Effect of route of breathing on the ventilatory and arousal responses to hypercapnia in awake and sleeping dogs.

Abstract

SUMMARY1. The influence of the upper airway on the ventilatory and arousal responses to hypercapnia in wakefulness and sleep was investigated using a chronic animal model.2. Experiments were performed in five unrestrained dogs trained to sleep naturally in the laboratory. The animal rebreathed through a chronic tracheostoma (thus excluding the upper airway from the breathing circuit), or through the snout (intact upper airway). Resistance to breathing and volume of dead space during quiet tracheal breathing were matched to those in quiet nasal breathing during wakefulness and sleep. CO2 rebreathing tests were performed during wakefulness, rapid eye movement (REM) and non-REM (NREM) sleep, during nasal and tracheal breathing.3. The ventilatory response to hypercapnia was significantly lower in nasal breathing compared with tracheal breathing, in all behavioural states. This was due to a smaller tidal volume and lower breathing frequency.4. The ventilatory response to CO2 was lowest during REM sleep, irrespective of route used for breathing.5. Alveolar partial pressure of CO2 (PACO2) level at arousal was identical in NREM nasal and tracheal rebreathing tests. Differences in PACO levels at arousal between NREM and REM sleep were not significant in nasal tests and only marginally different during tracheal breathing.6. We conclude that nasal breathing influences the hypercapnic ventilatory response in wakefulness and sleep, and that the presence of CO2 in the upper airway does not affect arousal in NREM and REM sleep.

Neural-mechanical coupling of breathing in REM sleep

“…The only advance our findings have made in understanding the nature of this REM-induced blunted response of ventilatory output and pressure development to the asphyxia of airway occlusion is to show that it occurs at the level of the neural activation of the diaphragm. Other respiratory mechanoreceptor reflex responses from lung stretch and from airway stimulation have also been shown to be blunted in phasic REM sleep (10,15,17,27,30). However, we think it unlikely that these reflexes are involved in the reduced ventilatory responses in REM sleep, because 1) they tend to be inhibitory, and blunting an inhibitory reflex should, if anything, enhance ventilation, and 2) the increase of ventilatory efforts over the duration of occlusion strongly suggests to us a buildup of chemical stimuli (5).…”

The effects of repeated exposure to hypercapnia on arousal and cardiorespiratory responses during sleep in lambs

“…This study adds to previous animal studies showing that arousability is less in active sleep compared with quiet sleep. Other animal studies have found delayed arousal in active sleep in response to hypercapnia (dogs, Phillipson et al 1977; Issa & Bitner, 1993; lambs, Fewell & Baker, 1989). Also arousal responses are slower in REM in response to hypoxia (Phillipson et al 1978; Henderson‐Smart & Read, 1979; Jeffery & Read, 1980; Neubauer et al 1981; Fewell & Baker, 1987) and airway stimulation or obstruction (Sullivan et al 1978; Davidson & Fewell, 1994).…”

Ventilatory neural drive in chronically hypercapnic patients with COPD: effects of sleep and nocturnal noninvasive ventilation

“…In health, chemosensory responses to both hypercapnia [48] and hypoxia [49] are reduced in NREM and REM sleep [50]. Typically, responses to hypercapnia have been measured through Read's rebreathing protocol, in which P aCO 2 is increased by taking an individual's expired air and having them re-inspire it [48,[51][52][53]. Hypercapnic sensitivity can also be assessed through artificial increases in CO 2 through a breathing circuit [54].…”