Co2-sensitive olfactory and pulmonary receptor modulation of
episodic breathing in bullfrogs.
Kinkead, Richard, and William K. Milsom.
Department of Zoology, University of British Columbia, 6270
University Blvd., Vancouver, British Columbia, Canada, V6T 1Z4
APStracts 2:0211R, 1995.
Breathing was monitored during normocarbia, hypercarbia (6% CO2 in
air) and the period immediately following the return to normocarbic
conditions in intact, olfactory denervated and vagotomized bullfrogs.
In intact frogs, ventilation increased during hypercarbia, but the
breathing pattern remained episodic. Immediately upon return to air,
there was a further paradoxical increase in breathing frequency, and
breathing became continuous in most frogs. Results obtained from
animals following olfactory receptor denervation indicate that tonic
stimulation of olfactory receptors by airway CO2 inhibited breathing
during hypercarbia. Measurements of the kinetics of changes in airway
and arterial blood CO2 levels support the suggestion that the sudden
release of this inhibition on the return to normocarbic conditions
was responsible for the post-hypercarbic hyperpnea. Vagotomy
increased ventilation during normocarbia. Hypercarbia now caused a
change in breathing pattern but had no net effect on total
ventilation suggesting that pulmonary vagal feedback inhibited
ventilation during normocarbia but stimulated ventilation during
hypercarbia. Although olfactory and pulmonary receptor feedback shape
the breathing pattern, they were not responsible for initiating or
terminating the episodes of breathing.
Received 6 January 1995; accepted in final form 17 July 1995.
APS Manuscript Number R16-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.