烧伤后高代谢伴多器官功能不全的大鼠枯否细胞一氧化氮的改变

Changes of nitric oxide produced by Kupffer cells in postburn hypermetabolic rats with multiple organ dysfunction syndromes

目的和方法：给大鼠造成３０％体表面积的全层烧伤并延迟输液复制大鼠烧伤后高代谢伴多器官功能不全的模型，观察该模型动物血浆一氧化氮（ＮＯ）及枯否细胞产生ＮＯ的量。结果：烧伤后大鼠血浆ＮＯ含量升高，并与其中ＴＮＦα的含量呈正相关。烧伤后大鼠枯否细胞在受ＬＰＳ刺激下ＮＯ的含量明显高于对照组。

Abstract AIM and METHODS:Systemic activation of inflammatory cascades including hypermetabolism has been implicated in the pathogenesis of the multiple organ dysfunction syndromes(MODS).The animal model of hypermetabolism with MODS postburn in rats was established for this study.The role of nitric oxide(NO)in the development of MODS was studied.RESULTS:Oxygen consumption increased to 120%～130% of baseline postburn.There is a positive correlation between secreted TNF α in plasma and oxygen consumption.A positive correlation between NO - in plasma and oxygen consumption also can be observed.The production of NO - and TNF α in plasma and broncho-alveolar lavage fluid increased postburn.A positive correlation can be seen between NO - and secreted TNF α in plasma.Nitric oxide production increased in LPS-stimulated Kupffer cells at any timepoints examined after thermal injury.CONCLUSION:Increasing amount of NO postburn can be one of the mediators of septic shock and MODS. MeSH 〖WTBZ] Burns;Multiple organ failure;Kupffer cells; Tumor necrosis factor;Nitric oxide