Increases in Middle Ear Pressure Resulting from Counter-Diffusion of Oxygen and Carbon Dioxide into the Middle Ear of Monkeys

Abstract

The mechanism of middle ear (ME) pressure regulation is incompletely understood. Previously, Hergels and Magnuson reported an unexpected increase in ME pressure for human subjects who partially evacuated their relative positive ME pressures by swallowing. They suggested that a novel, but unknown mechanism for the generation of gas was responsible for the pressure increase. In this experiment, the MEs of rhesus monkeys were inflated with N2 via the eustachian tube and post inflation ME pressures were recorded for up to three hours. Eleven of 20 experiments showed an initial increase in ME pressure caused by the inflation followed by stable pressures for the remainder of the followup period. In 9 of the experiments, a rapid and temporally discrete decrease in ME pressure was observed during the course of followup. Following the observed pressure decrease which was interpreted as a transient eustachian tube opening, ME pressures showed a progressive increase characterized by a kinetic pattern similar to that of the human experiment. To understand the mechanism responsible for this effect, the monkey experiment was simulated using a mathematical model of ME pressure regulation. Free parameters of the model were taken from experimental data for monkeys. The model accurately predicted the time course of pressure change documented in the monkey experiments. The effect is driven by a decrease in the preexisting ME partial pressures of CO2, O2 and H2O consequent to tubal openings at relative positive pressures, with the subsequent counter diffusion of those gases from blood to ME causing the observed increase in total ME pressure. The results reported by Hergels and Magnuson can also be explained by this mechanism.