TNE is well tolerated and can be safely performed in patients with dysphagia in an office setting. TNE may have a role in the comprehensive evaluation of the dysphagic patient in the office.

Most medical schools in the United States offer some teaching and clinical exposure to OTO, with considerable variability in the type of experience.

Oxygen free radical damage has been demonstrated in the middle ear mucosa of a guinea pig model of acute otitis media (AOM). Potential sources of free radicals include both neutrophils responding to infection and Streptococcus pneumoniae, a common AOM pathogen. This project was conducted to examine the middle ear fluid in a guinea pig model of AOM for evidence of elevated lipid peroxide (LPO) as a marker of free radical damage. Twenty-one guinea pigs were injected transtympanically with bacteria into the left (infected) middle ear cavity and sterile saline into the right (control) middle ear. Middle ear fluid was recovered on postoperative day 5. The fluid was weighed and analyzed for quantity of LPO. Results indicated an increased absolute level of LPO, as well as an increased level of LPO divided by the weight of the fluid recovered. Histologic examination confirmed leukocyte infiltration and mucosal edema that were consistent with mucosal damage. While free radical damage to the middle ear mucosa in a guinea pig model of AOM is well documented, this is the first study to demonstrate evidence of free radical damage in middle ear fluid. These results are relevant because they correlate mucosal damage with lipoperoxidation in fluid. Additionally, this serves as an important precursor to human studies, since middle ear fluid is readily available in patients with otitis media.

Evidence has emerged that oxygen free radicals contribute to middle-ear mucosa damage in acute otitis media (AOM). Streptococcus pneumoniae is the most common pathogen in AOM and produces hydrogen peroxide, a free radical intermediate, as it grows. To better characterize the mechanism of free radical damage in AOM, an experiment was conducted to examine the production of hydrogen peroxide. Thirty-two guinea pigs were injected transtympanically with bacteria in the left (infected) middle ear and sterile saline into the right (control) middle ear. Middle-ear fluid was removed and analyzed for quantity of hydrogen peroxide. Results indicated significantly greater hydrogen peroxide levels in infected versus control middle-ear fluid at 6, 12, and 24 h. Likely sources of hydrogen peroxide include both the neutrophil response to infection and pneumococcal growth and death.

Free radicals participate in the development of disease under inflammatory conditions. Lipid peroxides such as malondialdehyde are regarded as markers of cell membrane damage by oxidative stresses. Previous work from our laboratory has demonstrated that lipidperoxidation is increased in acute otitis media in guinea pigs, implicating a role for free radicals as contributors to inflammation. In this study we examined the effect of lazaroid U-74389G, a 21-aminosteroid, on acute otitis media in guinea pigs. Streptococcus pneumoniae organisms were inoculated into the right tympanic cavity; sterilized phosphate-buffered saline solution was injected into the left ear to serve as a control. The guinea pigs were given intraperitoneal injections of 40 mg/kg of a lazaroid compound or its vehicle every 12 hours. Middle ear mucosa was collected and used for assay. We quantified lipid peroxide by means of the methylene blue-hemoglobin method and by means of measurement of thiobarbituric acid reactive substance. Lazaroid significantly (p < 0.05) suppressed production of lipid hyproperoxide of the middle ear mucosa of the guinea pigs with acute otitis media for up to 24 hours. These results suggest that lazaroid may reduce lipoperoxidation in the middle ear at an early stage of acute otitis media.