Effects of vagal deafferentation on oesophageal motility and transit in the sheep.

Abstract

SUMMARY1. Effects of vagal deafferentation on oesophageal motility and transit were studied in conscious sheep by recording the electromyographic activity of different parts of oesophagus during swallowing of saliva, or balloons inflated with 20 ml of air.2. Surgical isolation and subsequent sectioning of the nodose ganglion, leaving the bundle of motor fibres intact, can be performed in sheep. Division of both ganglia led to immediate death of sheep. However, vagal deafferentation of the thoracic oesophagus could be achieved by sectioning the thoracic vagus nerve in association with suctioning the contralateral nodose ganglion.3. The sectioning of one vagus nerve did not affect primary oesophageal peristalsis during swallowing of saliva or of a bolus. Balloons inflated in the pharyngeal cavity and left free to move caudally, failed to pass into the stomach within the normal time of 2-2-3 s in only 4-16 % of the tests. In these cases, they were always stopped in the thoracic oesophagus.4. Following total deafferentation of the thoracic oesophagus, balloons were prevented from being propelled into the stomach in each test. They were stopped for several minutes at the beginning of the deafferented part of the oesophagus. Electromyographic activity recorded from the deafferented part was reduced during swallowing of balloons or saliva.5. Deafferentation was confirmed by the failure of the presumed deafferented segment of oesophagus to respond to distension.6. These experiments provide direct evidence that the vagus carries information from the oesophagus which influences the central pattern generator during swallowing of a bolus or saliva. In sheep, this feed-back is essential for the effective swallowing of a bolus although not for saliva.

Remifentanil alters sensory neuromodulation of swallowing in healthy volunteers: quantification by a novel pressure-impedance analysis

“…Animal experiments have shown that stimulation of superior laryngeal nerve afferents evokes a short-latency response in oropharyngeal and proximal esophageal DSG neurons, providing evidence that vagal sensory afferents monosynaptically innervate this part of the swallowing CPG (15,25). Importantly, in the context of the present findings, several previous studies have reported that sensory feedback is a powerful modulator of neuronal activation in the swallowing CPG (6, 10) that can adjust motor outputs depending on the bolus swallowed (6). Given the high level of -opioid receptors in the NTS, it is therefore likely that any centrally acting -opioid receptor agonist can modulate the activity of the swallowing CPG, in particular that of the DSG located in the NTS.…”

Brain Stem Control of the Phases of Swallowing

“…As described previously, studies in infants [20,24] and animals [22,23] found that the pharyngeal phase of swallowing is not activated as part of the initiation of the oral phase but must be activated by intraphase reflexes, i.e., the presence of the bolus in the pharynx. Deafferentation of the thoracic esophagus [46] in unanesthetized sheep eliminates the esophageal phase at the deafferented region of the esophagus during physiologically activated swallowing. More directly, it was found [14] that the initiation of the esophageal phase of swallowing does not occur as part of prior phases but must be activated by intraphase reflexes, i.e., the presence of the bolus in the esophagus.…”

“…While pharyngeal stimulation increases pharyngeal premotor neuronal discharge somewhat [56], esophageal stimulation greatly increases esophageal premotor discharge [56,95]. On the other hand, elimination of sensory afferent feedback does not significantly reduce the discharge of the pharyngeal premotor neurons [91], but it does significantly reduce the discharge of the esophageal premotor [56,95] and motor [46,56,80] neurons. Therefore, the pharyngeal premotor neurons, once activated, do not require peripheral stimulation to attain near maximal output, whereas the esophageal premotor neurons require significant sensory afferent feedback to maintain activation.…”

Effects of remifentanil on esophageal and esophagogastric junction (EGJ) bolus transit in healthy volunteers using novel pressure‐flow analysis

“…25 Central sensory relay occurs in the nucleus tractus solitarius (NTS), 26 and motor outputs are modulated in response to sensory input for different bolus characteristics. 27,28 In our study, remifentanil exposure reduced proximal esophageal contractility, suggesting either central effects leading to attenuated motor neurone activation or, alternatively, peripheral effects at the striated neuromuscular junction. Central modulation may occur at the level of the NTS as it has been shown to contain MOR.…”

“…The central nervous system, via brainstem‐based central pattern generators of swallowing, initiates and controls proximal striated muscle peristalsis via sequential activation of motor neurone pools within the nucleus ambiguus . Central sensory relay occurs in the nucleus tractus solitarius (NTS), and motor outputs are modulated in response to sensory input for different bolus characteristics . In our study, remifentanil exposure reduced proximal esophageal contractility, suggesting either central effects leading to attenuated motor neurone activation or, alternatively, peripheral effects at the striated neuromuscular junction.…”