Ion transports in the middle ear epithelium have been recently charact
erized. Experimental data using cell culture have found the existence
of a sodium transepithelial transport that drives a water flow. This i
s thought to play a key role in the maintain of air-filled and fluid-f
ree cavities. Impairment of this process is involved in the pathogenes
is of secretory otitis media, which is the main cause of acquired hear
ing loss. Several modulations of this transport have been evidenced: (
i) reactive oxygen species induced an endogenous synthesis of prostagl
andin E-2 (PGE(2)), which in turn increased the cAMP level and modulat
ed ion transport rate; (ii) steroids increased the expression of the c
u subunit sodium channel mRNA, which changes paralleled the modulation
of ion transport in the middle ear epithelium; (iii) moderate hypoxia
selectively and reversibly decreased the rate of sodium transport, as
a result of a parallel decrease in oc epithelial sodium channel subun
it mRNA level. These modulations may explain the course of middle ear
pathology. However, the development of an in vivo model has become man
datory to assess the relevance of these data in the pathophysiology of
the middle ear.