线粒体一氧化氮合酶与炎症及败血症休克

Mitochondrial nitric oxide synthase in the inflammation and septic shock

一氧化氮（NO）和其他细胞因子是炎症和败血症休克中重要的细胞内信使和分子标志物。重症炎症可引发败血症休克，损害组织线粒体。败血症休克分子机制之一就是由于线粒体一氧化氮合酶（mtNOS）持续催化NO生成，导致过量过氧化亚硝酸阴离子（ONOO^-）产生，使线粒体功能异常，肌肉收缩功能减弱。在炎症和败血症休克过程中脏器的化学发光（其发射光在440-600nm）与自发光不同，很可能由于NO和ONOO^-与其他化学物质反应，形成自由基时所激发的。因此，用表面化学发光法监测原位炎症和氧化应激，是非常客观的指标。

Nitric oxide （NO） and other cytokines are the intercellular messengers and molecular markers of inflammation and septic shock. Exacerbated inflammatory response can cause septic shock and damage mitochondria. One of the molecular mechanisms of septic shock is that the enhanced NO production by mitochondrial nitric oxide synthase （mtNOS） lead to product excessive peroxynitrite （ONOO^-）,mitochondrial dysfunction and muscle contractile failure. Organ chemiluminescence in inflammation and septic shock have been found spectrally different from spontaneous organ chemiluminescence with increased 440-600nm emission, maybe due to NO and ONOO^- reaction with other chemical materials leading to the formation of other flee radicals. Therefore, it is very objective to test in vivo inflammation and oxidative stress using organ surface chemiluminescence.