2000 Volume 49 Issue 8 Pages 646-652
Exercise is a common stimulus of bronchoconstriction in subjects with asthma. Exercise-induced asthma(EIA)may be caused by heat loss and/or water loss during exercise. These changes cause the release of mediators and the development of bronchoconstriction. Recent studies have implicated the cysteinyl leukotrienes in the pathogenesis of EIA. Therefore we investigated the effect of a leukotriene antagonist, pranlukast hydrate, on EIA. Subjects were 11 EIA positive patients and were all atopic type bronchial asthma. 450mg of pranlukast hydrate was given for 14 days and the exercise test was performed before and after treatment. Pulmonary function tests were done before and 0, 5, 15 and 30min after completion of the each exercise. Prostaglandin E_2, thromboxane B_2, leukotriene E_4 and B_4 in urine were measured before and after the treatment. Pranlukast hydrate did not affect FEV_<1.0>, PF and Flow volume curve at rest and also levels of medicators in urine. The mean maximal percentage fall in FEV_<1.0> after exercise was -54.9±5.7% without therapy and -30.1±7.5% after pranlukast hydrate therapy. There was a significant difference between FEV_<1.0> values before and treatment at each time(ρ<0.005). This study demonstrated that pretreatment with a potent and selective leukotriene antagonist, pranlukast hydrate, attenuated EIA, and it suggests that leukotriene plays a role in EIA.
