Middle ear gas loss in inflammatory conditions: the role of mucosa thickness and blood flow.

Several middle ear (ME) pathologies are associated with ME gas deficit. These include in particular the chronic otitis media diseases that are associated with inflammation (hence, increased ME mucosal blood flow) and/or reduced Eustachian tube (ET) function. The present study models the trans-mucosal gas exchange in normal and inflamed middle ears of rats. The model evaluates the role of the gas diffusion path in the ME mucosa using mucosa thickness as its index and the role of the mucosal blood flow rate on ME gas economy in order to compare between normal and inflamed MEs. An experimental method employing ME gas volume changes at constant pressure due to trans-mucosal gas exchange, and blood gas values from the literature, was used in anaesthetized rats to corroborate the model. Mucosa thickness was measured as an index of the gas diffusion path between the ME space and the ME circulation. ME inner surface area was estimated from its measured gas volume. Inflammation was inflicted by applying lipopolysaccharide (LPS) into one ear. The contralateral ear served as control. ME gas volume decreased significantly faster with time (p=0.02) in inflamed ears (-0.107 microL min(-1) +/- 0.034 S.D., n=10) versus control ears (-0.067 microL min(-1) +/- 0.036 S.D., n=10). Mucosa thickness was significantly thicker in inflamed ears (48.4 microm +/- 11.0 S.D.) versus controls (20.5 microm +/- 10.1 S.D.). The mathematical model, the experimental results, and the blood gas values were used to estimate the relative effective mucosal blood flow rate. The model predicts that in spite of almost doubling mucosa thickness in LPS treated ears, the increased gas loss in inflamed ears may be explained by increased mucosal blood flow rate. We suggest that the ability to estimate ME blood flow as obtained by applying the model to the measurements, is relevant to medical management of inflamed ME.