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Open AccessArticle

Characterizing Vascular Dysfunction in Genetically Modified Mice through the Hyperoxia Model

1
CBIOS—Universidade Lusófona’s Research Center for Biosciences and Health Technologies, Campo Grande, 1749 024 Lisboa, Portugal
2
Pharmacological Sciences Department—Universidade de Lisboa, Faculty of Pharmacy, Av Prof Gama Pinto 1649 003 Lisboa, Portugal
3
IBEB—Biophysics and Biomedical Engineering Institute, Universidade de Lisboa Faculty of Sciences, Campo Grande 1749 016 Lisboa, Portugal
4
INSERM U1034, Adaptation cardiovasculaire à l’ischémie, F-33600 Pessac, France
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(9), 2178; https://doi.org/10.3390/ijms20092178
Received: 9 April 2019 / Revised: 25 April 2019 / Accepted: 30 April 2019 / Published: 2 May 2019
(This article belongs to the Special Issue Microcirculation in Inflammation)
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Abstract

Modelling 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. View Full-Text
Keywords: hyperoxia; mouse; LDF; wavelet transform; diabetes; cardiac hypertrophy hyperoxia; mouse; LDF; wavelet transform; diabetes; cardiac hypertrophy
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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MDPI and ACS Style

Monteiro Rodrigues, L.; Nazaré Silva, H.; Ferreira, H.; Gadeau, A.-P. Characterizing Vascular Dysfunction in Genetically Modified Mice through the Hyperoxia Model. Int. J. Mol. Sci. 2019, 20, 2178.

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