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dc.contributor.authorBogaard, Harm Jen
dc.contributor.authorLegchenko, Ekaterinaen
dc.contributor.authorChaudhary, Ketul Ren
dc.contributor.authorSun, Xiao-Qingen
dc.contributor.authorStewart, Duncan Jen
dc.contributor.authorHansmann, Georgen
dc.date.accessioned2019-11-20T16:35:50Z
dc.date.available2019-11-20T16:35:50Z
dc.date.issued2019-12en
dc.identifier.issn1073-449X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/299068
dc.description.abstractTranslational research is essential to develop strategies for the treatment of pulmonary arterial hypertension (PAH) using animal models which reproduce the severity, the progressive nature and resistance to treatment of human PAH, including severe arterial remodeling and progressive right ventricular (RV) failure. We read with interest the letter by Kojonazariov et al. who propose to have found “severe emphysema in the SU5416/Hypoxia (SuHx) rat model of pulmonary hypertension”. The authors report that Wistar-Kyoto rats exposed to the combination of VEGFR2 inhibition by SU5416 and chronic hypoxia had moderately increased RVSP and RV mass compared to normoxic untreated animals. They applied in vivo micro-computed tomography (CT) to demonstrate an increase in lung volume and decreased lung density, an unaltered amount of lung tissue, but an increased air-to-tissue ratio, and claim these findings were confirmed by histological analysis, including mean linear intercept as surrogate of emphysema. Indeed, SU5416 has been previously shown to induce emphysema in normoxia, but this required repetitive SU5416 dosing (3 times weekly over 3 weeks) and occurred more predominantly in rats younger than 4 weeks of age (Norbert Voelkel, personal communication). In addition, emphysema could be negated, at the cost of the development of severe angioproliferative hypertension, by concomitant exposure to hypoxia.
dc.format.mediumPrinten
dc.languageengen
dc.rightsAll rights reserved
dc.rights.uri
dc.subjectAnimalsen
dc.subjectRatsen
dc.subjectHypertension, Pulmonaryen
dc.subjectEmphysemaen
dc.subjectPyrrolesen
dc.subjectIndolesen
dc.subjectPhenotypeen
dc.subjectHypoxiaen
dc.subjectPulmonary Arterial Hypertensionen
dc.titleEmphysema Is-at the Most-Only a Mild Phenotype in the Sugen/Hypoxia Rat Model of Pulmonary Arterial Hypertension.en
dc.typeArticle
prism.endingPage1450
prism.issueIdentifier11en
prism.publicationDate2019en
prism.publicationNameAmerican journal of respiratory and critical care medicineen
prism.startingPage1447
prism.volume200en
dc.identifier.doi10.17863/CAM.46129
dcterms.dateAccepted2019-07-11en
rioxxterms.versionofrecord10.1164/rccm.201906-1200leen
rioxxterms.versionAM*
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-12en
dc.contributor.orcidBogaard, Harm J [0000-0001-5371-0346]
dc.contributor.orcidLegchenko, Ekaterina [0000-0001-7949-2973]
dc.contributor.orcidChaudhary, Ketul R [0000-0003-1725-7438]
dc.contributor.orcidStewart, Duncan J [0000-0002-9113-8691]
dc.contributor.orcidHansmann, Georg [0000-0003-0709-3935]
dc.identifier.eissn1535-4970
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idEuropean Commission / European Respiratory Society (ERS) Marie Sklodowska-Curie Postdoctoral Research Fellowships (RESPIRE) (R3201800-00506)
cam.orpheus.successThu Jan 30 10:36:54 GMT 2020 - Embargo updated*
rioxxterms.freetoread.startdate2020-12-31


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