Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

Abstract

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat

“…Thus activation of PCF receptors with the low dose of capsaicin appears to "override" PEEPinduced excitation of Pre-I neurons, and the impact of vagal afferents on the overall activity of Pre-I facial motor output may represent balance among excitatory and inhibitory influences. Consistent with this suggestion, E abdominal activity can be inhibited by PCF receptor activation but excited by SARs (17). This result raises the intriguing possibility that pharmacologically antagonizing PCF receptor activation, or activating SARs, may benefit patients with sleep-disordered breathing, such as sleep apnea syndrome.…”

Effects of pulse lung inflation on chest wall expiratory motor activity

“…Second, thoracic expiratory inhibition could be reproduced by threshold electrical vagal stimulation that has been shown to selectively activate reflexes from pulmonary stretch receptors (22,27). Although activation of pulmonary C-fiber receptors has been shown to inhibit expiratory muscle activity (23,24), the threshold for their activation is higher by one order of magnitude. Third, other studies (4) have demonstrated that the neural responses to step inflations have a relatively slow adaptation rate consistent with pulmonary stretch receptor activation.…”

The abdominal muscles in anaesthesia and after surgery

“…capsaicin inhibits the effects of positive airway pressure. 41 This inhibition of the re¯ex response to positive airway pressure may explain why patients with lung disease, who may have lung in¯ammation, allow their lung volume to increase when constant positive airway pressure is applied, rather than re¯ex contracting their abdominal muscles to offset the increase. However, some of the control of the abdominal muscles must also be from muscle afferents, as dorsal root section, which will interrupt stretch receptor activity also inhibits the response to positive airway pressure.…”