Читать книгу The Esophagus - Группа авторов - Страница 138

Elsewhere in the gut, the myogenic control system has two fundamental characteristics: (i) electrical oscillations of the smooth muscle cells, usually called “slow waves”; and (ii) communication among smooth muscle cells allowing the tissue to operate as a functional unit [258, 259]. Both of these features are also present in the esophageal smooth muscle and can manifest with adequate cholinergic stimulation [165, 218, 219, 231, 260, 261]. A significant component of a myogenic system is contributed by the ICCs [131, 156]. It is not surprising, therefore, that with the esophagus isolated in vitro and with nerves blocked, a myogenic peristaltic contraction can be readily demonstrated in the smooth muscle segment [165, 218, 219, 262].

Regional gradients in the cholinergic and nitrergic innervation along the esophagus are believed to be sufficient for local control of peristalsis in the smooth muscle section. However, regional differences in the circular smooth muscle likely contribute to peristaltic contraction along the esophagus, including the responses to cholinergic and nitrergic innervation. These include a resting membrane potential gradient [228, 263], potassium and calcium ion channel diversity [251, 263, 264], and differences in muscle length–tension relationships and responses to cholinergic stimulation [264]. There are also differences in muscle proteins [265] and in intracellular signaling in response to cholinergic stimulation between esophageal body and LES muscle [266, 267].

Figure 5.13 Interplay of cholinergic (ACh) and non‐cholinergic (NANC) influences along the smooth muscle esophagus in the production of peristalsis. The cholinergic influence is most prominent proximally and decreases distally; the reverse is true for the NANC influence. Proximally, the contraction occurs earlier but is atropine sensitive, with cholinergic blockade delaying its appearance. Distally, the contraction normally appears later, but NANC blockade, such as with block of nitric oxide (NO) release, shortens the time to onset of the contraction. In either case of blockade, peristaltic velocity can significantly increase. LES, lower esophageal sphincter; UES, upper esophageal sphincter.

Source: Clouse RE, Diamant NE. Esophageal motor and sensory function and motor disorders of the esophagus. In: Feldman M, Freidman LS, Sleisenger MH, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 8th ed. © 2006, Elsevier.

The longitudinal muscle is not an innocent bystander, as it contracts sequentially in close association with circular muscle peristalsis and is involved in esophageal reflexes [268, 269]. Cholinergic stimulation, substance P, and, in contrast to circular muscle, NO are mediators of longitudinal muscle contraction [246, 270, 271]. Heightened sensitivity to longitudinal muscle stimulation may be a potential mechanism for esophageal shortening and hiatus hernia development in association with esophagitis [272, 273]. It is not known how the sequencing of longitudinal muscle by cholinergic excitation occurs during peristalsis in the absence of an inhibitory NO mechanism. Stimulation of the cut vagus results in simultaneous contraction [224]. Since the central vagal fibers connect to neurons in the enteric nervous system, excitation must finally result from an intramural mechanism, either primarily directed by the sequential vagal firing or from a coordinating intramural network.