Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria.
Biochim Biophys Acta Mol Basis Dis. 2017 Oct;1863(10 Pt B):2627-2632. doi: 10.1016/j.bbadis.2016.12.020. Epub 2017 Jan 5.
Changes in nitric oxide (NO) levels have been often associated with various forms of trauma, including secondary damage after traumatic brain injury (TBI). Several studies demonstrate the upregulation of NO synthase (NOS) enzymes, and concomitant increases in brain NO levels, which contribute to the TBI-associated glutamate cytotoxicity, including the pathogenesis of mitochondrial dysfunction. TBI is also associated with elevated NO levels in remote organs, indicating that TBI can induce systemic changes in NO regulation, which can be either beneficial or detrimental. Here we review the possible mechanisms responsible for changes in NO metabolism during TBI. Better understanding of the changes in NO homeostasis in TBI will be necessary to design rational therapeutic approaches for TBI. This article is part of a Special Issue entitled: Immune and Metabolic Alterations in Trauma and Sepsis edited by Dr. Raghavan Raju.
一氧化氮（NO）水平的变化常与各种形式的创伤有关，包括创伤性脑损伤（TBI）后的继发性损伤。多项研究表明，NO 合酶（NOS）酶的上调以及脑内 NO 水平的相应增加导致与 TBI 相关的谷氨酸细胞毒性，包括线粒体功能障碍的发病机制。TBI 还与远程器官中 NO 水平升高有关，这表明 TBI 可诱导 NO 调节的全身变化，这些变化可能有益或有害。在这里，我们回顾了 TBI 期间 NO 代谢变化的可能机制。为了设计针对 TBI 的合理治疗方法，有必要更好地了解 TBI 中 NO 动态平衡的变化。本文是由 Raghavan Raju 博士编辑的题为“创伤和败血症中的免疫和代谢改变”的特刊的一部分。
