Journal of Applied Physiology AJP: Cell Physiology
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J Appl Physiol 76: 756-759, 1994;
8750-7587/94 $5.00
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Journal of Applied Physiology, Vol 76, Issue 2 756-759, Copyright © 1994 by American Physiological Society

ARTICLES

Cardiovascular and respiratory effects of adenosine in humans after pulmonary denervation

N. J. Morgan-Hughes, P. A. Corris, M. D. Healey, J. H. Dark and J. M. McComb
Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne, United Kingdom.

Adenosine infusion causes tachycardia in normal subjects. A proposed mechanism is secondary pulmonary stretch receptor activation due to hyperventilation, induced by direct stimulation of carotid body chemoreceptors by adenosine. We examined responses to adenosine (incremental doses given by intravenous infusion, 5 min each rate) in six normal volunteers and six lung-transplant recipients with pulmonary denervation. Adenosine caused chemoreceptor stimulation in both groups with minute ventilation increasing from 5.8 +/- 0.4 to 10.7 +/- 1.3 l/min (P < 0.05) in the volunteers and from 4.8 +/- 0.4 to 9.2 +/- 0.8 l/min (P < 0.001) in the lung-transplant recipients. There was no difference in the magnitude of the ventilatory increase between the two groups (P = NS at all infusion rates). Adenosine produced tachycardia in both groups, with heart rate increasing from 66 +/- 5 to 84 +/- 3 beats/min (P < 0.01) in the volunteers and from 82 +/- 6 to 110 +/- 6 beats/min (P < 0.05) in the lung-transplant recipients. There was no difference in the magnitude of the heart rate response between the two groups (P = NS at all infusion rates). These data suggest, contrary to previous thinking, that pulmonary stretch receptor activation does not contribute to adenosine-induced tachycardia in humans.


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