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dc.rights.licenseopenen_US
dc.contributor.authorMONTEIRO RODRIGUES, Luis
dc.contributor.authorNAZARÉ SILVA, Henrique
dc.contributor.authorFERREIRA, Hugo
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain-Pierre
dc.date.accessioned2020-11-09T10:54:09Z
dc.date.available2020-11-09T10:54:09Z
dc.date.issued2019-05
dc.identifier.issn1422-0067en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/12151
dc.description.abstractEnModelling is essential for a better understanding of microcirculatory pathophysiology. In this study we tested our hyperoxia-mouse model with healthy and non-healthy mice. Animals (n = 41) were divided in groups—a control group, with 8 C57/BL6 non-transgenic male mice, a diabetic group (DB), with 8 C57BLKsJ-db/db obese diabetic mice and the corresponding internal controls of 8 age-matched C57BLKsJ-db/+ mice, and a cardiac hypertrophy group (CH), with 9 FVB/NJ cα-MHC-NHE-1 transgenic mice prone to develop cardiac failure and 8 age-matched internal controls. After anesthesia, perfusion data was collected by laser Doppler flowmetry (LDF) during rest (Phase 1), hyperoxia (Phase 2), and recovery (Phase 3) and compared. The LDF wavelet transform components analysis (WA) has shown that cardiorespiratory, myogenic, and endothelial components acted as main markers. In DB group, db/+ animals behave as the Control group, but WA already demonstrated significant differences for myogenic and endothelial components. Noteworthy was the increase of the sympathetic components in the db/db set, as in the cardiac overexpressing NHE1 transgenic animals, reported as a main component of these pathophysiological processes. Our model confirms that flow motion has a universal nature. The LDF component’s WA provides a deeper look into vascular pathophysiology reinforcing the model’s reproducibility, robustness, and discriminative capacities.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/
dc.subjectArticle RECHERCHE
dc.title.enCharacterizing Vascular Dysfunction in Genetically Modified Mice through the Hyperoxia Model
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/ijms20092178en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
bordeaux.journalInternational Journal of Molecular Sciencesen_US
bordeaux.page2178en_US
bordeaux.volume20en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue9en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
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