Bronchodilatation and inhibition of allergen-induced bronchoconstriction by circulating epinephrine in asthmatic subjects.

The influence of circulating epinephrine on basal bronchial tone and its ability to counteract the bronchial response to specific allergen challenge was investigated in eight patients with extrinsic seasonal asthma. A pretrial bronchial allergen challenge was positive for birch or timothy pollen. The patients were free from all medication at least 1 wk before experiments. On two separate occasions placebo (saline) or epinephrine (0.25 and 0.50 nmol X kg-1 X min-1) were infused. Epinephrine caused dose-dependent increases in end expiratory flow rates but did not influence peak expiratory flow rates or specific airway conductance, indicating dilatation of predominantly smaller airways. During placebo infusions allergen provocation induced clear-cut bronchoconstriction but no increase in circulating epinephrine levels. Elevation of circulating epinephrine (to 5 to 6 nmol/L in venous plasma) counteracted the allergen-induced bronchoconstriction. During epinephrine infusions all patients tolerated higher allergen doses than during placebo infusions. When the allergen dose was increased sufficiently to cause bronchoconstriction also during epinephrine infusions, the bronchoconstriction observed was similar in terms of changes in lung function parameters but less responsive to treatment with a high dose of the beta-2-agonist, salbutamol. This may have therapeutic implications since protection offered by treatment with, e.g. beta 2-agonists, may lead to exposure to higher allergen doses and similarly aggravated asthmatic reactions when they do occur despite this treatment.