THE EFFECT OF INHALED FENOTEROL AND IPRATROPIUM BROMIDE ON PROPRANOLOL INDUCED BRONCHOCONSTRICTION IN THE ASTHMATIC AIRWAYS

SUMMARY 1. The provocative dose of inhaled propranolol, (PC20P, mg/mL) needed to induce a 20% reduction in the forced expired volume in 1 s (FEV1, L) was determined for 15 adult asthmatics following randomized pre‐treatment with placebo, ipratropium bromide (40, 160 μg) and fenoterol (200, 800 μg) aerosols using a double‐blind protocol. 2. Fenoterol 200 μg, 800 μg increased the baseline FEV1 0.28±0.16, 0.32±0.16 L (P= 0.04, P= 0.008 respectively). Fenoterol 800 μg moved the PC20P rightwards from placebo geometric mean 10.95, 95% Confidence Intervals (95% CI) 4.43–27.22 mg/mL to mean 20.41, 95% CI 10.13 to 40.64 mg/mL (P= 0.01). Fenoterol 200 μg was not protective; mean PC20 16.22, 95% CI 7.83–34.35 mg/mL (P= 0.08). Neither 40 or 160 μg ipratropium changed the FEV1 or PC20P values compared with placebo; increase in FEV1 0.15±0.27 L (P= 0.22), 0.24±0.12 L (P= 0.14) and geometric mean PC20P 16.59±0.57 mg/mL 95% CI 8.01–34.51 mg/mL (P= 0.90), 15.48±0.66 mg/mL, 95% CI 6.72–36.05 mg/mL (P= 0.34) respectively after ipratropium treatments. 3. Bronchoconstriction induced by inhaled propranolol (P) appears to be only weakly antagonized by inhaled β‐agonist and not reduced by antimuscarinic anticholinergic aerosol. This finding argues against the activation of a cholinergic reflex to explain propranolol induced bronchoconstriction (PIB).