Mucosal surface area determines the middle ear pressure response followingestablishment of sniff-induced underpressures

Introduction: Miura and colleagues presented data that they interpreted as evidencing a pressure-regulating function of the mastoid mucosa. Specifical ly. they reported different responses after sniff-induced middle ear (ME) u nderpressure for ears with and without a history of otitis media with effus ion (OME). To understand the mechanism underlying that effect, a previously developed mathematical model was adapted to their experiment and used to s imulate the expected pressure-time functions under different conditions. Me thods: A simple, two-compartment model of passive, gradient-driven, trans-m ucosal gas exchange was used to simulate ME pressure behaviour. Initial con ditions for the free parameters of the model were taken fi um published dat a for humans and monkeys. Functions relating surface area to volume for geo metric representations of the ME were constructed and used as model paramet ers. The effect of sniffing on ME gas partial pressure was modelled as a fr actional reduction proportional to gas representation in the ME. Results: T he model accurately simulated the time course and magnitude of the post-sni ffing pressure change reported for both normal and abnormal MEs. The post-s niffing pressure increase is driven by sniff-induced blood-ME partial press ure gradients for CO2, O-2 and H2O, which cause passive counter-diffusion o f those gases. The effect of disease oil the rate of pressure increase is a ttributable to the reduced surface area for exchange caused by underdevelop ment of the mastoid in ears with a history of OME. Conclusions: These resul ts do not support a pressure-regulating role for the mastoid mucosa. Contra ry to currently held beliefs, the model simulation suggests that small, not large mastoid volumes buffer ME pressure from rapid change due to trans-mu cosal gas transfers.