Abstract

Animal and human studies have shown that various kinds of chemical mediators may participate in the pathogenesis of bronchial asthma. Among these mediators, thromboxane A2 (TXA2) is recognised as important in bronchial responses and the pathogenesis of airway hyperresponsiveness. The reasons are as follows. (i) TXA2 (or mimetics) is a powerful constrictor of bronchial muscle in vitro and in vivo. (ii) Levels of TXB2, a metabolite of TXA2, increase in blood or bronchoalveolar lavage fluid after allergen challenge in atopic asthmatic patients. (iii) TXA2 mimetics induce airway hyperresponsiveness to nonspecific stimuli such as acetylcholine or methacholine. (iv) TXA2 synthetase inhibitors or TXA2 receptor antagonists inhibit asthmatic responses or airway hyperresponsiveness in various animal models and in patients with asthma.

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