Relationship between cough due to hypotonic aerosol and the ventilatory response to CO2 in normal subjects.

This study tests the hypothesis that susceptibility to the tussive effect of hypotonic aerosol is related to the ventilatory response to CO2. The threshold concentration of saline required to elicit cough and the ventilatory response to CO2 were determined in 18 normal subjects. Twelve subjects coughed with hypotonic aerosol (responders), and six did not (nonresponders). The CO2 ventilatory responses, which were normalized for vital capacity, were greater in the responders than in the nonresponders (0.64 +/- 0.16 and 0.43 +/- 0.12 L/min/mm Hg/L, respectively, p less than 0.02). The differences in the ventilatory responses to CO2 were consequent to a lesser increase in respiratory frequency in the nonresponders as compared to the responders (0.35 +/- 0.33 and 0.77 +/- 0.32 breaths/min/mm Hg, respectively, p less than 0.02). There were no differences in vital capacity-normalized tidal volume responses between the 2 groups (0.02 +/- 0.01 and 0.02 +/- 0.01 L/mm Hg/L). These findings suggest that susceptibility to the tussive effect of hypotonic aerosol and CO2 ventilatory response may be determined by a common neural mechanism. Differences in the respiratory patterns assumed by the responders and nonresponders during CO2 rebreathing suggest that the blunted CO2 response in the nonresponders may be related to a decrease in gain of volume-related vagal feedback. It is suggested that hypotonic cough threshold and CO2 ventilatory responses may be mediated by similar airway receptors.