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Animal and human studies have shown that various kinds of chemical mediators may participate in the pathogenesis of bronchial asthma. Among these mediators, thromboxane A(2) (TXA(2)) is recognised as important in bronchial responses and the pathogenesis of airway hyperresponsiveness. The reasons are as follows. TXA(2) (or mimetics) is a powerful constrictor of bronchial muscle in vitro and in vivo.Levels of TXB(2), a metabolite of TXA(2), increase in blood or bronchoalveolar lavage fluid after allergen challenge in atopic asthmatic patients.TXA(2) mimetics induce airway hyperresponsiveness to nonspecific stimuli such as acetylcholine or methacholine.TXA(2) synthetase inhibitors or TXA(2) receptor antagonists inhibit asthmatic responses or airway hyperresponsiveness in various animal models and in patients with asthma. In Japan, the TXA(2) synthetase inhibitor ozagrel and the TXA(2) receptor antagonist seratrodast are now used in the treatment of patients with bronchial asthma. In multicentre double-blind studies, these 2 agents were shown to have beneficial effects in adult patients with asthma, and no serious adverse effects were reported. This review deals with the role of TXA(2) in the pathogenesis of bronchial asthma and the clinical potential of anti-TXA(2) agents in the treatment of bronchial asthma.