Response of Respiratory-Related Hypoglossal Nerve Activity to Capsaicin-Induced Pulmonary C-Fiber Activation in Rats

Abstract

This study was designed to examine respiratory-related hypoglossal nerve activity in response to activation of pulmonary C-fibers by capsaicin. Rats were anesthetized with urethane (1.2 g/kg, i.p.). Tracheostomy was performed. Catheters were introduced into the femoral vein and artery. Another catheter was placed near the entrance of the right atrium via the right jugular vein. Rats were paralyzed with gallamine triethiodide (5 mg/kg, i.v.), and ventilated artificially. Activities of the phrenic nerve (PNA) and the hypoglossal nerve (HNA) were recorded simultaneously. Varied doses of capsaicin (0.625, 1.25, and 5 µg/kg) were delivered into the right atrium to activate pulmonary C-fibers. Before bilateral vagotomy, apnea, decreases in PNA and HNA were observed in response to pulmonary C-fiber activation by the low and moderate doses of capsaicin. The high dose of capsaicin evoked an increase in PNA, an immediate tonic discharge of the hypoglossal nerve, and a decrease in phasic HNA. The onset time of HNA preceding PNA was abolished and replaced by a time lagged pattern as pulmonary C-fibers were activated. Raising CO₂ concentration did not attenuate the inhibitory effect of pulmonary C-fiber activation upon PNA and HNA. After bilateral sectioning of the vagi, administration of the moderate dose of capsaicin to activate non-vagal C-fibers produced increases in PNA and HNA. These results suggest that pulmonary vagal C-fiber activation may narrow the diameter at the oropharyngeal level by a decrease in phasic HNA, which may be disadvantageous for the maintenance of a patent upper airway.

Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat

“…The compliance and geometry of this region are influenced by a number of skeletal muscles. Among them are the alae nasi, tongue, and laryngeal muscles, which are innervated by the facial (FN), hypoglossal (HN) and superior (SLN), and recurrent laryngeal nerves (RLN), respectively (1,26,41).Many studies have shown that the inspiratory (I) discharge of the HN precedes the phrenic I burst (5,6,13,17,23,33). This preinspiratory (Pre-I) activity has been suggested to benefit UAW patency by dilating and stiffening the UAW before the onset of I airflow (30).…”

“…Many studies have shown that the inspiratory (I) discharge of the HN precedes the phrenic I burst (5,6,13,17,23,33). This preinspiratory (Pre-I) activity has been suggested to benefit UAW patency by dilating and stiffening the UAW before the onset of I airflow (30).…”

“…For example, activation of both pulmonary stretch receptors and vagal C fiber receptors inhibits respiratory bursting in UAW muscles and their corresponding motor nerves (11,23,25,40,42). This inhibition is associated with a delay in the onset of the UAW muscle I activity relative to the phrenic burst (23,25).…”

Hypersensitivity of lung vagal C fibers induced by acute intermittent hypoxia in rats: role of reactive oxygen species and TRPA1

“…Right-atrial injection of capsaicin evoked an inhibitory response of phrenic nerve activity that resulted in reflex apnea appearing as a prolonged TE, as previously described (29,34). This reflex apnea resulted in an increased apneic ratio, reflecting the magnitude of the apneic response.…”

“…For the studies of apneic reflex, expiratory time (TE) was analyzed as the interval between two successive phrenic bursts (29). The baseline TE was calculated on a breath-by-breath basis as the average value over the 10-breath period immediately before injection of chemical stimulants.…”