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.

Lee K-Z, Fuller DD, Tung L-C, Lu I-J, Ku L-C, Hwang J-C. Uncoupling of upper airway motor activity from phrenic bursting by positive end-expired pressure in the rat. J Appl Physiol 102: [878][879][880][881][882][883][884][885][886][887][888][889] 2007. First published November 2, 2006; doi:10.1152/japplphysiol.00934.2006.-Phasic bursting in the hypoglossal nerve can be uncoupled from phrenic bursting by application of positive end-expired pressure (PEEP). We wished to determine whether similar uncoupling can also be induced in other respiratory-modulated upper airway (UAW) motor outputs. Discharge of the facial, hypoglossal, superior laryngeal, recurrent laryngeal, and phrenic nerves was recorded in anesthetized, ventilated rats during stepwise changes in PEEP with a normocapnic, hyperoxic background. Application of 3-to 6-cmH 2O PEEP caused the onset inspiratory (I) UAW nerve bursting to precede the phrenic burst but did not uncouple bursting. In contrast, application of 9-to 12-cmH2O PEEP uncoupled UAW neurograms such that rhythmic bursting occurred during periods of phrenic quiescence. Single-fiber recording experiments were conducted to determine whether a specific population of UAW motoneurons is recruited during uncoupled bursting. The data indicate that expiratory-inspiratory (EI) motoneurons remained active, while I motoneurons did not fire during uncoupled UAW bursting. Finally, we examined the relationship between motoneuron discharge rate and PEEP during coupled UAW and phrenic bursting. EI discharge rate was linearly related to PEEP during preinspiration, but showed no relationship to PEEP during inspiration. Our results demonstrate that multiple UAW motor outputs can be uncoupled from phrenic bursting, and this response is associated with bursting of EI nerve fibers. The relationship between PEEP and EI motoneuron discharge rate differs during preinspiratory and I periods; this may indicate that bursting during these phases of the respiratory cycle is controlled by distinct neuronal outputs. uncoupled activity; motoneurons; expiratory-inspiratory; preinspiratory THE MAMMALIAN UPPER AIRWAY (UAW) consists of the airflow passages extending from the trachea to the external nares and is thus composed of the nasal cavity, pharynx, and larynx (34). 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). Similar to the HN, the onset of FN, SLN, and RLN I bursting occurs before the onset of phrenic bursting (16,25).The respiratory-related discharge of the UAW muscles is influenced by various chemical and mechanical ...

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Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH(2)O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH(2)O (baseline) to 9 cmH(2)O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH(2)O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN (P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.