Effect of β-Blocker Therapy on Airway Function

Summary

The ability of β-blockers to cause bronchoconstriction in asthmatic patients is related to their degree of cardioselectivity. The assessment of cardioselectivity in animals should be complemented by appropriate testing in man. Such tests are unpleasant for asthmatic patients, and not without risk, so that studies have been carried out on highly selected patients. Because of changes in sympathetic drive and airway calibre in asthmatic patients the results can only be considered to be semi-quantitative.

Bronchial β-blockade in normal subjects was assessed after different doses of β-blockers, by measuring the displacement of the airway dose-response curve to an inhaled β-agonist, salbutamol. This has been compared with the heart rate reduction in the same subjects after the same dose of β-blocker on a separate occasion. The combined results of 3 studies show that practolol (100 and 200mg), atenolol (50 and 100mg), and bevantolol (75 and I50mg) caused relatively little bronchial β-blockade, less than that seen with labetalol (150 and 300mg) and acebutolol (100 and 200mg), and considerably less than that with propranolol (40 and 80mg). In a further study, metoprolol (200mg) was compared with atenolol (100mg) and propranolol (80mg) at 2, 12 and 24 hours post-ingestion. At 2 hours, atenolol caused less bronchial β-blockade than metoprolol, and both caused much less than propranolol. By 24 hours there was no evidence of bronchial β-blockade with atenolol or metoprolol in contrast to propranolol. However, all 3 drugs caused some reduction in exercise heart rate at 24 hours; atenolol more than propranolol. These results suggest that atenolol is more cardio-selective than metoprolol.