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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/87    most recent expphysiol.2006.035758v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dick, T. E. Articles by Prabhakar, N. Search for Related Content PubMed PubMed Citation Articles by Dick, T. E. Articles by Prabhakar, N. Related Collections Themed Issue papers

¹ Division of Pulmonary Critical Care and Sleep Medicine, Department of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4941, USA

Abstract

The respiratory system expresses multiple forms of plasticity, defined as alterations in the breathing pattern that persist or develop after a stimulus. Stimulation of breathing with intermittent hypoxia (IH) elicits long-term facilitation (LTF), a type of plasticity in which respiratory motor activity progressively increases in anaesthetized animals, even after the stimuli have ceased and blood gases have normalized. It is unknown whether the sympathetic nervous system similarly expresses IH-induced plasticity, but we predicted that IH would evoke LTF in sympathetic nerve activity (SNA) because respiratory and sympathetic control systems are coupled. To test this idea, we recorded splanchnic (sSNA) and phrenic nerve activities (PNA) in equithesin-anaesthetized rats. Animals were exposed to 10 45 s episodes of 8% O₂–92% N₂, separated by 5 min intervals of 100% O₂, and recordings were continued for 60 min following the last hypoxic exposure. Cycle-triggered averages of integrated PNA and sSNA from periods preceding, and 5 and 60 min following the hypoxic stimuli were compared. Intermittent hypoxia significantly increased both sSNA and PNA. Treatment with methysergide (3 mg kg^–1, I.V.) 20 min before the intermittent hypoxic exposures prevented the increases in integrated PNA and sSNA 60 min after IH, indicating a role of serotonergic pathways in this form of plasticity. No increases in PNA and sSNA occurred at comparable times (60 and 120 min) in rats not exposed to hypoxia. The increased sSNA was not simply tonic, but was correlated with respiratory bursts, and occurred predominantly during the first half of expiration. These findings support the hypothesis that sympathorespiratory coupling may underlie the sustained increase in SNA associated with the IH that occurs during sleep apnoea.

(Received 12 September 2006; accepted after revision 15 November 2006; first published online 30 November 2006)
Corresponding author T. E. Dick: Biomedical Research Building BRB B55, 10900 Euclid Avenue, Cleveland, OH 44106-4941, USA. Email: ted3{at}po.cwru.edu

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