肽白三烯介导乙醛诱导的豚鼠支气管高反应性。

Peptide leukotrienes mediate acetaldehyde-induced bronchial hyper-responsiveness in guinea-pigs.

作者信息

Fujimura M, Myou S, Amemiya T, Tachibana H, Kita T, Matsuda T

机构信息

Third Department of Internal Medicine, Kanazawa University School of Medicine, Ishikawa, Japan.

出版信息

Clin Exp Allergy. 1997 Jan;27(1):104-9.

PMID: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.

摘要

背景

我们之前报道过，吸入乙醛（乙醇的一种代谢产物，也是酒精诱发哮喘的一个主要因素）会导致哮喘患者出现支气管高反应性（BHR）。然而，其机制尚不清楚。

目的

本研究的目的是探讨肽白三烯（LT）在乙醛诱发的BHR中的作用。

方法

在豚鼠中，采用改良的Konzett-Rössler方法，检测LT拮抗剂ONO-1078（0.1-1.0毫克/千克）和ICI-198,615（0.03-0.3毫克/千克）对乙醛诱发的支气管收缩以及对吸入乙酰甲胆碱的BHR的影响。

结果

0.8毫克/毫升的乙醛未能引起气道开口压力（Pao）的显著变化，但增强了随后吸入递增剂量（50-200微克/毫升）乙酰甲胆碱所诱发的Pao升高，这表明乙醛对支气管反应性有增强作用。虽然ONO-1078对递增剂量（5.0-20毫克/毫升）乙醛引起的支气管收缩没有抑制作用，但ONO-1078和ICI-198,615降低了乙醛诱发的BHR。