4.5 Article

Influence of vagal afferents on supraspinal and spinal respiratory activity following cervical spinal cord injury in rats

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 109, Issue 2, Pages 377-387

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01429.2009

Keywords

plasticity; positive end-expired pressure; vagotomy; crossed phrenic phenomenon; hypoglossal nerve

Funding

  1. National Institutes of Health [1R01-HD-052682-01A1, 1R01-NS-054025]
  2. University of Florida
  3. Paralyzed Veterans of America Research Foundation [2691]

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Lee KZ, Sandhu MS, Dougherty BJ, Reier PJ, Fuller DD. Influence of vagal afferents on supraspinal and spinal respiratory activity following cervical spinal cord injury in rats. J Appl Physiol 109: 377-387, 2010. First published May 27, 2010; doi:10.1152/japplphysiol.01429.2009.-C(2) spinal hemisection (C2HS) interrupts ipsilateral bulbospinal pathways and induces compensatory increases in contralateral spinal and possibly supraspinal respiratory output. Our first purpose was to test the hypothesis that after C2HS contralateral respiratory motor outputs become resistant to vagal inhibitory inputs associated with lung inflation. Bilateral phrenic and contralateral hypoglossal (XII) neurograms were recorded in anesthetized and ventilated rats. In uninjured (control) rats, lung inflation induced by positive end-expired pressure (PEEP; 3-9 cmH(2)O) robustly inhibited both phrenic and XII bursting. At 2 wk post-C2HS, PEEP evoked a complex response associated with phrenic bursts of both reduced and augmented amplitude, but with no overall change in the mean burst amplitude. PEEP-induced inhibition of XII bursting was still present but was attenuated relative to controls. However, by 8 wk post-C2HS PEEP-induced inhibition of both phrenic and XII output were similar to that in controls. Our second purpose was to test the hypothesis that vagal afferents inhibit ipsilateral phrenic bursting, thereby limiting the incidence of the spontaneous crossed phrenic phenomenon in vagal-intact rats. Bilateral vagotomy greatly enhanced ipsilateral phrenic bursting, which was either weak or absent in vagal-intact rats at both 2 and 8 wk post-C2HS. We conclude that 1) compensatory increases in contralateral phrenic and XII output after C2HS blunt the inhibitory influence of vagal afferents during lung inflation and 2) vagal afferents robustly inhibit ipsilateral phrenic bursting. These vagotomy data appear to explain the variability in the literature regarding the onset of the spontaneous crossed phrenic phenomenon in spontaneously breathing (vagal intact) vs. ventilated (vagotomized) preparations.

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