Nasal prostaglandin challenge increases N2O exchange from blood to middle ear

Nasal inflammation (NI) resulting from allergy or virus infection is causally associated with otitis media. Impaired Eustachian tube (ET) function consequent to NI may mediate this relationship. Moreover, the functional demand placed upon the ET for gas supply may be increased by NI, a hypothesis tested here. A total of five experiments were done at a minimum 2-week interval on four monkeys. For each experiment, the monkey was anesthetized and acclimated for 60 min. Then, the monkey was breathed with a 40% N2O gas mixture for 60 min followed by air breathing for 100 min. Fifteen minutes into air breathing, the nose was challenged with one of the five substances: saline, PGD2, capsaicin, histamine or bradykinin. Throughout, middle ear (ME) pressures were recorded at 5-min intervals. All pressure-time curves had a similar form consisting of a curvilinear decrease during acclimation, a linear increase during N2O breathing and a linear decrease during air breathing. The rates of pressure increase were ear-specific and not different across experiments. Compared to saline, the rate of pressure decrease was greater for challenge with all the substances and significantly greater after PGD2 challenge. Like N2, N2O is an inert gas whose transmucosal exchange is perfusion-limited for the ME. The measured pressure change is linearly related to the volume gas exchange between ME and blood. Therefore, nasal challenge with PGD2 and perhaps the other substances increases transmucosal inert gas exchange. ME to blood N2 transfer rate determines the physiological demand placed upon the ET for gas supply. That demand is increased by nasal exposure to certain inflammatory mediators.