Effect of Carbon Dioxide Breathing on Specific Airway Conductance in Normal and Asthmatic Subjects1,2

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Abstract
The effect of breathing 2.5 to 10 per cent carbon dioxide in air on specific airway conductance was determined by plethysmography in 9 normal subjects and in 8 subjects with mild asthma. In 9 normal subjects, during breathing of 5, 7.5, and 10 per cent carbon dioxide, mean (± SE) values of specific airway conductance decreased by 15.8 ± 6.1, 24.4 ± 6.0, and 28.4 ± 7.9 per cent with increases in end-tidal carbon dioxide tension of 5.0 ± 1.6, 12.3 ± 2.3, and 20.2 ± 2.5 mm Hg, respectively. These changes were not significantly affected by prior administration of atropine or propranolol except that atropine prevented the decrease in specific airway conductance during 5 per cent carbon dioxide breathing. Isocapnic hyperventilation decreased specific airway conductance (15 ± 6 per cent) but to a lesser extent than during similar increases in ventilation due to breathing of 10 per cent carbon dioxide. In contrast, in 8 subjects with asthma, specific airway conductance did not change during carbon dioxide breathing with or without prior atropine or during isocapnic hyperventilation. After propranolol, however, 5 to 10 per cent CO2 resulted in significant decreases in specific airway conductance (14.1 ± 4.7 to 27.2 ± 6.1 per cent) of a magnitude similar to that noted in normal subjects. These results suggest that, in normal subjects, hypercapnia due to 7.5 to 10 per cent carbon dioxide breathing constricts airways by a mechanism that is not principally related to a mechanical effect of hyperventilation and is not vagally mediated whereas airway constriction during lesser degrees of hypercapnia is apparently mediated by cholinergic pathways. In patients with asthma, on the other hand, hypercapnic airway constriction appears to be prevented by a concomitant sympathetic dilator effect on airways that is unmasked by β-adrenergic blockade.

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