Influence of the vagal afferent on supraspinal and spinal respiratory activity following cervical spinal cord injury (SCI) in rats

Abstract

Vagal afferents influence respiratory pattern after SCI, but their influence on spinal and supraspinal respiratory motor output is unclear. We tested the following hypotheses using rats with C2 spinal hemisection (C2HS): 1) vagal afferents attenuate ipsilateral (IL) phrenic bursting, 2) contralateral (CL) phrenic output becomes resistant to vagal inhibition after injury, and 3) vagal inhibition of C.N. XII output is altered following injury. Efferent discharge was recorded from IL and CL phrenic nerves and the CL XII nerve in uninjured rats and C2HS rats at 2 or 8 weeks post‐injury. Vagal inhibition associated with lung inflation was varied by manipulating positive‐end expired pressure (PEEP; 3–9 cmH2O). Bilateral vagotomy greatly enhanced IL phrenic inspiratory bursting which was weak or absent in vagally intact rats at both 2 and 8 weeks post‐C2HS. PEEP‐induced inhibition of CL phrenic and XII activity was attenuated at 2 but not 8 weeks post‐C2HS. We conclude that that 1) vagal afferents have a robust inhibitory effect on eupneic IL phrenic bursting, and 2) compensatory increases in both CL spinal (phrenic) and supraspinal (XII) output after C2HS attenuate the inhibitory influence of vagal afferents. Our vagotomy data appear to explain the variability regarding the onset of the spontaneous crossed phrenic phenomenon in spontaneously breathing (vagal intact) vs. ventilated (vagotomized) preparations.