Abstract
BackgroundWe have shown that intravenous adenosine in normal subjects does not cause bronchospasm, but causes dyspnea, most likely by an effect on vagal C fibers in the lungs [Burki et al. J Appl Physiol 2005; 98:180-5]. Since airways inflammation and bronchial hyperreactivity are features of asthma, it is possible that intravenous adenosine may be associated with an increased intensity of dyspnea, and may cause bronchospasm, as noted anecdotally in previous reports.MethodsWe compared the effects of placebo and 10 mg intravenous adenosine, in 6 normal and 6 asthmatic subjects.ResultsPlacebo injection had no significant (p > 0.05) effect on the forced expiratory spirogram, heart rate, minute ventilation (Ve), or respiratory sensation. Similarly, adenosine injection caused no significant changes (p > 0.05) in the forced expiratory spirogram; however, there was a rapid development of dyspnea as signified visually on a modified Borg scale, and a significant (p < 0.05) tachycardia in each subject (Asthmatics +18%, Normals + 34%), and a significant (p < 0.05) increase in Ve (Asthmatics +93%, Normals +130%). The intensity of dyspnea was significantly greater (p < 0.05) in the asthmatic subjects.ConclusionThese data indicate that intravenous adenosine does not cause bronchospasm in asthmatic subjects, and supports the concept that adenosine-induced dyspnea is most likely secondary to stimulation of vagal C fibers in the lungs. The increased intensity of adenosine-induced dyspnea in the asthmatic subjects suggests that airways inflammation may have sensitized the vagal C fibers.
Highlights
We have shown that intravenous adenosine in normal subjects does not cause bronchospasm, but causes dyspnea, most likely by an effect on vagal C fibers in the lungs [Burki et al J Appl Physiol 2005; 98:180-5]
In rats we have shown that intravenous adenosine directly stimulates pulmonary vagal C fibers through activation of A1 receptors [4], and it is likely that the dyspnea in man is a direct consequence of pulmonary C fiber activation
Neither saline injection nor intravenous adenosine resulted in any significant change (p > 0.5) in the spirogram (Table 1)
Summary
We have shown that intravenous adenosine in normal subjects does not cause bronchospasm, but causes dyspnea, most likely by an effect on vagal C fibers in the lungs [Burki et al J Appl Physiol 2005; 98:180-5]. Amongst the reported side effects [2] of intravenous adenosine in asthmatics are bronchospasm and dyspnea; in normal subjects we have shown [3] that while intravenous adenosine is dyspnogenic, and stimulates ventilation and tachycardia, it does not cause bronchospasm. In rats we have shown that intravenous adenosine directly stimulates pulmonary vagal C fibers through activation of A1 receptors [4], and it is likely that the dyspnea in man is a direct consequence of pulmonary C fiber activation.
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