Wong J M, Billiar T R
Department of Surgery, University of Pittsburgh, Pennsylvania 15213, USA.
Adv Pharmacol. 1995;34:155-70. doi: 10.1016/s1054-3589(08)61084-4.
During sepsis and inflammation profound changes in physiological function are induced by a variety of mediators, including endotoxin, various cytokines, and NO. Many of these mediators, in addition to their other functions, induce the synthesis of NO through the induction of iNOS within a variety of cell types. The regulation of iNOS expression is quite complex. Of interest is the fact that the functions of NO during sepsis range from modulating perfusion to mediating cytotoxicity. In addition, it is unique that many tissues not characterized as being involved in immune function express iNOS in a manner similar to that of tissues involved in immune function. The role of NO during episodes of acute inflammation appears to be a protective one; however, there are examples of chronic localized inflammation in both animal and human models which suggest that chronic iNOS expression may be detrimental. Further investigations into the regulation and function of NO in both the acute and chronic settings are necessary in order to fully understand this small yet unique molecule.
在脓毒症和炎症期间，多种介质会引起生理功能的深刻变化，这些介质包括内毒素、各种细胞因子和一氧化氮（NO）。除了其他功能外，这些介质中的许多还通过在多种细胞类型中诱导诱导型一氧化氮合酶（iNOS）来诱导NO的合成。iNOS表达的调节相当复杂。有趣的是，脓毒症期间NO的功能范围从调节灌注到介导细胞毒性。此外，许多未被归类为参与免疫功能的组织以与参与免疫功能的组织相似的方式表达iNOS，这一点很独特。急性炎症发作期间NO的作用似乎具有保护作用；然而，在动物和人类模型中都有慢性局部炎症的例子，这表明慢性iNOS表达可能是有害的。为了充分了解这种虽小但独特的分子，有必要对急性和慢性情况下NO的调节和功能进行进一步研究。
