Ca. Smith et al., VENTILATORY EFFECTS OF SPECIFIC CAROTID-BODY HYPOCAPNIA IN DOGS DURING WAKEFULNESS AND SLEEP, Journal of applied physiology, 79(3), 1995, pp. 689-699
We used extracorporeal perfusion of the vascularly isolated carotid si
nus region to determine the effects of specific carotid body chemorece
ptor hypocapnia-alkalosis on ventilatory control in the unanesthetized
dog. Eight female dogs were studied during wakefulness, non-rapid-eye
-movement (NREM) sleep, and rapid eye movement (REM) sleep. Carotid bo
dy perfusions lasted from 1 to 2 min, and each trial was preceded by a
1-min control period. Two levels of carotid body hypocapnia were empl
oyed, similar to 7 and 14 Torr below eupneic levels in a given dog. We
found that 1) During wakefulness and NREM sleep, carotid body hypocap
nia caused reduced tidal volume (VT) but not apnea or expiratory time
prolongation. 2) The inhibition of ventilation in response to carotid
body hypocapnia was graded below normocapnia, showing the highest sens
itivity at carotid body Pco(2) near 7 Torr below eupneic values. Inhib
ition reached a maximum near 14 Torr below the eupneic level; VT, insp
iratory minute ventilation (VI), and VT-to-inspiratory time ratio fell
31, 23, and 27% in wakefulness and 30, 23, and 30% in NREM sleep. 3)
Reductions in ventilation in response to carotid body hypocapnia are l
essened but still persist throughout perfusion (up to at least 130 s)
despite significant systemic hypercapnia. 4) During REM sleep, carotid
body hypocapnia had no consistent inhibitory effect on ventilation un
til carotid body Pco(2) was reduced to values near 14 Torr below the e
upneic level, at which point ventilation was similar to wakefulness an
d NREM. 5) Moderate carotid body hypocapnia was as effective as caroti
d body hyperoxia in reducing VT and VI. We conclude that carotid body
hypocapnia-alkalosis can significantly inhibit eupneic VT and ventilat
ion during wakefulness and NREM sleep and, if the hypocapnia is severe
enough, during REM sleep.