Phrenic activity during severe hypercapnia in vagotomized rabbits.

The central control mechanism of respiratory frequency under varied alveolar carbon dioxide pressure (PACO2 20--200 Torr) was investigated in anesthetized, vagotomized, immobilized, and artificially ventilated rabbits. Central inspiratory activity indicated by phrenic motor discharge was tolerant of the extensive hypercapnia. Under light anesthesia the respiratory frequency (f) decreased in a hyperbolic fashion with increasing PACO2. Under deeper anesthesia or after mesencephalic decerebration the hyperbolic f response to PACO2 was abolished or changed to a hill-type f response (initial increase and subsequent decrease in f) and, on the average, the changes in frequency were much less. We conclude that in the absence of vagal control the respiratory frequency is primarily determined by 1) the periodicity of the bulbopontine inspiratory activity, which is little dependent on PACO2, and 2) a suprapontine acceleratory mechanism, which is depressed by increased PACO2 and highly sensitive to anesthetics. The mechanism of changes in the type of f response to CO2 is discussed.