K. Kwong et al., ROLE OF PULMONARY C-FIBERS IN ADENOSINE-INDUCED RESPIRATORY INHIBITION IN ANESTHETIZED RATS, Journal of applied physiology, 84(2), 1998, pp. 417-424
The clinical use of adenosine is commonly associated with pulmonary si
de effects, namely dyspnea, that suggest the possible involvement of b
ronchopulmonary sensory afferents. Our objective in this study was to
characterize the effects of adenosine on breathing and to determine wh
ether the vagal pulmonary afferents play a role in mediating these eff
ects. We measured respiratory and cardiovascular changes in anesthetiz
ed, spontaneously breathing rats after bolus injections of adenosine a
t 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 occu
rs immediately after injection. Perineural capsaicin treatment of the
cervical vagi blocked the adenosine-induced respiratory inhibition. Le
ft ventricular administration of adenosine failed to elicit an apneic
response. Pretreatment with the adenosine Al-receptor antagonist 8-cyc
lopentyl-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 A(1)
-receptor is probably involved. It is unclear, however, what accounts
for the exceedingly long latency in this response.