Effect of beta adrenergic blockage on bronchial sensitivity to inhaled acetylcholine in normal subjects.

Dose-responses curves were established in 10 normal subjects by measuring, with a body plethysmograph, the changes of specific airway conductance (SGaw) produced by aerosolized acetylcholine. Doses of acetylcholine producing a 50 per cent decrease of control SGaw (ED50) were found to be largely variable among individuals. Beta-adrenergic blockade with intravenous propranolol (0.2 mg per kilogram) resulted in a mean potentiation of the acetycholine effect (mean ED50 after propranolol was significantly lower than mean ED50 before). This potentiating effect of propranolol, however, was also subjected to individual variations, suggesting individual variability of the sympathetic system. The range of variation in acetylcholine sensitivity was not narrowed by propranolol treatment and no correlation was found between initial acetylcholine sensitivity and propranolol potentiation. This suggests that variability of the sympathetic system is not the main factor in determining individual variation in acetylcholine sensitivity. Even when propranolol was very effective in increasing airway sensitivity, this sensitivity was still less marked than usually encountered in asthmatic patients. This suggests that beta-adrenergic blockade cannot create, if alone, the bronchial hypersensitivity characteristic of asthma.

RCT Entities:   Population Interventions Outcomes