Animal and human studies have shown that various kinds of chemical med
iators 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 hyperresponsiven
ess. The reasons are as follows. (i) TXA(2) (or mimetics) is a powerfu
l constrictor of bronchial muscle in vitro and in vivo. (ii) Levels of
TXB2, a metabolite of TXA(2), increase in blood or bronchoalveolar la
vage fluid after allergen challenge in atopic asthmatic patients. (iii
) TXA(2) mimetics induce airway hyperresponsiveness to nonspecific sti
muli such as acetylcholine or methacholine. (iv) TXA(2) synthetase inh
ibitors or TXA(2) receptor antagonists inhibit asthmatic responses or
airway hyperresponsiveness in various animal models and in patients wi
th asthma. In Japan, the TXA(2) synthetase inhibitor ozagrel and the T
XA(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 revie
w deals with the role of TXA(2) in the pathogenesis of bronchial asthm
a and the clinical potential of anti-TXA(2) agents in the treatment of
bronchial asthma.