Abstract
The nature of peripheral and central chemoreceptor interaction in the neonatal period is unknown. Given recent findings in adult rodents, the hypothesis addressed here is that mild systemic hypercapnia will blunt the respiratory response to sudden excitation and inhibition of the peripheral chemoreceptors. To test this, postnatal day 12 mouse pups were exposed to three brief (30 sec) episodes of 10% O2/balance N2 (HPX) or 100% O2 (HPRX) using a mask‐pneumotach system that allowed re‐breathing. Challenges were given during normocapnic conditions (inspired CO2= 0‐0.5%; NC (n=6)), or when inspired CO2 was increased ~1.5% (HC; n=6) via re‐breathing. Respiratory frequency (fB), tidal volume (VT) and ventilation (VE) were calculated, on a breath‐to‐breath basis, during room air and during each HPX or HPRX exposure. The hyperventilation induced by HPX reached steady‐state by 50 breaths (~15‐20 sec). The HPX‐induced increase in fB and VE was significantly greater in NC (+45 ± 6 breaths.min‐1 and +560 ± 81 ml.min‐1.kg‐1, respectively) than in HC (+19 ± 9 and +311 ± 109, respectively) (P<0.05 for both). Hypoventilation was induced by HPRX in the first 25 breaths (~5‐10 sec). The HPRX‐induced reduction in VT and VE was greater in NC (‐1.1 ± 0.5 mL/breath and ‐364 ± 141 ml.min‐1.kg‐1, respectively) than in HC (+0.3 ± 0.3 and ‐15 ± 79, respectively) (P<0.01 for both). These data show that when CO2 is slightly elevated, respiration is relatively unresponsive to sudden stimulation or inhibition of the peripheral chemoreceptors. This suggests that in neonatal life, a hypo‐additive interaction exists between peripheral and central chemoreceptor inputs.
Published Version
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