Rhinology · 2010
Azelastine nasal spray inhibiting parasympathetic function of tracheal smooth muscle.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wang Hsing-Won, Chou Ying-Liang, Chu Yueng-Hsiang
Аннотация
BACKGROUND: Azelastine hydrochloride is a histamine receptor-1 (H(1)) antagonist with anti-inflammatory properties that is available in the United States as Astelin Nasal Spray for rhinitis patients who are suffering from sneezing and rhinorrhea. The effect of H(1) antagonists on nasal mucosa in vivo is well known; however, the effect of the drug on tracheal smooth muscle has rarely been explored. During administration via oral intake or inhalation of the H(1) antagonist for nasal symptoms, it might affect the trachea.
METHODS: We examined the effectiveness of azelastine on isolated rat tracheal smooth muscle by testing: 1) the effect on tracheal smooth muscle resting tension; 2) the effect on contraction caused by 10(-6) M methacholine as a parasympathetic mimetic; and 3) the effect on electrically induced tracheal smooth muscle contractions.
RESULTS: The results indicated that addition of methacholine to the incubation medium caused the trachea to contract in a dose-dependent manner. Addition of azelastine at doses of 10(-5) M or above elicited a significant relaxation response to 10(-6) M methacholine-induced contraction. Azelastine could inhibit electrical field stimulation-induced spike contraction. It alone had a minimal effect on the basal tension of trachea as the concentration increased.
CONCLUSIONS: This study indicated that high concentrations of azelastine might actually inhibit parasympathetic function of the trachea. Azelastine might reduce asthma attacks in rhinitis patients because it could inhibit parasympathetic function and reduce methacholine-induced contraction of tracheal smooth muscle.
METHODS: We examined the effectiveness of azelastine on isolated rat tracheal smooth muscle by testing: 1) the effect on tracheal smooth muscle resting tension; 2) the effect on contraction caused by 10(-6) M methacholine as a parasympathetic mimetic; and 3) the effect on electrically induced tracheal smooth muscle contractions.
RESULTS: The results indicated that addition of methacholine to the incubation medium caused the trachea to contract in a dose-dependent manner. Addition of azelastine at doses of 10(-5) M or above elicited a significant relaxation response to 10(-6) M methacholine-induced contraction. Azelastine could inhibit electrical field stimulation-induced spike contraction. It alone had a minimal effect on the basal tension of trachea as the concentration increased.
CONCLUSIONS: This study indicated that high concentrations of azelastine might actually inhibit parasympathetic function of the trachea. Azelastine might reduce asthma attacks in rhinitis patients because it could inhibit parasympathetic function and reduce methacholine-induced contraction of tracheal smooth muscle.