Our purpose was to examine the influence of steady-state changes in chemical stimuli, as well as discrete peripheral chemoreceptor stimulation, on abdominal expiratory motor activity. In decerebrate, paralyzed, vagotomized, and ventilated cats that had bilateral pneumothoraces, we recorded efferent activity from a phrenic nerve and from an abdominal nerve (cranial iliohypogastric nerve L1). All cats showed phasic expiratory abdominal nerve dischange at normocapnia [end-tidal PCO2 38 ± 2 Torr], but small doses (2-6 mg/kg) or pentobarbital sodium markedly depressed this activity. Hyperoxic hypercapnia consistently enhanced abdominal expiratory activity and shortened the burst duration. Isocapnic hypoxia caused inhibition of abdominal nerve discharge in 11 of 13 case. Carotid sinus nerve denervation (3 cats) exacerbated in hypoxic depression of abdominal nerve activity and depressed phrenic motor output. Stimulation of peripheral chemoreceptors with NaCN increased abdominal nerve discharge in 7 of 10 cats, although 2 cats exhibited marked inhibition. Four cats with intact neuraxis, but anesthetized with ketamine, yielded qualitatively similar results. We conclude that when cats are subjected to steady-state chemical stimuli in siolation (no interference from proprioceptive inputs), hypercapnia potentiates, but hypoxia attenuates abdominal expiratory nerve activity. Mechanisms to explain the selective inhibition of expiratory motor activity by hypoxia are proposed, and physiological implications are discussed.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Applied Physiology|
|State||Published - Jan 1 1987|
ASJC Scopus subject areas
- Physiology (medical)