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Life Sci ; 239: 116912, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31634465

RESUMO

AIMS: Cardiac dysfunction is a major cause of multi-organ dysfunction in critical care units following severe burns. The purpose of this study was to investigate the role of inducible nitric oxide synthase (iNOS) in cardiac dysfunction in burned mice. MATERIALS AND METHODS: Wild-type and iNOS-knockout mice were subjected to 30% total body surface area burns. Next, the expression of iNOS was measured at 1, 3 and 7 days post-burn. Cardiac function, insulin sensitivity, inflammation, oxidative stress, and apoptosis in the hearts of the mice were assessed at 3 days post-burn. KEY FINDINGS: Compared to control mice, iNOS expression was increased and reached a maximum in the heart of burned mice at 3 days post-burn. iNOS deficiency significantly alleviated the cardiac dysfunction and insulin resistance in burned mice. In addition, burn-induced inflammation, oxidative stress, and apoptosis in the heart were markedly reduced in iNOS-knockout burned mice when compared to corresponding values in wild-type burned mice. SIGNIFICANCE: Our study demonstrates that iNOS contributes to insulin resistance in the hearts of mice following burn injury, and iNOS deficiency protects cardiac function against burn injury in mice, suggesting iNOS as a potential therapeutic target to treat burn injuries.


Assuntos
Queimaduras/fisiopatologia , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico Sintase Tipo II/fisiologia , Animais , Apoptose , Queimaduras/complicações , Coração , Cardiopatias/metabolismo , Inflamação/metabolismo , Resistência à Insulina/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Músculo Esquelético/metabolismo , Miocárdio/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo I/metabolismo , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo III/metabolismo , Estresse Oxidativo/fisiologia , Ratos , Ratos Sprague-Dawley
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