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1 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: nrp{at}po.cwru.edu.
Carotid bodies are functionally immature at birth and exhibit poor sensitivity to hypoxia. Previous studies have shown that continuous hypoxia at birth impairs hypoxic sensing at the carotid body. Intermittent hypoxia (IH) is more frequently experienced in neonatal life. Previous studies on adult animals have shown that IH facilitates hypoxic sensing at the carotid bodies. Based on these studies, in the present study we tested the hypothesis that neonatal IH facilitates hypoxic sensing of the carotid body and augments ventilatory response to hypoxia. Experiments were performed on 2-day old rat pups that were exposed to 16h of IH soon after the birth. IH paradigm consisted of 15s of 5% O2 (nadir) followed by 5min of 21% O2 (9 episodes/h). In one group of experiments (IH and control, n =6 pups each), sensory activity was recorded from ex vivo carotid bodies, and in the other (IH and control, n =7 pups each) ventilation was monitored in unanesthetized pups by plethysmography. In control pups, sensory response of the carotid body was weak and was slow in onset (~100s). In contrast, carotid body sensory response to hypoxia was greater and the time course of the response was faster (~30s) in IH compared to control pups. The magnitude of the hypoxic ventilatory response was greater in IH compared to control pups, whereas changes in VO2 and VCO2 during hypoxia were comparable between both groups. The magnitude of ventilatory stimulation by hyperoxic hypercapnia (7% CO2 balance O2), however, was the same between both groups of pups. These results demonstrate that neonatal IH facilitates carotid body sensory response to hypoxia and augments hypoxic ventilatory chemoreflex.
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