No abstract

Quinolinic acid (QUIN) is an endogenous metabolite that exerts a neurotoxic effect by binding to specific neuronal receptors. Studies involving a broad spectrum of infectious and inflammatory central nervous system diseases have suggested a role for QUIN in causing neuronal injury. Since there is evidence for presence of the QUIN receptor in mammalian cochleas, QUIN was measured in middle ear effusions (MEEs). Gas chromatography/mass spectrometry detected QUIN in each of 65 diluted human MEEs, with a mean of 482 +/- 75 (SEM) nmol/L and a range from 15 to 2667 nmol/L. QUIN was also detected in each of 197 chinchilla MEEs from five different models of otitis media, with a mean of 10.6 +/- 1.3 (SEM) mumol/L and a range from 0.23 to 146.0 mumol/L (corrected for dilution). To determine whether QUIN causes sensorineural hearing loss (SNHL), QUIN solutions were placed on round window membranes (RWM) for 20 to 240 minutes, in 20 chinchillas. SNHL was detected by electrocochleography in QUIN-exposed animals, but not in saline controls. We conclude that QUIN is present in MEEs and that QUIN in the middle ear has the potential to cross the RWM and cause sensorineural hearing loss, possibly by binding to specific neuronal receptors in mammalian cochleas.

Objective: Assess the changes in Eustachian tube (ET) function (ETF) with balloon dilation of Eustachian tube (BDET). Study Design: Prospective cohort for repeated testing measures. Setting: Clinical research center. Patients: Eleven adults with at least one patent ventilation tube (VT) inserted for chronic ET dysfunction (ETD) and history of otitis media with effusion. Interventions: Subjects with evidence of moderate to severe ETD on the side with a VT underwent unilateral BDET. Main Outcome Measures: Changes in ETF parameters after BDET measured by Forced Response Test (FRT), Inflation Deflation Test (IDT), and Pressure Chamber test. Results: With the FRT at 11 ml/min, opening pressure (OP) decreased from 458 ± 160 to 308 ± 173 daPa and closing pressure (CP) from 115 ± 83 to 72 ± 81 daPa at the 3-month post-BDET visit. The IDT and Pressure Chamber test showed that the percentage of middle ear (ME) pressure gradient equilibrated with swallows improved from 28 ± 34 to 53 ± 5% for positive and from 20 ± 28 to 38 ± 43% for negative ME pressure. Images from the pre- and post-BDET functional CT scans did not show apparent changes in the anatomy. Comparisons of ETF test parameters pre- and post-BDET suggested that the ET was easier to open and stayed open longer after the procedure. However, during the limited duration of follow-up most subjects continued to have ETD, some requiring VT re-insertion after the study period. Conclusions: Adults with severe ETD may benefit from BDET, however ETD may not be completely resolved and patients may continue to need VTs.

Middle ear negative pressure and effusions, decreased middle ear compliance, and abnormal tympanometry results have been described after diving on oxygen. Middle ear gas hyperoxia has been shown to down-regulate the eustachian tube ventilatory function (ETVF). The purpose of the present study was to investigate to what extent systemic hyperoxia in the face of air-equivalent middle ear gas composition might interfere with the ETVF. ETVF was investigated in four young adult female cynomolgus monkeys by the forced-response and inflation-deflation tests using air while the animals breathed either room air or 100% normobaric oxygen. Higher opening, closing, and steady-state pressures were observed under systemic hyperoxia. The percentage of the applied pressure equalized, and the maximal pressure change on a single swallow in the deflation test were both lower under hyperoxic conditions. The results show that systemic hyperoxia might impair ETVF. This observation adds to our understanding of the pathophysiology of middle ear dysfunction observed after diving on oxygen.