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Vol. 84, Issue 2, 417-424, February 1998
Department of Physiology, University of Kentucky, Lexington, Kentucky 40536
Kwong, Kevin, Ju-Lun Hong, Robert F. Morton, and Lu-Yuan
Lee. Role of pulmonary C fibers in adenosine-induced respiratory inhibition in anesthetized rats. J. Appl.
Physiol. 84(2): 417-424, 1998.
The clinical use
of adenosine is commonly associated with pulmonary side effects, namely
dyspnea, that suggest the possible involvement of bronchopulmonary
sensory afferents. Our objective in this study was to characterize the
effects of adenosine on breathing and to determine whether the vagal
pulmonary afferents play a role in mediating these effects. We measured
respiratory and cardiovascular changes in anesthetized, spontaneously
breathing rats after bolus injections of adenosine at therapeutic
doses. Right atrial injection of adenosine (0.04-0.6 mg/kg)
elicits, in a dose-dependent manner, a pulmonary chemoreflex-like
response consisting of a delayed apnea, bradycardia, and hypotension.
In contrast, the classic capsaicin-elicited pulmonary chemoreflex occurs immediately after injection. Perineural capsaicin treatment of
the cervical vagi blocked the adenosine-induced respiratory inhibition.
Left ventricular administration of adenosine failed to elicit an apneic
response. Pretreatment with the adenosine A1-receptor antagonist
8-cyclopentyl-1,3-dipropylxanthine attenuated the
adenosine-induced apnea. These results indicate that adenosine elicits
a respiratory inhibition via stimulation of pulmonary C fibers and that
activation of the A1-receptor is
probably involved. It is unclear, however, what accounts for the
exceedingly long latency in this response.
dyspnea; vagus nerve; pulmonary chemoreflex; A1-receptor; 8-cyclopentyl-1,3-dipropylxanthine
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