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Selectivity of beta adrenoreceptor antagonist drugs assessed by histamine bronchial provocation
Author(s) -
Ruffin R. E.,
Frith P. A.,
Anderton R. C.,
Kumana C. R.,
Newhouse M. T.,
Hargreave F. E.
Publication year - 1979
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt1979255part1536
Subject(s) - placebo , provocation test , propranolol , bronchoconstriction , histamine , medicine , heart rate , context (archaeology) , asthma , bronchospasm , anesthesia , terfenadine , antagonist , metoprolol , pharmacology , cardiology , blood pressure , paleontology , alternative medicine , receptor , pathology , biology
In a double‐blind, within‐patient, randomized study, 12 mild asthmatics were given single oral doses of propranolol (80 mg), metoprolol (100 mg), timolol (10 mg), or placebo. Resting heart rate and forced expiratory volume in one sec (FEV 1 ) were measured before and 90 min after treatment. Nonspecific bronchial reactivity was measured by inhaled histamine at 90 min. Following each active drug, resting heart rate changed to a similar extent and to a greater degree than after placebo (p < 0.01). Changes in FEV 1 were small and not different from those after placebo. In contrast, after each active drug, bronchial reactivity increased more than after placebo. The degree of reactivity with each active drug was similar but the differences from corresponding placebo values were significant (p < 0.05). We conclude that, in mild asthmatics, nonspecific bronchial reactivity is a more sensitive index of airway effects than resting FEV 1 . Moreover, in the context of this study, since the β‐blockers were given in doses likely to induce equivalent cardiac β‐blockade, there is no evidence to suggest that any one of them is more “cardioselective” than the others.