Jr. Rodman et al., Carotid body denervation in dogs: eupnea and the ventilatory response to hyperoxic hypercapnia, J APP PHYSL, 91(1), 2001, pp. 328-335
We assessed the time course of changes in eupneic arterial PCO2 (Pa-CO2) an
d the ventilatory response to hyperoxic rebreathing after removal of the ca
rotid bodies (CBX) in awake female dogs. Elimination of the ventilatory res
ponse to bolus intravenous injections of NaCN was used to confirm CBX statu
s on each day of data collection. Relative to eupneic control (Pa-CO2 = 40
+/- 3 Torr), all seven dogs hypoventilated after CBX, reaching a maximum Pa
-CO2 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 hyperox
ic CO2 ventilatory (change in inspired minute ventilation/change in end-tid
al 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 t
o hyperoxic hypercapnia over the ensuing 19 days. We conclude that 1) the c
arotid bodies contribute similar to 40% of the eupneic drive to breathe and
the ventilatory response to hyperoxic hypercapnia and 2) there is no recov
ery in the eupneic drive to breathe or the ventilatory response to hyperoxi
c hypercapnia after removal of the carotid chemoreceptors, indicating a lac
k of central or aortic chemoreceptor plasticity in the adult dog after CBX.