Abstract
Gas exchange in the middle ear, as well as ventilation through the eustachian tube, has been thought to be important in the physiology and pathophysiology of the middle ear. From the clinical point of view, it should be determined whether the impairment of gas exchange is related to the development or prolongation of middle ear diseases. We found that normally developed mastoid air cells contribute greatly to gas exchange in the middle ear. Experiments in cats also revealed that tubal dysfunction alone does not necessarily cause either profound negative middle ear pressure or middle ear effusion. Thus, middle ear gas exchange, in cooperation with ventilation through the eustachian tube, is considered to keep the middle ear in a physiological condition, whereas in pathological conditions of the middle ear, such as otitis media with effusion, abnormal gas exchange appears to cause negative middle ear pressure due to absorption of oxygen in the middle ear cavity; in this process, cells either in the mucous membrane or in the effusion of the middle ear may consume oxygen in the middle ear cavity. In refractory otitis media, in which both poor mastoid pneumatization and intractable tubal dysfunction are generally observed, ventilation and pressure equalization of the middle ear are very difficult. Further investigation of gas exchange should be conducted in ears with both sclerotic mastoids and tubal dysfunction.
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