Submitted on December 11, 2008
Revised on February 10, 2009
Accepted on February 23, 2009
Contribution of the Carotid Body Chemoreceptors to Eupneic Ventilation in the Intact, Unanesthetized Dog
Gregory M. Blain1*, Curtis A. Smith2, Kathleen S. Henderson2, and Jerome A. Dempsey1
1 University of Wisconsin - Madison
2 University of Wisconsin
* To whom correspondence should be addressed. E-mail: gblain{at}wisc.edu.
We used extracorporeal perfusion of the reversibly isolated carotid sinus region to determine the effects of specific carotid body (CB) chemoreceptor inhibition on eupneic ventilation (VI) in the resting, awake, intact dog. Four female spayed dogs were studied during wakefulness when CB was perfused with 1) normoxic, normocapnic blood, and 2) hyperoxic (> 500 mmHg), hypocapnic (
20 mmHg) blood to maximally inhibit the CB tonic activity. We found that CB perfusion per se (normoxic, normocapnic) had no effect on ventilation. CB inhibition caused marked reductions in VI (-60%, range 49-80%) and inspiratory flow rate (-58%, range 44-87%) 24 to 41 seconds following the onset of CB perfusion. Thereafter, a partial compensatory response was observed and a steady state in VI was reached after 50 to 76 seconds following the onset of CB perfusion. This steady-state tidal volume-mediated hypoventilation (31 %) coincided with a significant reduction in mean diaphragm EMG (-24%) and increase in mean arterial pressure (+12 mmHg, MAP), which persisted for 7 to 25 minutes until CB perfusion was stopped despite a substantial increase in CO2 retention (+9 mmHg, PaCO2) and systemic respiratory acidosis. We interpret these data to mean that CB chemoreceptors contribute more than one half to the total eupneic drive to breathe in the normoxic, intact awake animal. We speculate that this CB contribution consists of both the normal tonic sensory input from the CB chemoreceptors to medullary respiratory controllers as well as a strong modulatory effect on central chemoreceptor responsiveness to CO2.
