are present that can also function in a sensory mode.
There are other ICCs that likely operate in sensory–motor activity as part of myogenic control systems for peristalsis, similar to elsewhere in the gut. In such a capacity in the esophagus, the ICCs have the potential to act as transducers for nerve‐to‐muscle signaling, as pacemakers for the smooth muscles themselves, and as conduction pathways for muscle‐to‐muscle communication within muscle bundles or between bundles and muscle layers. Independent of the ICCs, there are free nerve endings close to the smooth muscle cells for release of neurotransmitters directly on the cells.
Functional motor activity
Primary peristalsis
Normal swallow‐induced contraction of the esophagus is called primary peristalsis. Following closure of the UES and entry of the bolus into the esophagus, a progressive circumferential contraction begins in the upper esophagus and passes distally along the esophageal body to reach the relaxed LES. The LES then contracts in sequence. The velocity of the peristaltic wave varies between 2.5 and 5 cm/s along the esophagus in a bimodal fashion [160–162] (Figure 5.9). The duration of normal swallow‐induced contraction is less than 7 s, and contraction amplitudes rarely exceed 200 mmHg [163]. Figure 5.10 shows these events as recorded by both conventional and high‐resolution manometry.
Figure 5.9 Velocity of the peristaltic wave front along the esophagus. The bimodal velocity was apparent using axial reconstructions of pressure data. The two modes represent propagation through the proximal striated muscle and distal smooth muscle regions, with deceleration near the lower esophageal sphincter. There is no break in velocity in the smooth muscle region.
Source: Clouse RA, Diamant NE. Motor function of the esophagus. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract, 4th ed; 2006. © 2006, Elsevier.
For peristalsis to progress distally, the proximal esophagus needs to contract before the distal esophagus at any point along the esophagus. This is ensured by esophageal inhibition, which ensures a latency gradient progressing from proximally towards the distal esophagus. The following are key factors that contribute to the latency gradient: (i) sequential firing of preganglionic efferent vagal nerve; (ii) varying discharge latency to firing of vagal efferent fibers [164]; (iii) shorter latency to contraction in the proximal esophageal muscle compared to distally [165, 166]; and (iv) gradient of cholinergic and nitrergic nerves and neurotransmitters along the esophagus [166].
Esophageal shortening of 2–2.5 cm also occurs with swallow‐induced contraction. This is mediated by longitudinal muscle contraction, which proceeds distally at 2–4 cm/s slightly in advance of the circular muscle contraction [167–169] or very close to it [169–171]. The onset, peak, and duration of circular and longitudinal muscle contraction are precisely coordinated throughout the esophagus [172, despite different neural control of the two muscle layers [173]. Longitudinal muscle contraction augments circular muscle contraction and reduces stress on the esophageal wall [174]. Simultaneous circular and longitudinal muscle contraction stiffens the esophageal wall and augments contraction to better propel a bolus. Longitudinal muscle contraction thins the distal esophageal wall, allowing distal accommodation of the bolus as it moves forward. Axial stretch induces distal esophageal and LES relaxation as well as deglutitive inhibition, potentially by activating mechanosensitive inhibitory motor neurons, resulting in NO‐mediated inhibition in the distal esophagus [175–177]. Swallow‐induced UES elevation also stretches the esophagus longitudinally, with similar results [172]. Coordination of the longitudinal and circular muscle layers is partly a function of cholinergic innervation, which can be abnormal in spastic disorders such as nutcracker esophagus [178, 179].
Of interest, the amplitude of the circular muscle contraction shows a consistent decrease in a short segment 4–6 cm below the UES. This is termed the transition zone, the region where striated (segment 1) and smooth muscle (segments 2 and 3) have interspersed and/or innervation changes from the RLN proximally to the more distal vagal branches. There are two other troughs in amplitude: one separating the smooth muscle segment into two (segment 2, segment 3) and the other separating the distal smooth muscle segment from the LES [160, 162, 180]. It is not known if these findings are due to separate neuromuscular units governed by output from subunits in the SPG, or by peripheral intramural mechanisms within regional differences in muscle or nerve. If central, it raises the possibility that SPG control of the esophagus may be grouped into distinct functional subunits defined by sphincters and contracting segments.
The contraction amplitude determines the efficacy of bolus propulsion and esophageal emptying, with this efficacy decreasing as amplitude decreases [181]. At a threshold of 30 mmHg, incomplete bolus transit is identified with a sensitivity of 85% and specificity of 66% [182]. Gravity facilitates transport, especially of liquids, and distal contraction amplitude can decrease in the more upright position [183].
Secondary peristalsis
Secondary peristalsis originates in the esophagus in response to local sensory stimulation, such as from retained food not cleared by the primary wave or from refluxed acid. This peristaltic wave is similar to primary peristalsis but begins in the esophagus at or above the level of the stimulus. However, distention high in the esophagus may at times initiate the process at the pharyngeal stage [184].
Figure 5.10 Esophageal peristalsis: relationship between videofluoroscopic, manometric, impedance, and topographic representations. (A) Depiction of intraluminal manometry/impedance measurement with five sensors at 4 cm intervals, and a sleeve sensor in the lower esophageal sphincter (LES). (B) Representation by overlaying manometry and impedance measurements with the videofluoroscopic appearance of a 5 mL swallowed barium bolus. The pressure scale for the thick, dark line is on the left, and the impedance scale for the light, thin line is on the right. The arrows point to the distribution of the bolus at the times indicated. As the bolus enters the esophagus, there is a slight increase in pressure at most sites, the “bolus pressure.” As the contraction reaches each site, the pressure increases and the impedance decreases. As the lumen closes and the upstroke of the pressure wave occurs, the tail of the barium bolus is evident. (C) Comparison of conventional manometric pressure tracing at five sites and the LES, as positioned in A, with the pressure profile obtained with high‐fidelity (high‐resolution) manometry and displayed topographically as an isocontour plot. The overlay places the two representations at similar locations. In the isocontour plot, deepening shades of gray indicate higher pressures. There are three pressure troughs: at the junction of the striated and smooth muscle esophagus; in the mid‐portion of the smooth muscle portion; and at the end of the peristaltic segment just before the LES. The troughs separate four different pressure segments, the last fronting the contraction closing the LES. The end of the LES relaxation measured with conventional manometry coincides with arrival of the contraction at the start of the fourth pressure segment and the LES.
Source: Pandolfino et al. [90] with permissions of Elsevier.
Tertiary peristalsis
If connections to the central control of the SPG are absent, a local intramural mechanism can produce peristalsis in the smooth muscle segment of the intact animal [185–187]. This contraction is called tertiary peristalsis and is different from the “tertiary” uncoordinated or simultaneous contractions