VENTILATORY EFFECTS OF SPECIFIC CAROTID-BODY HYPOCAPNIA IN DOGS DURING WAKEFULNESS AND SLEEP

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.