| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Research Abstract |
We reported that release of Substance-P from C-fiber of bronchial nerves has an important role in the mechanisms of the exercise-induced asthma (EIA).
This time, therefore, we examined the effect of leukotrien C4, D4, E4 antagonist (ONO-1078) on the EIA in order to determine the role leukotrien to cause EIA.Futhermore, to clarify the involvement of Substance-P and leukotriene released by mast cell, we take the NK1 receptor antagonist (FK888), NK1 and NK2 receptor antagonist (FK224) and Leukotriene C4, D4, E4 antagonist (ONO-1078) to EIA in guinea pig immunized byOA.And to determine the effect of probocation of cold air to hyperresponsiveness, we measured the Rr and airway responsiveness to histamine and investigated the histamine and Substnace-P level in BALF in guinea pig immunized by OA after cold air porbocation.
It is recognized that Rr in guinea pig dosen't increase 5 minutes after exercise, but increased significantly 15 minutes after exercise. Histamine concentration in BAlF of guinea pig 15 minutes after exercise was higher than before, but not significantly. Substance-P level were significantly higher than before. Proportion do neutrophiles in BALF increase 15 minutes after exerciase. ONO-1078 inhibited EIA and so did FK888 and FK224. Although the Rr increased and threshhold to histamined decrease 15 minutes after inhalation of cold air (-10ﾟC), histamine and Substance-P level in BALF didn't significantly change respectively.
It is suggested that activation of mast cell and releasebility of C-fiber in the bronchus were induced after hyperventilation, mediators from mast cells and C-fiber play an important role in mechanisms of EIA.
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