OBJECTIVE: To show a relationship between intranasal histamine challenge, the development of middle ear effusion and Eustachian tube (ET) dysfunction in a rat model. METHODS: Non-allergic Sprague-Dawley rats weighing between 450-600 g were randomly assigned to receive an intranasal infusion of 16 microl of 10% histamine or normal saline. ET function was assessed by using the forced-response test to measure passive and active opening and closing pressures at time intervals of 6, 10, 14, 18, 22, and 26 min and 24 h post-infusion. Mucociliary clearance times (MCCTs) of the tubotympanum at 18 min post-infusion were measured by timing the transit of dye from the middle ear to the nasopharynx. Outcome measures were ET dysfunction and evidence of clinical effusion. RESULTS: Intranasal histamine caused acute ET dysfunction when introduced into the nasopharynx demonstrated by significant elevations in passive and active opening and closing pressures (P < or = 0.001) compared to controls. The largest difference was seen at 26 min post-infusion. Furthermore, MCCTs were 2.4 times longer after infusing intranasal histamine than after saline infusion. No clinically significant effusions were evident in either group at any time interval. CONCLUSION: These data demonstrate a successful development of an intranasal histamine rat model, in addition to a relationship between intranasal histamine challenge and development of acute ET dysfunction.
OBJECTIVE: To show a relationship between intranasal histamine challenge, the development of middle ear effusion and Eustachian tube (ET) dysfunction in a rat model. METHODS: Non-allergic Sprague-Dawley rats weighing between 450-600 g were randomly assigned to receive an intranasal infusion of 16 microl of 10% histamine or normal saline. ET function was assessed by using the forced-response test to measure passive and active opening and closing pressures at time intervals of 6, 10, 14, 18, 22, and 26 min and 24 h post-infusion. Mucociliary clearance times (MCCTs) of the tubotympanum at 18 min post-infusion were measured by timing the transit of dye from the middle ear to the nasopharynx. Outcome measures were ET dysfunction and evidence of clinical effusion. RESULTS: Intranasal histamine caused acute ET dysfunction when introduced into the nasopharynx demonstrated by significant elevations in passive and active opening and closing pressures (P < or = 0.001) compared to controls. The largest difference was seen at 26 min post-infusion. Furthermore, MCCTs were 2.4 times longer after infusing intranasal histamine than after saline infusion. No clinically significant effusions were evident in either group at any time interval. CONCLUSION: These data demonstrate a successful development of an intranasal histaminerat model, in addition to a relationship between intranasal histamine challenge and development of acute ET dysfunction.