Читать книгу The Esophagus - Группа авторов - Страница 129

There is significant redundancy of control mechanisms for smooth muscle peristalsis that interact effectively for normal peristalsis. Vagal fibers enter the esophagus at different levels and travel various distances within the esophagus to reach the neurons within the intramural plexuses. Sympathetic supply arises from spinal segments T1–10 with post‐ganglionic fibers passing to the esophagus from paraspinal sympathetic ganglia 127]. These fibers also go mainly to the intramural plexuses, to modulate neuronal activity. Few sympathetic fibers go directly to the smooth muscle cells. The role of the sympathetics appears to be limited [150, 151], although activation of beta‐receptors causes membrane hyperpolarization and muscle relaxation [151, 152], and catecholamines may release other inhibitory peptides from nerves [153]. As in the striated muscle portion, the myenteric ganglion cells have many different peptides [143, 154, 155]. Some of these peptides may have a modulatory role. However, for practical purposes, functionally there are only two types of motor neurons: excitatory cholinergic neurons that also contain substance P; and inhibitory nitrergic (NO) neurons that also contain VIP.

The longitudinal muscle forms a continuous layer of smooth muscle cells that do not make gap junction contact with each other. ICCs are present in this layer in the human [156] and cat esophagus [131], but not the dog or opossum [135, 157, 158]. Nerve fibers enter this layer from the myenteric plexus.

The circular layer is not a continuous sheet of muscle cells but is separated into lamellae or muscle bundles by connective tissue septa that are in intimate contact with the myenteric plexus region [131, 156]. Smooth muscle cells make gap junction contacts between themselves and the ICCs, but not with nerves. The ICCs are found within the muscle bundles and in the connective tissue septa. There are few ICCs in the myenteric plexus region. It is proposed that many of these ICCs function as sensory receptors since the presence and structural integrity of some ICCs are dependent on the presence of intact afferent vagal innervation [131, 159]. IGLEs 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.