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Department of Physiology, University of Kentucky Medical Center, Lexington, Kentucky 40536-0084; and Department of Pharmacology, Karolinska Institut, S-104 01 Stockholm, Sweden
Received 18 April 1996; accepted in final form 22 July 1996.
Lee, Lu-Yuan, Robert F. Morton, and Jan M. Lundberg.
Pulmonary chemoreflexes elicited by intravenous injection of
lactic acid in anesthetized rats. J. Appl.
Physiol. 81(6): 2349-2357, 1996.
Experiments were
carried out to characterize the cardiorespiratory reflex responses to
intravenous injection of lactic acid and to determine the involvement
of vagal bronchopulmonary C-fiber afferents in eliciting these
responses in anesthetized rats. Bolus injection of lactic acid (0.2 mmol/kg iv) immediately elicited apnea, bradycardia, and hypotension,
which were then followed by a sustained hyperpnea. The immediate apneic
and bradycardiac responses to lactic acid were completely abolished by
bilateral vagotomy and were absent when the same dose of lactic acid
was injected into the left ventricle. The subsequent hyperpneic
response was substantially attenuated by denervation of carotid body
chemoreceptors. After a perineural capsaicin treatment of both vagus
nerves to block the conduction of C fibers, lactic acid no longer
evoked the immediate apnea and bradycardia, whereas the hyperpneic
response became more pronounced and sustained, presumably because of
the removal of the inhibitory effect on breathing mediated by pulmonary
C-fiber activation. Single-unit electrophysiological recording showed
that intravenous injection of lactic acid consistently evoked an abrupt
and intense burst of discharge from the vagal C-fiber afferent endings
in the lungs. In conclusion, the cardiorespiratory depressor responses induced by lactic acid are predominantly elicited by activation of
vagal pulmonary C fibers.
pulmonary C fibers; vagal reflexes; apnea; hyperpnea; capsaicin; perineural capsaicin treatment
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