Objectives: The aim of this study was to evaluate the effects of non-bronchoconstrictive doses of propranolol on airway hyperresponsiveness to methacholine. Methods: Double increasing concentrations (from 0.03 to 64 mug/ml) of inhaled propranolol were administered to a study population which included ten patients with mild asthma, tell rhinitics, and ten healthy control subjects. After the baseline bronchial responses to propranolol and methacholine, expressed as the cumulative provocative dose producing a 20% fall in forced expiratory volume in 1 a (PD20FEV1), were assessed, methacholine challenge was repeated after pretreatment with non-bronchoconstrictive doses of propranolol. Results: The pharmacologically induced beta -blockade did not cause any effect in normal individuals, but it worsened airway responsiveness to methacholine in all asthmatics (geometric mean PD20 FEV1: 257 and 87 mug, respectively) and some rhinitics (geometric mean PD20 FEV1: 724 and 446 mug, respectively). Conclusion: Asthmatic patients were extremely sensitive to beta -blockers, whereas we observed a variable response to propranolol within the group of rhinitic subjects. This variability in the latter group is possibly because these individuals had different degrees of airway inflammation, increased parasympathetic activity, and beta -adrenoceptor dysfunction.

Effects of non-bronchoconstrictive doses of inhaled propranolol on airway responsiveness to methacholine.

VATRELLA, Alessandro;
2001-01-01

Abstract

Objectives: The aim of this study was to evaluate the effects of non-bronchoconstrictive doses of propranolol on airway hyperresponsiveness to methacholine. Methods: Double increasing concentrations (from 0.03 to 64 mug/ml) of inhaled propranolol were administered to a study population which included ten patients with mild asthma, tell rhinitics, and ten healthy control subjects. After the baseline bronchial responses to propranolol and methacholine, expressed as the cumulative provocative dose producing a 20% fall in forced expiratory volume in 1 a (PD20FEV1), were assessed, methacholine challenge was repeated after pretreatment with non-bronchoconstrictive doses of propranolol. Results: The pharmacologically induced beta -blockade did not cause any effect in normal individuals, but it worsened airway responsiveness to methacholine in all asthmatics (geometric mean PD20 FEV1: 257 and 87 mug, respectively) and some rhinitics (geometric mean PD20 FEV1: 724 and 446 mug, respectively). Conclusion: Asthmatic patients were extremely sensitive to beta -blockers, whereas we observed a variable response to propranolol within the group of rhinitic subjects. This variability in the latter group is possibly because these individuals had different degrees of airway inflammation, increased parasympathetic activity, and beta -adrenoceptor dysfunction.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11386/3798878
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