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  • Title: Peptide leukotrienes mediate acetaldehyde-induced bronchial hyper-responsiveness in guinea-pigs.
    Author: Fujimura M, Myou S, Amemiya T, Tachibana H, Kita T, Matsuda T.
    Journal: Clin Exp Allergy; 1997 Jan; 27(1):104-9. PubMed ID: 9117874.
    Abstract:
    BACKGROUND: We previously reported that inhaled acetaldehyde, a metabolite of ethanol and a main factor in alcohol-induced asthma, causes bronchial hyper-responsiveness (BHR) in asthmatics. However, the mechanisms are unclear. OBJECTIVE: The purpose of this study was to investigate a role of a peptide leukotriene (LT) in acetaldehyde-induced BHR. METHODS: Effects of LT antagonists, ONO-1078 (0.1-1.0 mg/kg) and ICI-198, 615 (0.03-0.3 mg/kg), on acetaldehyde-induced bronchoconstriction and BHR to inhaled methacholine were examined using a modified Konzett-Rössler method in guinea pigs. RESULTS: Acetaldehyde at 0.8 mg/ml, which failed to induce significant changes in Pao (pressure at the airway opening), enhanced an increase in Pao induced by subsequent inhalations of ascending doses (50-200 micrograms/ml) of methacholine, suggesting a potentiating effect of acetaldehyde on bronchial responsiveness. Although ONO-1078 had no inhibitory effect on bronchoconstriction caused by ascending doses (5.0-20 mg/ml) of acetaldehyde, ONO-1078 and ICI-198, 615 reduced the acetaldehyde-induced BHR. CONCLUSION: Acetaldehyde causes BHR via LT release in guinea-pigs.
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