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J Appl Physiol 94: 399-409, 2003. First published July 12, 2002; doi:10.1152/japplphysiol.00374.2002
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Vol. 94, Issue 1, 399-409, January 2003

HIGHLIGHTED TOPICS
Plasticity in Respiratory Motor Control
Selected Contribution: Intermittent hypoxia induces phrenic long-term facilitation in carotid-denervated rats

Ryan W. Bavis and Gordon S. Mitchell

Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin 53706

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 after three 5-min isocapnic hypoxic episodes [arterial PO2 (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 (inspired oxygen fraction = 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 after 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 1 h after 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 central nervous system effects.

plasticity; respiratory control; carotid body; episodic hypoxia


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