Ryan A F, Bennett T
Department of Surgery/Otolaryngology, UCSD School of Medicine and VA Medical Center, La Jolla, California 92093, USA.
Laryngoscope. 2001 Feb;111(2):301-5. doi: 10.1097/00005537-200102000-00021.
OBJECTIVES/HYPOTHESIS: Nitric oxide (NO) is a small, short-lived free radical involved in cellular signaling and known to play a role in inflammation. It is generated on demand by the enzyme nitric oxide synthase (NOS) on arginine. We have previously found that mRNA encoding NOS is produced in the middle ear during otitis media. The role of NO was therefore explored in an experimental model of immune-mediated otitis media.
Guinea pigs were systemically immunized and later challenged in the middle ear with the same antigen. One ear of each animal was challenged with antigen alone. In the opposite ear, antigen was combined with a potent inhibitor of NOS, N(G)-amino-L-arginine (L-NAA). After survival for 24, 48, or 72 hours, the middle ears were evaluated for otitis media.
Inhibition of NOS resulted in significantly increased middle ear effusion at all three time periods. This increase was blocked by the addition of excess 1-arginine, which bypasses the inhibitory effects of L-NAA. The infiltration of cells into the middle ear lumen and the hyperplasia of the middle ear mucosa were unaffected by L-NAA administration.
The results suggest that NO is involved in regulating the permeability of the middle ear vascular, the transudation of serum into the middle ear mucosa, and/or the movement of extracellular fluid across the middle ear mucosal epithelium.
目的/假设：一氧化氮（NO）是一种参与细胞信号传导的小分子、短寿命自由基，已知其在炎症中发挥作用。它由一氧化氮合酶（NOS）在精氨酸上按需生成。我们之前发现，在中耳炎期间中耳会产生编码NOS的mRNA。因此，在免疫介导性中耳炎的实验模型中探讨了NO的作用。
豚鼠经全身免疫，随后在中耳用相同抗原进行激发。每只动物的一只耳朵仅用抗原激发。在对侧耳朵，抗原与一种强效NOS抑制剂N（G）-氨基-L-精氨酸（L-NAA）联合使用。存活24、48或72小时后，对中耳进行中耳炎评估。
在所有三个时间段，抑制NOS均导致中耳积液显著增加。添加过量的L-精氨酸可阻断这种增加，L-精氨酸可绕过L-NAA的抑制作用。L-NAA给药对细胞浸润到中耳腔以及中耳黏膜增生没有影响。
结果表明，NO参与调节中耳血管的通透性、血清渗入中耳黏膜以及/或者细胞外液穿过中耳黏膜上皮的移动。
