Ventilatory responses to transient hypoxia and hypercapnia in man

The contribution of the peripheral (arterial) chemoreceptors to the ventilatory response to acute hypoxia and hypercapnia in intact unanesthetized man has been evaluated by methods which assume that ventilatory responses to transient stimuli reflect their effects upon the arterial chemoreceptors while responses to steady-state stimuli reflect their effects upon both arterial chemoreceptors and the central nervous system. Transient eucapneic hypoxia was produced by inhalation of several breaths of N₂ while breathing room air; transient hypercapneic hypoxia was produced by inhalation of several breaths of N₂ with CO₂ added while breathing CO₂ enriched air. Transient euoxic hypercapnia was produced by inhalation of single breaths of from 6 to 20% CO₂ in 21 % O₂ while the subject breathed air; transient hypoxic hypercapnia was produced by inhalation of single breaths of CO₂ enriched hypoxic gas while the subjects breathed a similarly hypoxic gas mixture. The ventilatory responses to transient hypoxia were qualitatively similar to the responses to steady-state hypoxia although they were quantitatively significantly greater by an average of 18%. The responses to transient euoxic hypercapnia averaged approximately one-third the responses to steady-state euoxic hypercapnia. Responses to transient hypercapnia were much less enhanced by hypoxia than were responses to steady-state hypercapnia. The findings suggest that: (1) A slight. centrally mediated, depressant effect of hypoxia may be present in unanesthetized man; (2) The peripheral chemoreceptors are responsible for approximately one-third of the overall (steady-state) ventilatory response to hypercapnia; (3) The phenomenon of stimulus interaction (enhancement of ventilatory response to hypercapnia by hypoxia) occurs at both the peripheral chemoreceptors and within the central nervous system but the central effect is the predominant one.