The respiratory network that generates rhythmic activity is continuously subjected to excitatory and inhibitory inputs which regulate tidal breathing and respiratory timing: inspiratory (Ti) and expiratory (Te) duration. Recently we have shown in unrestrained, 5 day (but not 3 wk old) rat pups, that hypercapnia induced increases in tidal volume are accompanied by reduction in frequency due to an increase in Te. To identify if this maturational change in timing response to CO2 is central or peripheral in origin, we examined the effect of graded increases in inhaled CO2 on phrenic activity in decerebrate, vagotomized, paralyzed, and mechanically ventilated rat pups at 4-6 (n=8), 12-17 (n=9), and 36-40 (n=8) days. Hypercapnia always induced an increase in peak phrenic activity, which was associated with a CO2 concentration-dependent increase in Te at 4-6 but not 12-17 or 36-39 days (Fig). Hypercapnia had no significant effect on Ti. These results indicate that in early postnatal life CO2 increases phrenic output in parallel with a prolongation of Te which is centrally mediated and not related to changes in vagal or upper airway reflexes. We postulate that in the youngest animals, prolongation of Te during hypercapnia provides sufficient time to empty the lungs, regulate functional residual capacity and optimize work of breathing. Excessive prolongation of Te during hypercapnia, however, might compromise the ventilatory response.
Support: NIH 56470.