AR Berman, MC Liu, EM Wagner and D Proud
Department of Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224-6801, USA.

To determine if bradykinin, a potential mediator of asthma, acts, at least in part, at the level of the peripheral airways, we used a wedged bronchoscope technique to study asthmatic and normal subjects. Baseline peripheral airways resistance (Rp) was measured in the right upper lobe. Subjects then received saline, followed by increasing doses of bradykinin, aerosolized through the bronchoscope. Rp was measured after each challenge. At the end of the procedure, bronchoalveolar lavage was performed in both the challenged and a control segment. Fibrinogen content of recovered lavage fluids was measured as an index of plasma exudation. Bradykinin induced a dose-dependent increase in Rp in the asthmatics, but did not effect Rp in normal subjects. In asthmatics, there was no significant correlation between peripheral airways reactivity and whole lung reactivity to bradykinin. Fibronogen increased significantly in both groups after bradykinin challenge, and there was no significant difference between postchallenge levels for the two groups. Thus, hyperreactivity of the peripheral airways in asthmatics is not directly due to plasma exudation. The ability of bradykinin to increase peripheral airways resistance in asthmatic, but not in normal, subjects is consistent with a role of this peptide as a mediator of asthma.

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