Nitric Oxide: A Mediator of Endotoxin‐Induced Middle Ear Effusions

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Abstract
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 35μL 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.
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