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1 Department of Medicine, Division of Pulmonary Medicine, University of Connecticut Health Center, Farmington, CT, USA
2 Department of Medicine, University of Kentucky Medical Center, Lexington, KY, USA
3 Department of Physiology, University of Kentucky Medical Center, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: nburki{at}uchc.edu.
Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm, dyspnea, and increase in ventilation in man but these effects have not been systematically studied. We therefore compared the effects of 10 mg intravenous adenosine to placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change (p>0.1) in lung resistance as measured by the interrupter technique. There were significant increases (p<0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in 20 of 21 subjects, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analysed (18.9 ± 5.8 s, 20.3 ± 5.5 s, and 19.7 ± 4.5s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared to the normoxic state, the intensity of the dyspneic response was significantly (p<0.05) reduced, whereas the heart rate response increased significantly (p<0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.
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