[Evaluation of arachidonic acid metabolites in experimental rat otitis media with effusion]

Leukotrienes B4, C4 (LTB4, LTC4) and prostaglandin E2 (PGE2) are arachidonic acid metabolites which are released from various types of cells, and are considered to be the mediators of inflammation because of their potent vascular permeability increasing activity (LTC4 and PGE2) and chemotactic activity (LTB4). In this study, to evaluate the involvement of arachidonic acid metabolites in otitis media with effusion, we measured the LTB4, LTC4 and PGE2 in rat middle ear effusion (MEE) by radioimmunoassay (RIA). SD rats weighing about 200g were used. The animals were divided into two groups, and lipopolysaccaride (LPS) or concanavalin A (ConA) was injected into the right middle ear cavity through the tympanic membrane. The left middle ear cavities were injected with 200 microliters of phosphate balanced buffered saline (PBS) and used as controls. After stimulation, middle ear effusion and accumulation of inflammatory cells such as neutrophils, macrophages, and lymphocytes was observed in the middle ear cavity. In contrast, no inflammatory cells were observed in the control ears. Proteins exudated into the middle ear cavity after LPS or ConA injection. The protein content increased up to 3 days, and then decreased. Substantial amounts of LTs and PG were detected in experimental rat OME, although hardly and LTs or PG was detected in the control ears or serum. LTs levels increased up to 7 days, and then decreased. PGE2 levels increased up to 3 days, and decreased thereafter. Dexamethasone effectively suppressed protein exudation, cell accumulation and production of arachidonic acid metabolites in the middle ear.