Influence of hypercapnic acidosis and hypoxia on abdominal expiratory nerve activity in the rat.

We studied the influence of hypercapnic acidosis and hypoxia on the neural drive to abdominal muscles in anesthetized and decerebrate rats; this information is unavailable despite widespread use of the rat as an experimental model in respiratory physiology and neurobiology. To minimize confounding influences from receptors in the lungs and chest wall, the animals were vagotomized, paralyzed and mechanically ventilated, and electrical activity was recorded from abdominal muscle nerves. In anesthetized and decerebrate rats, both stimuli evoked steady, low amplitude expiratory discharge that persisted throughout the expiratory phase (E-all activity), but was inhibited during inspiration. We also observed late expiratory, high-amplitude bursts (E2 activity) superimposed on this steady activity, but only at the highest levels of respiratory drive. Hypoxia enhanced abdominal motor activity transiently, whereas hypercapnic acidosis caused a sustained increase in activity. Thus, both hypercapnic acidosis and hypoxia activate abdominal muscle motoneurons in the absence of phasic afferent inputs.