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J Appl Physiol (September 15, 2005). doi:10.1152/japplphysiol.00926.2005
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Submitted on August 1, 2005
Accepted on September 7, 2005

Response Time and Sensitivity of the Ventilatory Response to CO2 in Unanesthetized Intact Dogs: Central vs. Peripheral Chemoreceptors

Curtis A Smith1*, Joshua R Rodman1, Bruno J Chenuel1, Kathleen S Henderson1, and Jerome A Dempsey1

1 Population Health Sciences, University of Wisconsin, Madison, WI, USA

* To whom correspondence should be addressed. E-mail: casmith4{at}wisc.edu.

We assessed the speed of the ventilatory response to square-wave changes in PACO2 and the relative gains of the steady-state ventilatory response to CO2 of the central chemoreceptors vs. the carotid body chemoreceptors in intact, unanesthetized dogs. We used extracorporeal perfusion of the reversibly isolated carotid sinus to maintain normal tonic activity of the carotid body chemoreceptor while preventing it from sensing systemic changes in CO2, thereby allowing us to determine the response of the central chemoreceptors alone. We found: 1) The ventilatory response of the central chemoreceptors alone is 11.2 (SD=3.6) seconds slower than when CBs are allowed to sense CO2 changes. 2) On average, the central chemoreceptors contribute about 63% of the gain to steady-state increases in CO2. There was wide dog-to-dog variability in the relative contributions of central vs. carotid body chemoreceptors; the central exceeded the carotid body gain in 4 of 6 dogs but in 2 dogs carotid body gain exceeded central CO2 gain. If humans respond similarly to dogs, we propose that the slower response of the central chemoreceptors vs. the carotid chemoreceptors prevents the central chemoreceptors from contributing significantly to ventilatory responses to rapid, transient changes in PaCO2 such as those following periods of hypoventilation and hyperventilation ("ventilatory undershoots/overshoots") observed during sleep-disordered breathing. However, the greater average responsiveness of the central chemoreceptors to brain hypercapnia in the steady-state suggests that these receptors may contribute significantly to ventilatory overshoots once unstable/periodic breathing is fully established.




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