The movements of the small intestine, like those else where in the gastrointestinal tract, can be divided into mixing contractions and propulsive contractions. To a great extent, this separation is artificial because essentially all movements of the small intestine cause at least some degree of both mixing and propulsion. The usual classification of these processes is described in the following sections.
MIXING CONTRACTIONS (SEGMENTATION CONTRACTIONS)
When a portion of the small intestine becomes distended with chyme, stretching of the intestinal wall elicits localized concentric contractions spaced at intervals along the intestine and lasting a fraction of a minute. The contractions cause “segmentation” of the small intestine, as shown in Figure 1—that is, they divide the intestine into spaced segments that have the appearance of a chain of sausages. As one set of segmentation contractions relaxes, a new set often begins, but the contractions this time occur mainly at new points between the previous contractions. Therefore, the segmentation contractions “chop” the chyme two to three times per minute, in this way promoting progressive mixing of the food with secretions of the small intestine.
Fig1. Segmentation movements of the small intestine.
The maximum frequency of the segmentation contractions in the small intestine is determined by the frequency of electrical slow waves in the intestinal wall, which is the basic electrical rhythm described in Chapter 63. Because this frequency normally is not greater than 12 per minute in the duodenum and proximal jejunum, the maximum frequency of the segmentation contractions in these areas is also about 12 per minute, but this maximum frequency occurs only under extreme conditions of stimulation. In the terminal ileum, the maximum frequency is usually eight to nine contractions per minute.
The segmentation contractions become exceedingly weak when the excitatory activity of the enteric nervous system is blocked by the drug atropine. Therefore, even though it is the slow waves in the smooth muscle itself that cause the segmentation contractions, these contractions are not effective without background excitation mainly from the myenteric nerve plexus.
PROPULSIVE MOVEMENTS
Peristalsis in the Small Intestine. Chyme is propelled through the small intestine by peristaltic waves. These waves can occur in any part of the small intestine and move toward the anus at a velocity of 0.5 to 2.0 cm/sec— faster in the proximal intestine and slower in the terminal intestine. They are normally weak and usually die out after traveling only 3 to 5 centimeters. The waves rarely travel farther than 10 centimeters, so forward movement of the chyme is very slow—so slow that net movement along the small intestine normally averages only 1 cm/min. This rate of travel means that 3 to 5 hours are required for passage of chyme from the pylorus to the ileocecal valve.
Control of Peristalsis by Nervous and Hormonal Signals. Peristaltic activity of the small intestine is greatly increased after a meal. This increased activity is caused partly by the beginning entry of chyme into the duodenum, causing stretch of the duodenal wall. In addition, peristaltic activity is increased by the so-called gastroenteric reflex that is initiated by distention of the stomach and conducted principally through the myenteric plexus from the stomach down along the wall of the small intestine.
In addition to the nervous signals that may affect small intestinal peristalsis, several hormonal factors also affect peristalsis. These factors include gastrin, CCK, insulin, motilin, and serotonin, all of which enhance intestinal motility and are secreted during various phases of food processing. Conversely, secretin and glucagon inhibit small intestinal motility. The physiological importance of each of these hormonal factors for controlling motility is still questionable.
The function of the peristaltic waves in the small intestine is not only to cause progression of chyme toward the ileocecal valve but also to spread out the chyme along the intestinal mucosa. As the chyme enters the intestines from the stomach and elicits peristalsis, the peristalsis immediately spreads the chyme along the intestine, and this process intensifies as additional chyme enters the duodenum. Upon reaching the ileocecal valve, the chyme is sometimes blocked for several hours until the person eats another meal; at that time, a gastroileal reflex intensifies peristalsis in the ileum and forces the remaining chyme through the ileocecal valve into the cecum of the large intestine.
Propulsive Effect of the Segmentation Movements. The segmentation movements, although lasting for only a few seconds at a time, often also travel 1 centimeter or so in the anal direction, and during that time they help propel the food down the intestine. The difference between the segmentation and the peristaltic movements is not as great as might be implied by their separation into these two classifications.
Peristaltic Rush. Although peristalsis in the small intestine is normally weak, intense irritation of the intestinal mucosa, as occurs in some severe cases of infectious diarrhea, can cause both powerful and rapid peristalsis, called the peristaltic rush. This phenomenon is initiated partly by nervous reflexes that involve the autonomic nervous system and brain stem and partly by intrinsic enhancement of the myenteric plexus reflexes within the gut wall. The powerful peristaltic contractions travel long distances in the small intestine within minutes, sweeping the con tents of the intestine into the colon and thereby relieving the small intestine of irritative chyme and excessive distention.
Movements Caused by the Muscularis Mucosae and Muscle Fibers of the Villi. The muscularis mucosae can cause short folds to appear in the intestinal mucosa. In addition, individual fibers from this muscle extend into the intestinal villi and cause them to contract intermittently. The mucosal folds increase the surface area exposed to the chyme, thereby increasing absorption. Also, contractions of the villi—shortening, elongating, and shortening again— “milk” the villi so that lymph flows freely from the central lacteals of the villi into the lymphatic system. These mucosal and villous contractions are initiated mainly by local nervous reflexes in the submucosal nerve plexus that occur in response to chyme in the small intestine.
THE ILEOCECAL VALVE PREVENTS BACKFLOW FROM THE COLON TO THE SMALL INTESTINE
As shown in Figure 2, the ileocecal valve protrudes into the lumen of the cecum and therefore is forcefully closed when excess pressure builds up in the cecum and tries to push cecal contents backward against the valve lips. The valve usually can resist reverse pressure of at least 50 to 60 centimeters of water.
Fig2. Emptying at the ileocecal valve.
In addition, the wall of the ileum for several centimeters immediately upstream from the ileocecal valve has a thickened circular muscle called the ileocecal sphincter. This sphincter normally remains mildly constricted and slows emptying of ileal contents into the cecum. However, immediately after a meal, a gastroileal reflex (described earlier) intensifies peristalsis in the ileum, and emptying of ileal contents into the cecum proceeds.
Resistance to emptying at the ileocecal valve prolongs the stay of chyme in the ileum and thereby facilitates absorption. Normally, only 1500 to 2000 milliliters of chyme empty into the cecum each day.
Feedback Control of the Ileocecal Sphincter. The degree of contraction of the ileocecal sphincter and the intensity of peristalsis in the terminal ileum are controlled significantly by reflexes from the cecum. When the cecum is distended, contraction of the ileocecal sphincter becomes intensified and ileal peristalsis is inhibited, both of which greatly delay emptying of additional chyme into the cecum from the ileum. Also, any irritant in the cecum delays emptying. For instance, when a person has an inflamed appendix, the irritation of this vestigial remnant of the cecum can cause such intense spasm of the ileocecal sphincter and partial paralysis of the ileum that these effects together block emptying of the ileum into the cecum. The reflexes from the cecum to the ileocecal sphincter and ileum are mediated both by way of the myenteric plexus in the gut wall and of the extrinsic auto nomic nerves, especially by way of the prevertebral sympathetic ganglia.
