Ball S S, Prazma J, Dais D, Rosbe K W, Pillsbury H C
Ohio State University College of Medicine, Columbus, USA.
Laryngoscope. 1996 Aug;106(8):1021-7. doi: 10.1097/00005537-199608000-00022.
Using a rat model, the authors investigated the role of nitric oxide (NO) in endotoxin-induced middle ear effusion (MEE). After the eustachian tube was obstructed, the middle ear was transtympanically injected with 35 microL of either 1 mg/mL lipopolysaccharide (LPS) or LPS and 1 mmol/L N-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase. Over the next 6 hours, the fluid within the middle ear was collected every 2 hours, and the quantity of albumin in the fluid, an index of vascular leakage, was determined using enzyme-linked immunosorbent assay. L-NAME significantly reduced LPS-induced vascular extravasation into the middle ear. Inoculation of the ear with L-arginine, the substrate for NO synthase, reversed the effects of L-NAME. These results indicate that NO is a mediator of LPS-induced MEE. Therefore, inhibition of NO synthase may represent a novel approach to the treatment of otitis media with effusion.
作者利用大鼠模型研究了一氧化氮（NO）在内毒素诱导的中耳积液（MEE）中的作用。在咽鼓管阻塞后，经鼓膜向中耳注入35微升1毫克/毫升的脂多糖（LPS）或LPS与1毫摩尔/升N-硝基-L-精氨酸甲酯（L-NAME，一种NO合酶的竞争性抑制剂）。在接下来的6小时内，每2小时收集一次中耳内的液体，并使用酶联免疫吸附测定法测定液体中白蛋白的含量，白蛋白含量是血管渗漏的一个指标。L-NAME显著减少了LPS诱导的血管渗漏到中耳。用L-精氨酸（NO合酶的底物）接种耳朵可逆转L-NAME的作用。这些结果表明，NO是LPS诱导的MEE的介质。因此，抑制NO合酶可能代表一种治疗渗出性中耳炎的新方法。
