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Articles in PresS, published online ahead of print July 12, 2002
J Appl Physiol, 10.1152/jap.00374.2002
Submitted on April 29, 2002
Accepted on July 8, 2002
1 Department of Comparative Biosciences, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: bavisr{at}svm.vetmed.wisc.edu.
Episodic hypoxia elicits a long-lasting augmentation of phrenic inspiratory activity known as long-term facilitation (LTF). We investigated the respective contributions of carotid chemoafferent neuron activation and hypoxia to the expression of LTF in urethane-anesthetized, vagotomized, paralyzed and ventilated Sprague-Dawley rats. One hour following three 5-min isocapnic hypoxic episodes (PaO2=40±5 Torr), integrated phrenic burst amplitude was greater than baseline in both carotid denervated (n=8) and sham-operated (n=7) rats (P<0.05), indicating LTF. LTF was reduced in carotid denervated rats relative to sham (P<0.05). In this and previous studies, rats were ventilated with hyperoxic gas mixtures (FIO2=0.5) under baseline conditions. To determine whether episodic hyperoxia induces LTF, phrenic activity was recorded under normoxic (PaO2=90-100 Torr) conditions before and following three 5-min episodes of isocapnic hypoxia (PaO2=40±5 Torr; n=6) or hyperoxia (PaO2>470 Torr; n=6). Phrenic burst amplitude was greater than baseline one hour following episodic hypoxia (P<0.05), but episodic hyperoxia had no detectable effect. These data suggest that hypoxia per se initiates LTF independently from carotid chemoafferent neuron activation, perhaps through direct CNS effects.
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