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Ventricular Remodeling Induced by Tissue Vitamin A Deficiency in RatsAzevedo P.S.1 · Minicucci M.F.1 · Chiuso-Minicucci F.2 · Justulin Jr L.A.3 · Matsubara L.S.1 · Matsubara B.B.1 · Novelli E.4 · Seiva F.4 · Ebaid G.4 · Campana A.O.1 · Zornoff L.A.M.1 · Paiva S.A.R.1
1Internal Medicine Department, Botucatu Medical School, UNESP - São Paulo State University, Botucatu,2Department of Microbiology and Immunology, Institute of Biosciences, UNESP - São Paulo State University, Botucatu,3Department of Morphology, Institute of Biosciences, UNESP - São Paulo State University, Botucatu,4Chemistry and Biochemistry Department, Institute of Biosciences, Botucatu Medical School, UNESP - São Paulo State University, Botucatu Corresponding Author
Paula Schmidt Azevedo
Departamento de Clínica Médica, Faculdade de Medicina de Botucatu
Rubião Júnior s/n, Botucatu, CEP: 18618-000, SP (Brazil)
Tel. +55 14 38822969, Fax +55 14 38822238
Background/Aims: Experimental studies suggest that vitamin A plays a role in regulating cardiac structure and function. We tested the hypothesis that cardiac vitamin A deficiency is associated with adverse myocardial remodeling in young adult rats. Methods: Two groups of young female rats, control (C - n = 29) and tissue vitamin A deficient (RVA - n = 31), were subjected to transthoracic echocardiography exam, isolated rat heart study and biochemical study. Results: The RVA rats showed a reduced total vitamin A concentration in both the liver and heart [vitamin A in heart, µmol/kg (C = 0.95 ± 0.44 and RVA = 0.24 ± 0.16, p = 0.01)] with the same serum retinol levels (C = 0.73 ± 0.29 µmol/L e RVA = 0.62 ± 0.17 µmol/L, p = 0.34). The RVA rats showed higher left ventricular diameters and reduced systolic function. The RVA rats also demonstrated increased lipid hydroperoxide/total antioxidant capacity ratio and cardiac levels of IFN-γ and TNF-α but not of metalloproteinase (MMP)-2 and -9 activity. On the other hand, the RVA rats had decreased levels of β-hydroxyacylcoenzyme A dehydrogenase and lactate dehydrogenase. Conclusions: Tissue vitamin A deficiency stimulated cardiac remodeling and ventricular dysfunction. Additionally, the data support the involvement of oxidative stress, energy metabolism, and cytokine production in this remodeling process.
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