Journal of Applied Physiology, Vol 68, Issue 1 369-373, Copyright © 1990 by American Physiological Society
Cardiac receptors evoke ventilatory response with increased venous PCO2 at constant arterial PCO2
J. A. Estavillo
Department of Anatomy, School of Medicine, Southern Illinois University, Carbondale 62901.
The effects of elevated venous PCO2 and denervation of the cardiac
ventricles on ventilation were studied in 20 anesthetized open-chest
unidirectionally ventilated White Leghorn cockerels. Venous PCO2 was
increased by insufflating the gut with high CO2 while recording changes in
the amplitude of the sternal movements. Arterial blood gases were held
constant by unidirectionally ventilating the lungs with gas flows
approximately five times the animal's resting minute volume. Insufflating
the gut with 90% N2-10% O2 did not change the level of ventilation, whereas
with 90% CO2-10% O2 the amplitude of sternal movement increased 500% above
that with no gut gas flow. Exchange of N2 for the CO2 was followed by a
rapid reduction of ventilatory movements to control levels. Arterial blood
gases remained constant during gut gas insufflation, whereas mixed venous
PCO2 increased and mixed venous pH decreased when high CO2 was given to the
gut. Cutting the middle cardiac nerves, which primarily innervate the
ventricles of the heart, reduced the ventilatory response to CO2 gut
insufflation by 67%. Sympathetic denervation of the thoracic viscera did
not change the responses. It appears that, in the chicken, increasing the
mixed venous PCO2 while holding the arterial blood gases constant alters
ventilation by an afferent system located in the venous circulation or in
the right ventricle which is sensitive to changes in PCO2.
