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J Appl Physiol 91: 328-335, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 1, 328-335, July 2001

Carotid body denervation in dogs: eupnea and the ventilatory response to hyperoxic hypercapnia

J. R. Rodman, A. K. Curran, K. S. Henderson, J. A. Dempsey, and C. A. Smith

The John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin School of Medicine, Madison, Wisconsin 53705

We assessed the time course of changes in eupneic arterial PCO2 (PaCO2) and the ventilatory response to hyperoxic rebreathing after removal of the carotid bodies (CBX) in awake female dogs. Elimination of the ventilatory response to bolus intravenous injections of NaCN was used to confirm CBX status on each day of data collection. Relative to eupneic control (PaCO2 = 40 ± 3 Torr), all seven dogs hypoventilated after CBX, reaching a maximum PaCO2 of 53 ± 6 Torr by day 3 post-CBX. There was no significant recovery of eupneic PaCO2 over the ensuing 18 days. Relative to control, the hyperoxic CO2 ventilatory (change in inspired minute ventilation/change in end-tidal PCO2) and tidal volume (change in tidal volume/ change in end-tidal PCO2) response slopes were decreased 40 ± 15 and 35 ± 20% by day 2 post-CBX. There was no recovery in the ventilatory or tidal volume response slopes to hyperoxic hypercapnia over the ensuing 19 days. We conclude that 1) the carotid bodies contribute ~40% of the eupneic drive to breathe and the ventilatory response to hyperoxic hypercapnia and 2) there is no recovery in the eupneic drive to breathe or the ventilatory response to hyperoxic hypercapnia after removal of the carotid chemoreceptors, indicating a lack of central or aortic chemoreceptor plasticity in the adult dog after CBX.

chemoreception; ventilatory control; compensation; rebreathing


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