Recent reports suggest the involvement of vascular phenomena in exercise- induced asthma. Sensory neuropeptides, such as substance P (SP), which causes airway vascular dilatation and plasma leakage, have been demonstrated to play a role in hyperpnea-induced airway narrowing in animal studies. The purpose of this study was to investigate the importance of tachykinins in exercise- induced airway narrowing in patients with asthma using a selective neurokinin 1-receptor (NK1-receptor) antagonist, FK-888. In a double-blind, placebo- controlled, crossover trial, nine subjects with stable asthma were given FK- 888 (2.5 mg) or placebo by inhalation 20 min before each exercise at a level previously demonstrated to cause a fail of at least 40% in specific airway conduction (SGaw). Inhalation of FK-888 had no significant effect on baseline SGaw. While the recovery from exercise-induced airway narrowing was significantly faster after treatment with FK-888, the area under the curve for SGaw during the 50 min after exercise was significantly reduced (p < 0.05) and the time taken for the SGaw to recover to within 65% of baseline after exercise was also significantly shorter with FK-888 than with placebo (p < 0.05). However, treatment with FK-888 did not significantly attenuate the maximal fall in SGaw. These results suggest that NK1-receptor-mediated mechanisms are involved in the recovery phase of exercise-induced airway narrowing. The possible mechanisms of these phenomena are discussed.
|Number of pages||6|
|Journal||American journal of respiratory and critical care medicine|
|Publication status||Published - 1996 Jan 1|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine