W J Doyle1. 1. Department of Otolaryngology, Children's Hospital of Pittsburgh and the University of Pittsburgh School of Medicine, PA, USA.
Abstract
INTRODUCTION: Miura and colleagues presented data that they interpreted as evidencing a pressure-regulating function of the mastoid mucosa. Specifically, they reported different responses after sniff-induced middle ear (ME) underpressure for ears with and without a history of otitis media with effusion (OME). To understand the mechanism underlying that effect, a previously developed mathematical model was adapted to their experiment and used to simulate the expected pressure-time functions under different conditions. METHODS: A simple, two-compartment model of passive, gradient-driven, trans-mucosal gas exchange was used to simulate ME pressure behaviour. Initial conditions for the free parameters of the model were taken from published data for humans and monkeys. Functions relating surface area to volume for geometric representations of the ME were constructed and used as model parameters. The effect of sniffing on ME gas partial pressure was modelled as a fractional reduction proportional to gas representation in the ME. RESULTS: The model accurately simulated the time course and magnitude of the post-sniffing pressure change reported for both normal and abnormal MEs. The post-sniffing pressure increase is driven by sniff-induced blood-ME partial pressure gradients for CO2, O2, and H2O, which cause passive counter-diffusion of those gases. The effect of disease on the rate of pressure increase is attributable to the reduced surface area for exchange caused by underdevelopment of the mastoid in ears with a history of OME. CONCLUSIONS: These results do not support a pressure-regulating role for the mastoid mucosa. Contrary to currently held beliefs, the model simulation suggests that small, not large mastoid volumes buffer ME pressure from rapid change due to trans-mucosal gas transfers.
INTRODUCTION: Miura and colleagues presented data that they interpreted as evidencing a pressure-regulating function of the mastoid mucosa. Specifically, they reported different responses after sniff-induced middle ear (ME) underpressure for ears with and without a history of otitis media with effusion (OME). To understand the mechanism underlying that effect, a previously developed mathematical model was adapted to their experiment and used to simulate the expected pressure-time functions under different conditions. METHODS: A simple, two-compartment model of passive, gradient-driven, trans-mucosal gas exchange was used to simulate ME pressure behaviour. Initial conditions for the free parameters of the model were taken from published data for humans and monkeys. Functions relating surface area to volume for geometric representations of the ME were constructed and used as model parameters. The effect of sniffing on ME gas partial pressure was modelled as a fractional reduction proportional to gas representation in the ME. RESULTS: The model accurately simulated the time course and magnitude of the post-sniffing pressure change reported for both normal and abnormal MEs. The post-sniffing pressure increase is driven by sniff-induced blood-ME partial pressure gradients for CO2, O2, and H2O, which cause passive counter-diffusion of those gases. The effect of disease on the rate of pressure increase is attributable to the reduced surface area for exchange caused by underdevelopment of the mastoid in ears with a history of OME. CONCLUSIONS: These results do not support a pressure-regulating role for the mastoid mucosa. Contrary to currently held beliefs, the model simulation suggests that small, not large mastoid volumes buffer ME pressure from rapid change due to trans-mucosal gas transfers.