NO及NO合成酶与感染性休克

感染性休克病理生理学过程十分复杂。NO在其中的作用既具有有害的一面,同时也存在有利的一面。受内毒素、细胞因子等诱导,iNOS表达上调并产生大量NO,引起循环衰竭、组织细胞损伤以及通过调节炎症介质基因表达扩大全身炎症反应。另一方面,eNOS所产生的NO对机体具有保护作用。然而,感染性休克时,eNOS蛋白质合成及其功能受到损害,反而成为血管内皮功能失常、诱发多器官功能障碍的重要原因。

Nitric oxide, NO syntheses (NOS) and septic shock

The pathophysiological condition of septic shock is very complex. Nitric oride (NO) has both harmful and beneficial effect in this event. Induced by endotoxin as well as cytokines, inducible NOS (iNOS) was highly expressed and produced a large amount of NO, which could result in circulation failure, cell injury and amplification of systemic inflammatory responses. On the other hand, NO derived from eNOS has been identified to play a protective role in sepsis and septic shock. However, eNOS down-regulation and dysfunction, at least in part, induced endothelium dysfunction and multiple organ dysfunction syndrome (MODS).