ISSN:
1365-2222
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Background We previously reported that inhaled acetaldehyde, a metabolite of ethanol atid a maiti 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 (O.l-l.Omg/kg) and ICI-198, 615 (0.03–0.3 mg/kg), on acetaldehyde-induced bronchoconstriction and BHR to inhaled methacho-line were examined using a modified Konzett-Rössler method in guinea pigs.Results Aeetaldehyde at 0.8mg/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 μg/ml) of methacholine. suggesting a potentiating effect of acetaldehyde oti 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1365-2222.1997.tb00679.x
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