• Yongzheng Guo, Yuehua You, Dingyi Lv, Jianghong Yan, Fei-Fei Shang, Xiaowen Wang, Cheng Zhang, Qingdan Fan, and Suxin Luo.
• Division of cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China; Institute of Life Science, Chongqing Medical University, Chongqing, 400016, China.
• Life Sci. 2019 Dec 15; 239: 116912.

AimsCardiac 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 MethodsWild-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 FindingsCompared 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.SignificanceOur 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.Copyright © 2019 Elsevier Inc. All rights reserved.

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