Hsing-Won Wang1, Ying-Liang Chou, Yueng-Hsiang Chu. 1. Department of Otolaryngology-Head and Neck Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC. w0512n@ms15.hinet.net
Abstract
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.
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 rhinitispatients 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 rhinitispatients because it could inhibit parasympathetic function and reduce methacholine-induced contraction of tracheal smooth muscle.