• Nausherwan K Burki, Mohammad Sheatt, and Lu-Yuan Lee.
• Division of Pulmonary Medicine, University of Connecticut Health Center, Farmington, CT 06030-1321, USA. nburki@uchu.edu <nburki@uchu.edu>
• Pulm Pharmacol Ther. 2008 Jan 1; 21 (1): 208-13.

AbstractWe have recently shown that intravenous injection of adenosine causes dyspnea and hyperventilation in man, and we suggested that stimulation of vagal C-fibers in the airways and lungs is involved. To test this hypothesis further, the present study was performed in healthy subjects (n=12; age 32.4+/-10.2 yrs, 7 females) to determine if the effect of adenosine could be attenuated by blocking the airway sensory receptors by inhalation of aerosolized lidocaine, a local anesthetic. In each subject, the effects of intravenous injection of adenosine (10mg) on dyspneic sensation, minute ventilation, airway resistance and heart rate were measured after the subject inhaled lidocaine or placebo aerosol on two separate days. After a latency of approximately 20s, adenosine injection evoked a distinct dyspneic sensation, increase in minute ventilation (VE), and transient bradycardia followed by tachycardia in all subjects. The increase in VE resulted primarily from a significant increase in tidal volume. The intensity of adenosine-induced dyspnea was markedly reduced after the lidocaine pretreatment compared to placebo. In a sharp contrast, the VE and heart rate responses to adenosine were not affected by lidocaine. These results lend further support to our previous studies indicating that the origin of the dyspnogenic action of intravenous adenosine is most likely vagal bronchopulmonary C-fiber sensory nerves.

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