hypertension. The normal RV is a thin-walled flow generator able to accommodate large changes in venous return but unable to maintain flow output in the presence of a brisk increase in pulmonary artery pressure. The RV chronically exposed to pulmonary hypertension undergoes hypertrophic changes and an increase in contractility, allowing for preserved flow output in response to peripheral demand. Failure of systolic function adaptation (homeometric adaptation, described by Anrep's law of the heart) results in increased dimensions (heterometric adaptation; Starling's law of the heart), with a negative effect on diastolic ventricular interactions, limitation of exercise capacity, and vascular congestion. Ventricular function is described by pressure-volume relationships. The gold standard of systolic function is maximum elastance (E max ), or the maximal value of the ratio of pressure to volume. This value is not immediately sensitive to changes in loading conditions. The gold standard of afterload is arterial elastance (E a ), defined by the ratio of pressure at E max to stroke volume. The optimal coupling of ventricular function to the arterial circulation occurs at an E max /E a ratio between 1.5 and 2. Patients with severe pulmonary hypertension present with an increased E max , a trend toward decreased E max /E a , and increased RV dimensions, along with progression of the pulmonary vascular disease, systemic factors, and left ventricular function. The molecular mechanisms of RV systolic failure are currently being investigated. It is important to refer biological findings to sound measurements of function. Surrogates for E max and E a are being developed through bedside imaging techniques.Keywords: right ventricle, pulmonary hypertension, preload, afterload, maximum elastance, end-systolic elastance, arterial elastance. One must inquire how increasing pulmonary vascular resistance results in impaired right ventricular function.-J. T. Reeves, 1989 1 In 1988, Jack Reeves and his colleagues noted that pulmonary hypertension is a common complication of cardiac and pulmonary diseases, that associated alterations in right ventricular (RV) function cause symptoms and limit survival, and that, paradoxically, research in this area had been relatively scarce. 1 Accordingly, they called for more studies to improve the understanding of RV failure in health and disease. Twenty-five years later, there has been significant progress, but our present knowledge remains incomplete, and calls for more research have been repeated. 2,3 The right ventricle (RV) in mammals and birds is a thin-walled flow generator, designed to accommodate the entire systemic venous return undergoing gas exchange in the pulmonary circulation, which is a separate high-flow, low-pressure system. 4 The pulmonary vascular pressures at rest and at mild levels of exercise are so low that a mean systemic filling pressure in the range of 10-15 m...

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Section: Systolic Functionsupporting

confidence: 77%

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Naeije¹,

Brimioulle²,

Dewachter³

2014

Pulm. circ.

107

View full text Add to dashboard Cite

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“…were reported (Faber et al, 2006;Bartelds et al, 2011;Kapur et al, 2013;Borgdorff et al, 2013Borgdorff et al, , 2015bde Raaf et al, 2015;Szulcek et al, 2016). However, opening the chest and insertion of the catheter through the RV free wall cause loss of intrathoracic pressure, changes of myocardial integrity and trauma.…”

Section: Introductionmentioning

confidence: 93%

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Böehm

Lawrie

Wilhelm

et al. 2017

Experimental Physiology

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This is the peer reviewed version of the following article: Boehm, M. et al (2016), Maintained right ventricular pressure overload induces ventricular-arterial decoupling in mice. Exp Physiol., which has been published in final form at https://doi.org/10.1113/EP085963. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request.This is an Accepted Article that has been peer-reviewed and approved for publication in the Experimental Physiology, but has yet to undergo copy-editing and proof correction. Please cite this article as an Accepted Article; doi: 10.1113/EP085963. This article is protected by copyright. All rights reserved. AbstractNew Findings: What is the central question of this study?The aim is to investigate whether complementary assessment of non-invasive ultrasound imaging along with closed chest-derived intra-cardiac pressure-volume catheterization is applicable to mice for an in-depth characterization of right ventricular (RV) function even upon maintained pressure overload. What is the main finding and its importance?Characterization

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“…Occlusion of the LAo likely causes pathological, pressure overload hypertrophy of the right ventricle (Eme et al, 2009a) [see Faber et al (Faber et al, 2006) and Leeuwenburgh et al (Leeuwenburgh, 2008) for mammalian examples], whereas chronic exercise can increase alligator heart mass (Eme et al, 2009b), possibly leading to a greater stroke volume (e.g. Rowell, 1974;Scheuer and Tipton, 1977).…”

Section: Exercise and Lao Occlusion Cause A Synergistic Increase In Vmentioning

confidence: 99%

Turning crocodilian hearts into bird hearts: growth rates are similar for alligators with and without right-to-left cardiac shunt

Eme

Gwalthney

Owerkowicz

et al. 2010

Journal of Experimental Biology

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SUMMARYThe functional and possible adaptive significance of non-avian reptiles' dual aortic arch system and the ability of all non-avian reptiles to perform central vascular cardiac shunts have been of great interest to comparative physiologists. The unique cardiac anatomy of crocodilians -a four-chambered heart with the dual aortic arch system -allows for only right-to-left (R-L; pulmonary bypass) cardiac shunt and for surgical elimination of this shunt. Surgical removal of the R-L shunt, by occluding the left aorta (LAo) upstream and downstream of the foramen of Panizza, results in a crocodilian with an obligatory, avian/mammalian central circulation. In this study, R-L cardiac shunt was eliminated in age-matched, female American alligators (Alligator mississippiensis; 5-7 months of age). We tested the hypothesis that surgical elimination of R-L cardiac shunt would impair growth (a readily measured proxy for fitness) compared with sham-operated, age-matched controls, especially in animals subjected to exhaustive exercise. While regular exercise caused a decrease in size (snout-to-vent length, head length and body mass), elimination of the capacity for R-L cardiac shunt did not greatly reduce animal growth, despite a chronic ventricular enlargement in surgically altered juvenile alligators. We speculate that, despite being slightly smaller, alligators with an occluded LAo would have reached sexual maturity in the same breeding season as control alligators. This study suggests that crocodilian R-L cardiac shunt does not provide an adaptive advantage for juvenile alligator growth and supports the logic that cardiac shunts persist in crocodilians because they have not been selected against. Supplementary material available online at

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Right and left ventricular function after chronic pulmonary artery banding in rats assessed with biventricular pressure-volume loops

Cited by 113 publications

References 33 publications

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Biomechanics of the Right Ventricle in Health and Disease (2013 Grover Conference Series)

Maintained right ventricular pressure overload induces ventricular–arterial decoupling in mice

Turning crocodilian hearts into bird hearts: growth rates are similar for alligators with and without right-to-left cardiac shunt

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