Movement Of Material Through The Esophagus

The obvious function of the esophagus is to serve as a conduit for and to propel swallowed material to

Peristalsis Movement

FIGURE 4 Neural pathways involved in the regulation of pharyngeal and esophageal peristalsis. Vagal sensory input is relayed to the swallowing center in the medulla, where output to muscles is coordinated with respiration. Muscles of the pharynx and the striated esophagus are innervated via the nucleus ambiguus; smooth muscles of the esophagus are innervated via the dorsal motor nucleus. Enlarged area details the direct innervation of striated muscle by vagal fibers and indirect innervation of smooth muscle via the interneurons. The sequential nature of the innervation, which makes peristalsis possible, is also illustrated here. (Adapted from Johnson LR, ed., Gastrointestinal physiology, 6th ed. St. Louis: CV Mosby, 2001.)

FIGURE 4 Neural pathways involved in the regulation of pharyngeal and esophageal peristalsis. Vagal sensory input is relayed to the swallowing center in the medulla, where output to muscles is coordinated with respiration. Muscles of the pharynx and the striated esophagus are innervated via the nucleus ambiguus; smooth muscles of the esophagus are innervated via the dorsal motor nucleus. Enlarged area details the direct innervation of striated muscle by vagal fibers and indirect innervation of smooth muscle via the interneurons. The sequential nature of the innervation, which makes peristalsis possible, is also illustrated here. (Adapted from Johnson LR, ed., Gastrointestinal physiology, 6th ed. St. Louis: CV Mosby, 2001.)

the stomach. The esophagus, however, also has two important barrier functions: (1) It prevents the entry of air at the upper end and (2) the entry or reflux of gastric contents at the lower end. The barrier functions are carried out by two sphincters, one at each end. The propulsive function is accomplished by the coordinated contractions of the two muscle layers of the esophageal wall.

The anatomy of the esophagus follows the general pattern outlined in the previous chapter with an inner layer of circular muscle and an outer layer of longitudinal muscle. The major difference is that in the human the upper one-third to one-half of this muscle is striated. The lower one-half of the esophagus is smooth muscle, and there is a brief transition zone between the two types. The upper esophageal (or pharyngoeso-phageal) sphincter consists of a thickening of the circular layer of striated muscle, which is anatomically identified as the cricopharyngeal muscle. The lower esophageal (or gastroesophageal) sphincter cannot be identified anatomically, but consists of a 1- to 2-cm zone of increased pressure that is maintained at a level greater than the pressure in the stomach.

Material moves through the GI tract from regions of higher intraluminal pressure to regions of lower pressure. These pressures can be monitored by pressure-sensing devices placed (usually in swallowed tubes of known length) at various levels in the GI tract. Figure 5 depicts data from six such devices placed sequentially along the esophagus. Note that resting intraesophageal pressures are below atmospheric, because most of the esophagus is located in the thorax. In fact, intrathoracic pressure is determined by measuring intraesophageal pressure. The pressure at the upper esophageal sphincter is above atmospheric. The pressure becomes equal to atmospheric pressure as the esophagus passes through the diaphragm into the abdomen and then increases considerably at the lower esophageal sphincter. The upper esophageal sphincter produces pressures of approximately 60 mm Hg over a 1- to 2-cm zone. The body of the esophagus is a flaccid tube that directly reflects the pressures within the thorax and abdomen. Hence, within the thorax, the intraluminal pressure drops during inspiration and rises with expiration (Fig. 5A). After passing the diaphragm, the excursions reverse to reflect intra-abdominal pressures. The lower esophageal sphincter consists of a zone of increased pressure approximately 20-40 mm Hg higher than the pressures on either side of it. This zone may occur over distances of from a few millimeters to several centimeters.

During a swallow, the upper esophageal sphincter relaxes immediately before the lower pharyngeal muscles contract. This decreases the pressure in the area of the sphincter (Fig. 5B) and allows the bolus to enter the esophagus. The sphincter then contracts to prevent reflux and entry of air. Pressure at the sphincter returns to the basal level as the muscle assumes its resting tone. A primary peristaltic contraction of the esophageal body now begins just below the upper esophageal sphincter. The coordinated and sequential nature of the contractions produces a zone of increased pressure that moves down the esophagus with the bolus in front of it. As the peristaltic contraction passes, the esophageal muscle returns to its resting tone and becomes flaccid again. As the bolus approaches the lower esophageal sphincter, the sphincter relaxes (Fig. 5B), allowing the bolus to enter the stomach. The sphincter then contracts back to its resting tone, which results in a pressure higher than that in the stomach, thereby preventing reflux.

Esophageal peristalsis is slow, moving down the esophagus at velocities ranging from 2-6 cm/sec, and may take a total of 10 sec. However, the time it takes for

Material Your Esophagus
FIGURE 5 Intraluminal esophageal pressures recorded (A) between swallows and (B) during a swallow. X axis, time; UES, upper esophageal sphincter; LES, lower esophageal sphincter. (Adapted from Johnson LR, ed., Gastrointestinal physiology, 6th ed. St. Louis: CV Mosby, 2001.)

a bolus to reach the stomach also depends greatly on gravity and the physical nature of the material swallowed. Liquids swallowed in an upright position will reach the stomach before the peristaltic contraction. Therefore, although both esophageal sphincters must relax, peristalsis per se is not always necessary for esophageal transport. For most material, however, peristalsis is essential for transport to the stomach. The efficiency of esophageal peristalsis can be demonstrated readily by drinking a liquid while standing on ones head.

Frequently, however, the esophagus is not totally emptied by the original peristaltic contraction initiated by the swallow. The resulting distension, induced by the residual material, initiates another peristaltic contraction beginning just above the area of distension. This contraction, which occurs in the absence of a swallow or the pharyngeal phase, is called secondary peristalsis and is involuntary and not usually sensed. Secondary peristaltic contractions serve to "sweep" the esophagus clean of material left from a swallow or refluxed from the stomach. At times, it may take several secondary contractions to remove all material from the esophagus.

Esophageal motility is regulated by both central and peripheral mechanisms, all of which are not completely understood. Closure of the upper esophageal sphincter depends on the tone and elasticity of the cricophar-yngeal muscle. Relaxation of this muscle during a swallow is coordinated through the swallowing center, as previously discussed. The body of the esophagus receives innervation through the vagus nerves (see Fig. 4). Somatic motor nerves from the nucleus ambig-uus synapse directly with the striated muscle in the upper portion of the esophagus. Visceral motor nerves, arising from the dorsal motor nucleus, synapse with neurons of the myenteric plexus (between the circular and longitudinal layers of smooth muscle). These interneurons in turn innervate the smooth muscle layers (see Fig. 4). The interneurons also communicate signals with each other—in other words, up and down the esophagus—and relay input to the central nervous system (CNS) via afferent nerves in the vagus. Afferent input, for example, initiates secondary peristaltic contractions and alters the intensity of esophageal contractions.

Although primary esophageal peristalsis is initiated during a swallow via sequentially fired nerves from the swallowing center, the CNS is not necessary for the entire peristaltic contraction. Interruption of central influences by bilateral vagotomy produces abnormalities of peristalsis in the striated muscle portion of the esophagus, but peristalsis occurs normally in the smooth muscle portions. Peristalsis can also be induced in excised esophagi placed in physiologic salt solutions.

This indicates that the interneurons or smooth muscle cells themselves are able to coordinate the contractions.

Resting tone of the lower esophageal sphincter appears to be largely myogenic. Passive stretching of this portion of the esophagus results in smooth muscle contraction independent of neural and hormonal input. This resting tone, however, is modified by various agents. Gastrin increases tone, and numerous descriptions of lower esophageal sphincter regulation state that this is a physiologically important control mechanism. Current information, however, indicates that in physiologic amounts, gastrin does not play a normal role in the regulation of tone or contractions of the sphincter. Acetylcholine and related compounds increase resting tone, and prostaglandin E and isopro-terenol decrease tone.

Relaxation of the sphincter as a peristaltic wave approaches is mediated neurally. Vagal stimulation decreases sphincter tone and pressure. The mediator of this response is vasoactive intestinal peptide (VIP) (see Chapter 32), which initiates the synthesis of nitric oxide (NO). NO is a potent relaxer of smooth muscle and directly causes the lower esophageal sphincter to relax.

In the condition known as achalasia, the lower esophageal sphincter fails to relax during swallowing and the primary peristaltic contractions are weak and nonpropulsive. Thus, the esophagus becomes functionally obstructed and swallowed material builds up, the lower esophagus dilates, and aspiration may occur. Treatment involves stretching the sphincter with a balloon or surgically weakening the sphincter muscle.

Motor abnormalities of the esophagus also occur in diffuse esophageal spasm, resulting in simultaneous strong contractions of long duration. These contractions are largely nonpropulsive. Obstruction of the esophagus often occurs in esophageal cancer. Scleroderma frequently begins as nerve degeneration in the esophagus and progresses to the replacement of smooth muscle with noncontractile fibrous tissues. This patient experiences heartburn and dysphagia (difficulty swallowing).

Receptive Relaxation of the Stomach

Swallowing also involves the stomach. The pressure within the orad portion of the stomach is essentially equal to intra-abdominal pressure, which is slightly higher than atmospheric. During a swallow, the orad stomach relaxes before the arrival of the bolus at the same time that the lower esophageal sphincter relaxes. After the bolus enters the stomach, pressure returns slowly to basal levels. In this manner, the stomach can accommodate volume changes of as much as 1500 mL with negligible increases in pressure. Accommodation is

Clinical Note

The most common symptom associated with esophageal dysfunction is heartburn. This burning sensation is caused by the reflux of gastric acid into the esophagus and the resulting injury to the esophageal mucosa. This condition may be produced by motor abnormalities that result in abnormally low pressures in the lower esophageal sphincter or by the failure of secondary peristaltic contractions to effectively empty the esophagus. Reflux may also occur if intragastric pressure increases, as may occur after a large meal, during heavy lifting, or during pregnancy. In some cases, a region of proximal stomach may move through the diaphragm into the thorax, producing severe gastric reflux. This condition is termed hiatal hernia and is often treated by surgery. Reflux itself is not abnormal, occurring several times a day. Under normal conditions, the refluxed acid is cleared from the esophagus, and no symptoms develop.

made possible by the active relaxation of the gastric smooth muscle, a process referred to as receptive relaxation.

Receptive relaxation is mediated by a vagovagal reflex, which means that afferent information from the stomach is relayed to the CNS via the vagus and that the signal from the CNS resulting in relaxation also reaches the gastric smooth muscle via vagal efferents. Receptive relaxation can be elicited in the absence of a swallow by distending or stretching the stomach. Vagotomy abolishes this reflex. The neurotransmitter has not been identified but nitric oxide appears to be involved. The hormone cholecystokinin (CCK) functions physiologically to make the orad stomach more distensible, thus facilitating this process.

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