Kanwar S, Kubes P
Immunology Research Group, University of Calgary Medical Center, Alberta, Canada.
New Horiz. 1995 Feb;3(1):93-104.
There is growing evidence that nitric oxide (NO.), a biologically active gas continuously produced by endothelium, is a homeostatic regulator of leukocyte adhesion in the microcirculation. Inhibition of NO. production leads to increased leukocyte rolling and adhesion in various vascular beds and two adhesion molecules, P-selectin and CD11/CD18, have been implicated in these processes. The role of mast cells and mast cell-derived mediators as potential contributors to the increased adhesion are discussed in this review. Moreover, oxidants may initiate the leukocyte recruitment after NO. synthesis inhibition. Recent data demonstrating increased oxidative stress in endothelium deprived of NO. are summarized. The role of NO. as an anti-inflammatory and antiadhesive modulator in postischemic venules of various organs is also discussed. The beneficial effect of NO. donors in this inflammatory condition is summarized. Finally, the potential use of NO. donating drugs in concert with available pharmaceutical compounds to reduce inflammation is reviewed.
越来越多的证据表明，一氧化氮（NO.）作为内皮细胞持续产生的一种生物活性气体，是微循环中白细胞黏附的稳态调节因子。抑制NO.的产生会导致白细胞在各种血管床中的滚动和黏附增加，两种黏附分子P-选择素和CD11/CD18参与了这些过程。本综述讨论了肥大细胞及其衍生介质作为黏附增加潜在促成因素的作用。此外，氧化剂可能在NO.合成抑制后引发白细胞募集。总结了近期关于缺乏NO.的内皮细胞氧化应激增加的数据。还讨论了NO.作为各种器官缺血后微静脉中的抗炎和抗黏附调节剂的作用。总结了NO.供体在这种炎症状态下的有益作用。最后，综述了NO.供体药物与现有药物化合物协同使用以减轻炎症的潜在用途。
