Abstract
To evaluate the effect of Lipopolysaccharide (LPS), a bacterial endotoxin on cochlear microcirculation, and its mode of action. Twenty-five Dunkin-Hartley guinea pigs were divided into five groups of five animals each. After surgical preparation, cochlear microcirculation was quantified by in vivo fluorescence microscopy. Placebo or LPS (1mg, 10µg, and 100ng) was applied topically, and microcirculation was measured before and twice after application. A fifth group was pretreated with etanercept, a tumor necrosis factor (TNF) antagonist, and afterward the lowest LPS concentrations that yielded significant results (10µg) were applied. In the groups that had been treated with 1mg and 10µg LPS, a significant drop in cochlear microcirculation was observed after 30 (.791±.089 Arbitrary Units (AU), compared to baseline, and .888±.071AU) and 60 (.756±.101 AU and .817±.124 AU, respectively) minutes. The groups that had been treated with 100ng LPS and that had been pretreated with etanercept showed no significant change in cochlear blood flow compared to placebo. Lipopolysaccharide shows a dose-dependent effect on cochlear microcirculation; this effect can already be observed after 30min. Pretreatment with etanercept can abrogate this effect, indicating that TNF mediates the effect of LPS on cochlear microcirculation.
Highlights
Acute otitis media is one of the most common infectious diseases, affecting up to 11% of the worldwide population, reflecting between 300 and 700 million patients per year.[1]
It has been established that injection of lipopolysaccharide into the middle ear is a viable animal model for acuta bacterial otitis media.[7,8]
When it comes to permanent sensorineural hearing loss, it is commonly believed that this is caused by transition of toxins though the round[9] and oval[10,11] window membrane, causing inflammation of the cochlea.[12]
Summary
Acute otitis media is one of the most common infectious diseases, affecting up to 11% of the worldwide population, reflecting between 300 and 700 million patients per year.[1]. It has been established that injection of lipopolysaccharide into the middle ear is a viable animal model for acuta bacterial otitis media.[7,8]. When it comes to permanent sensorineural hearing loss, it is commonly believed that this is caused by transition of toxins though the round[9] and oval[10,11] window membrane, causing inflammation of the cochlea (suppurative labyrinthitis).[12] These findings had been reproduced in animal models of otitis media with suppurative labyrinthitis.[13]. We decided to investigate the effect of LPS on cochlear microcirculation and its mode of action
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