Literature DB >> 23729212

Distinct loading conditions reveal various patterns of right ventricular adaptation.

Marinus A J Borgdorff1, Beatrijs Bartelds, Michael G Dickinson, Paul Steendijk, Maartje de Vroomen, Rolf M F Berger.   

Abstract

Right ventricular (RV) failure due to chronically abnormal loading is a main determinant of outcome in pulmonary hypertension (PH) and congenital heart disease. However, distinct types of RV loading have been associated with different outcomes. To determine whether the adaptive RV response depends on loading type, we compared hemodynamics, exercise, and hypertrophy in models of pressure overload due to pulmonary artery banding (PAB), pressure overload due to PH, combined pressure and volume overload, and isolated volume load. Ninety-four rats were subjected to either PAB, monocrotaline-induced PH (PH), aortocaval shunt (shunt), or combined monocrotaline and aortocaval shunt (PH + shunt). We performed pressure-volume analysis and voluntary exercise measurements at 4 wk. We compared PAB to PH (part I) and PH + shunt to either isolated PH or shunt (part II). In part I, enhanced contractility (end-systolic elastance and preload recruitable stroke work) was present in PH and PAB, but strongest in PAB. Frank-Starling mechanism was active in both PAB and PH. In PAB this was accompanied by diastolic dysfunction (increased end-diastolic elastance, relaxation constant), clinical signs of RV failure, and reduced exercise. These distinct responses were not attributable to differences in hypertrophy. In part II, in PH + shunt the contractility response was blunted compared with PH, which caused pseudonormalization of parameters. Additional volume overload strongly enhanced hypertrophy in PH. We conclude that different types of loading result in distinct patterns of RV adaptation. This is of importance for the approach to patients with chronically increased RV load and for experimental studies in various types of RV failure.

Entities:  

Keywords:  contractility; monocrotaline; pressure-volume analysis; pulmonary hypertension; right ventricular failure

Mesh:

Substances:

Year:  2013        PMID: 23729212     DOI: 10.1152/ajpheart.00180.2013

Source DB:  PubMed          Journal:  Am J Physiol Heart Circ Physiol        ISSN: 0363-6135            Impact factor:   4.733


  21 in total

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7.  Estrogen Preserves Pulsatile Pulmonary Arterial Hemodynamics in Pulmonary Arterial Hypertension.

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8.  Emerging hemodynamic signatures of the right heart (Third International Right Heart Failure Summit, part 2).

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9.  Smooth muscle cytochrome b5 reductase 3 deficiency accelerates pulmonary hypertension development in sickle cell mice.

Authors:  Katherine C Wood; Brittany G Durgin; Heidi M Schmidt; Scott A Hahn; Jeffrey J Baust; Tim Bachman; Dario A Vitturi; Samit Ghosh; Solomon F Ofori-Acquah; Ana L Mora; Mark T Gladwin; Adam C Straub
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10.  Computational quantification of patient-specific changes in ventricular dynamics associated with pulmonary hypertension.

Authors:  Henrik Finsberg; Ce Xi; Xiaodan Zhao; Ju Le Tan; Martin Genet; Joakim Sundnes; Lik Chuan Lee; Liang Zhong; Samuel T Wall
Journal:  Am J Physiol Heart Circ Physiol       Date:  2019-11-01       Impact factor: 4.733

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