一氧化氮在烧伤小鼠腹腔巨噬细胞功能调节中的作用

作者探讨了烧伤时小鼠腹腔巨噬细胞（MΦ）产生一氧化氮（NO）、TNF-α及PGE_2的影响,以及烧伤活化的MΦ通过产生的NO对其本身功能的调节作用。实验发现烧伤早期MΦ能产生过量的NO、TNF及PGE_2,其中以NO产生较早,PGE_2产生较晚。NO的产生与iNOS活性呈明显正相关。iNOS特异性阻断剂甲基精氨酸（NMMA）能使NO产生明显下降,同时还使TNF-α及PGE_2产量分别卜降42. 9％和52. 8％,但对iNOS活性无影响。

NO Selfregulated Macrophages (MΦ) Function after Burn Injury

The purpose of this paper was to investigate the role of NO derived murine peritoneal MΦ could produce excessive NO, TNF, PGE2 at the early phase postburn in which NO producing was the earliest. The dymamic change of iNOS activity of MΦ postburn was just same as that of the NO production, but occured earlier and there was a significat positive correlation between them iNOS specific blocker NMMA could inhibit the NO production, but not affect the iNOS activity, meanwhile, NMMA also could attenuate the TNF and PGE2 productions by 42. 9% and 52. 8% respectively. Conclusion: NO produced by MΦ could upregulated the TNF and PGE2 productions from the same cells after burn injury.