Abstract

While it is well known that significant changes in ventilatory control occur during postnatal development, the maturational influence of peripheral chemoreceptor stimulation (PCS) during normoxia (N) and hypoxia (H) have not been systematically evaluated. Accordingly, in the present study, we separately assessed the ventilatory responses to PCS with sodium cyanide (NaCN), both during steady-state inhalation of 21% (N) and 10% (H) O2. Following tracheostomy and carotid artery catheterization under light ether anesthesia, pulmonary ventilation (VE) was continually monitored in newborn rabbits (age range: 1-30 days) placed in a body plethysmograph. During N, while saline had no effect, infusions of NaCN (dose range: 0.01 to 0.4 mg/kg) established reproducible dose-dependent increases in VE. The maximal percent increases in VE (VEmax) with NaCN systematically increased with age; however, “sensitivity” to NaCN, represented by the dose of NaCN producing 50% of VEmax, was not age related. In marked contrast to N, during steady-state H, lower doses of NaCN (i.e., less than 0.1 mg/kg) produced less VE stimulation, while higher doses produced VE depression resulting in some cases in acute apnea. Bilateral carotid body denervation abolished the VE responses to NaCN. These findings in maturing rabbits indicate that: (1) during normoxia, PCS with NaCN produces ventilatory stimulation; however, (2) during steady-state hypoxia PCS produces ventilatory depression which may lead to apnea.

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