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Afferent sensory stimulation

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The esophageal stage of the SPG is normally activated during swallowing [7], enhanced by pharyngeal and esophageal sensory feedback, but least prominent during the esophageal stage. Failed esophageal peristalsis in all or part of the esophagus is common in humans, particularly with “dry” swallows. The presence of a bolus increases the amplitude of the peristaltic wave and its completion [78, 189, 190]. Animal studies have been conflicting in determining the necessity for bolus stimulation of the esophagus for primary peristalsis to occur. In dogs that have a totally striated muscle esophagus, and with diversion of the bolus in the cervical esophagus, primary peristalsis is absent in the distal esophagus [191, 192]. In the decerebrate cat with absent cortical input and intact distal smooth muscle esophagus, the bolus must be present in the cervical esophagus for peristalsis to proceed [104]. In primates that also have a distal smooth muscle esophagus, the bolus is not always necessary [193]. Transcranial magnetic stimulation of the cortex in the anesthetized cat [50] or awake dog [194] can itself initiate swallowing. Transcranial magnetic stimulation does not initiate swallowing in the human, although muscles in the pharynx and upper and lower esophagus can be induced to contract [195–197]. The esophageal stage of the SPG must be adequately activated for primary esophageal peristalsis, and one or more of the three SPG inputs – cortical, pharyngeal, or esophageal – is sufficient for activation, with each input facilitating others [198]. However, involvement of all three may not be necessary, depending on species’ differences and experimental conditions.

The swallowed bolus is an important component of peristaltic integrity, and amplitude, duration, and velocity of the peristaltic wave are subject to the nature and size of the bolus. Sensory feedback regarding the swallowed bolus is transmitted by esophageal afferent nerves to the solitary nucleus, which modifies efferent output to the smooth esophageal muscles [199]. Bolus information can also modify peristalsis through intramural neuromuscular reflexes, thereby affecting the strength and speed of esophageal peristalsis [200–203]. Larger boluses and increased viscosity increase contraction amplitude and duration, and slow peristaltic velocity [189, 190, 200]. Additionally, hot water increases amplitude while decreasing the duration of contraction, whereas cold water decreases amplitude and increases the duration of contraction [199]. Increased intra‐abdominal pressure and esophageal obstruction also increase amplitude and slow velocity.

Under normal circumstances, secondary peristalsis is dependent on sensory activation of a central reflex, mediated by activation within the esophageal stage of the SPG [184, 204]. This is always true of the striated muscle esophagus because of its dependence on central control. Once initiated, this also activates neurons for the smooth muscle esophagus, and the contraction wave progresses distally in identical fashion to the primary wave [184, 205]. There is no convincing evidence that intramural neural or myogenic mechanisms stimulated locally in the smooth muscle segment could independently produce secondary peristalsis when central connections are intact. In the cat, vagal blockade in the neck abolishes secondary peristalsis [157]. However, local mechanisms in this segment can alter the response to the central control that is initiated by afferent signaling to the SPG, influenced by factors such as the location of the peripheral stimulus and whether the stimulus is a stationary distending balloon, collapsible barostat balloon, or movable bolus. When initiated by a moveable bolus or barostat balloon, secondary peristalsis proceeds relatively unaltered. A fixed distending balloon, not a physiologic stimulus, induces contractions proximal to the balloon and can significantly alter the distal contraction [40,206–212]. As with primary peristalsis, the local and central mechanisms must integrate effectively.

The Esophagus

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