Role of the Superior Cervical Ganglion in Response to Hypoxia in Juvenile Rats

Abstract

The superior cervical ganglion (SCG) sends sympathetic input to the carotid body (CB) via the ganglioglomerular nerve (GGN) in order to modulate carotid sinus nerve (CSN) chemosensory afferent discharge via controlling vascular tone. This chemoafferent discharge is then relayed to the nucleus tractus solitarius (NTS) where the information is processed resulting in a compensatory increase in respiration. Hypoxic gas challenge stimulates the GGN. However, little is known as to the effects of superior cervical ganglionecomy (SCGx) on carotid body chemosensory afferent response to hypoxia (HX).Our objective was to determine the effect of unilateral SCGx on the ventilatory responses elicited by HX (10% O2, 90% N2) gas challenge (5 episodes of 5 min in duration separated by 15 min) in freely‐moving juvenile (P25) Sprague‐Dawley rats.Male rats postnatal (P) 21 were subjected to sham or unilateral (right) SCGx and were allowed 4 days to recover. On the day of the experiment, P25 rats were placed in whole‐body plethysmography chambers and subjected to the hypoxic gas exposure. Ventilatory parameters included frequency of breathing, tidal volume, minute ventilation (= frequency x tidal volume), inspiratory and expiatory times, end inspiratory and expiratory pauses, peak inspiratory and expiratory flows, EF50 (expiratory flow at 50% expired tidal volume) and central inspiratory drive (tidal volume/inspiratory time).The HX challenge elicited robust ventilatory responses in sham‐operated rats compared to unilateral (right) SCGx. Frequency (breathes/min), minute ventilation (ml/min), peak inspiratory flow (msec), and peak expiratory flow (msec) were diminished in unilateral (right) SCGx rats compared to sham. End expiratory pause (msec) showed a faster return to baseline following hypoxic challenge in unilateral (right) SCGx compared to sham. These findings demonstrate a role for CB sympathetic input from the SCG in modulating the ventilatory response to hypoxia.Support or Funding InformationNIH‐SPARC 1OT2OD023860‐02 SJLewisThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.