Abstract
Histamine, which has been found in middle ear effusions, is a potent pharmacological mediator released at an early stage of allergic reactions or general inflammatory process, increasing permeability of small blood vessels. Histamine might be involved in the origin and chronicity of middle ear effusions. In this study we studied the effect of histamine on the mucociliary function. First we examined the effect of histamine and its H1 and H2 blockers on the ciliary activity in the middle ear. 10(-2) M of histamine deteriorated ciliary activity; however, at lower concentrations ciliostimulatory effects were demonstrated for histamine (between 10(-8) M and 10(-4) M). Such ciliostimulatory effects were not affected by diphenhydramine (H1-blocker) but were reduced by cimetidine (H2-blocker). Thus histamine stimulates ciliary activity by combining with H2-receptor. Intratympanic injection of 10(-4) M of histamine induced accumulation of middle ear effusions (MEEs). The volume of MEEs was largest at 1 day postinjection when its mucociliary clearance time was longest. Then the mucociliary clearance time became shorter, but it was still significantly longer than that of the control animal. Ciliary activity in the tubotympanum showed no recovery through the observation period. On the other hand, intratympanic injection of 10(-6) M of histamine produced MEEs at 1 and 3 days postinjection when the mucociliary clearance time was longer than that of the control group. At 8 days, when most ears did not demonstrate MEEs, the mucociliary clearance time and ciliary activity in the Eustachian tube and tympanic orifice reached the level of the control group. Our present study demonstrates that histamine can induce mucociliary dysfunction of the tubotympanum resulting in middle ear effusions, and that cilia, especially those present in the tube and the tympanic orifice, have a significant role in eliminating middle ear effusions.
Published Version
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