42 CHAPTER 5 Motility of the Small Intestine regulating MMC cycle length. Plasma levels of motilin
fluctuate with the same periodicity as for the phase of intense duodenal contractions, and exogenously adminis- tered motilin initiates a premature MMC. Enteric nerves also are involved because their disruption alters MMC ini- tiation and migration. Extrinsic nerves do not seem to be required. Segments of intestine that have been extrinsically denervated still exhibit MMCs. However, extrinsic neural activity can modify characteristics of the MMC.
Feeding abolishes MMCs and institutes a pattern of more or less continuous contractions of varying ampli- tude. The change in pattern caused by feeding proba- bly is brought about by hormones such as gastrin and CCK, which are released during feeding, and by neural mechanisms.
43 CHAPTER 5 Motility of the Small Intestine
CLINICAL TESTS
Auscultation to detect “bowel sounds” probably is the most common means used to assess bowel activity. In addition, observing the movement of barium by x-ray studies and of isotopes by scintigraphy (see Chapter 4) can yield some information on transit time through the small bowel. Unfortunately, these methods are not pre- cise. Advances in technology have made the recording
of intraluminal pressures rather easy in normal persons and in patients with minimal gastrointestinal dysfunc- tion. However, the inaccessibility of the small intes- tine and the difficulty in placing intraluminal sensors in patients with major dysmotility limit the routine use of direct recordings of intestinal contractions as a diagnostic tool.
Altered small intestinal motility resulting in delayed transit frequently accompanies a variety of diseases and clinical conditions. Perhaps the most common is the transient ileus or apparent paralysis of the small intes- tine sometimes seen after abdominal surgery. However, intraabdominal inflammation (e.g., pancreatitis, appendi- citis, abscess) may produce a similar picture. Systemic diseases such as diabetes mellitus and amyloidosis, metabolic alterations such as potassium depletion, and administration of drugs, particularly anticholinergics, all
may have an adverse effect on intestinal transit. Mixing probably is impaired as well, although this is less clinically apparent.
Alternatively, rapid intestinal transit is seen in certain malabsorptive states induced by infectious agents, allergic reaction, and various pharmacologic agents. In these con- ditions both motility and absorption are affected. In most disease states it is not clear whether changes in motility are primary (caused by the disease) or secondary (caused by the presence of unabsorbed or secreted material).
CLINICAL APPLICATIONS—cont’d
S U M M A R Y
• Movement of contents within the intestinal lumen depends on the type of contraction. Segmenting con- tractions cause mixing and local circulation of contents.
Peristaltic contractions cause net aboral transit.
• During digestion of a meal, most contractions are of the segmenting type, with short peristaltic contractions occurring randomly. During interdigestive periods, bursts of intense peristaltic contractions envelop each region of the intestine approximately every 90 minutes.
Each burst appears to begin in the stomach and migrate aborally along the intestine such that it reaches the ter- minal ileum in approximately 90 minutes. This activity is called the MMC.
• Intestinal slow waves are cyclic depolarizations and repolarizations of muscle cell membranes. At any locus of the intestine, slow waves are present at a constant fre- quency (i.e., approximately 12 cpm in the duodenum and 8 cpm in the ileum). At adjacent loci, slow waves appear to propagate aborally.
• Spike potentials are rapid fluctuations in membrane potential that are superimposed on the depolarization phase of the slow wave. These potentials, not the slow waves themselves, initiate contractions of the muscle.
Spike potentials do not accompany every slow wave.
Their presence and pattern depend on the digestive state and on neural and humoral activities.
• Enteric nerves coordinate both the types and patterns of contractions. The phase of intense contractions of the MMC in the upper intestine may be initiated by the release of motilin. The conversion of the MMC pat- tern to the digestive pattern may result in part from the release of hormones such as gastrin and CCK.
• Vomiting in humans usually involves nausea and retch- ing, which overcome the antireflux mechanisms of the GI tract, and occur in response to a variety of stimuli that are coordinated in the medulla.
44 CHAPTER 5 Motility of the Small Intestine
K E Y W O R D S A N D C O N C E P T S
Myenteric/Auerbach plexus Segmentation
Law of the intestines Migrating motor complex Slow wave activity
Spike potentials Peristaltic reflex
Intestino-intestinal reflex Idiopathic pseudoobstruction
S E L F - S T U D Y P R O B L E M S
1. What are the major differences between gastric and intestinal slow waves?
2. How does the motor activity aid in carrying out the major functions of the small intestines?
SUGGESTED READINGS
Hasler WL. Small intestinal motility. In: Johnson LR, ed.
Physiology of the Gastrointestinal Tract. 4th ed. Vol. 1. San Diego: Elsevier; 2006.
Weisbrodt NW. Motility of the small intestine. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. 2nd ed. Vol. 1.
New York: Raven Press; 1987.
Wingate DL. Backward and forward with the migrating complex.
Dig Dis Sci. 1981;26:641–666.
O B J E C T I V E S
• Describe the anatomy of the large intestine.
• Explain the function of the ileocecal reflex.
• Define a mass movement.
• Understand the motility of defecation and the recto- sphincteric reflex.
• Discuss the control of defecation and explain the loss of control that occurs with some spinal cord injuries.
Motility of the Large Intestine
6
Contractions of the large intestine are organized to allow for optimal absorption of water and electrolytes, net aboral movement of contents, and storage and orderly evacuation of feces.
ANATOMIC CONSIDERATIONS
Anatomically the human large intestine is divided into the following: the cecum; the ascending, transverse, descending, and sigmoid colon; the rectum; and the anal canal. The muscular layers of the large intestine are composed of both longitudinally and circularly arranged fibers. Longitudinal fibers are concentrated into three flat bands called the taeniae coli. These run from the cecum to the rectum, where the fibers fan out to form a more continuous longitudinal coat. The circular layer of muscle fibers is continuous from the cecum to the anal canal, where it increases in thickness to form the inter- nal anal sphincter. Overlapping and slightly distal to the internal anal sphincter are layers of striated muscle.
These striated muscle bundles make up the external anal sphincter.
In humans the external features of the large intestine differ from those of the small intestine. In addition to the presence of taeniae coli, the colon appears to be divided into segments called haustra or haustrations (Fig. 6.1).
Haustra probably are the result of structural and functional properties of the colon. Points of concentration of mus- cular tissue and mucosal foldings can be found in colons examined post mortem.
In addition, haustra are more prominent in areas of the colon that possess taeniae coli. Haustra are not fixed,
however. Segmental colonic contractions appear, dis- appear, and form again at another locus. Thus haustral formation also has a dynamic component because of the contractile activity of colonic musculature.
The large intestine, like other areas of the bowel, is innervated by the autonomic nervous system (ANS). The enteric system consists partly of many nerve cell bodies and endings that lie between the circular and the longitu- dinal muscle coats. In areas of the large intestine with tae- niae, this myenteric plexus is concentrated beneath them.
Cells of the myenteric plexus receive input from a variety of receptors within the intestine, as well as by way of the extrinsic nerves. Axons from these cells innervate the mus- cle layers. Extrinsic innervation to the large intestine comes from both parasympathetic and sympathetic branches of the ANS. There are two pathways of parasympathetic innervation: the cecum and the ascending and transverse portions of the colon are innervated by the vagus nerve;
the descending and sigmoid areas of the colon and the rec- tum are innervated by pelvic nerves from the sacral region of the spinal cord. The pelvic nerves enter the colon near the rectosigmoid junction and project orally and aborally within the plane of the myenteric plexus. These projec- tions, called shunt fascicles, innervate myenteric nerves en route. The vagus and pelvic nerves consist primarily of preganglionic efferent fibers and many afferent fibers.
The efferent fibers synapse with the nerve cell bodies of the myenteric and other intrinsic plexuses. The proximal regions of the large intestine are sympathetically inner- vated by fibers that originate from the superior mesenteric ganglion. More distal regions receive input from the infe- rior mesenteric ganglion. The distal rectum and anal canal
46 CHAPTER 6 Motility of the Large Intestine are innervated by sympathetic fibers from the hypogastric
plexus. Most of the sympathetic fibers are postganglionic efferent and afferent fibers. The external anal sphincter, a striated muscle, is innervated by the somatic pudendal nerves.
As in other regions of the gut, several diverse chem- icals serve as mediators at presynaptic and postsynaptic junctions within the autonomic innervation to the large intestine. Acetylcholine (ACh) and tachykinins such as substance P serve as major excitatory mediators, and nitric oxide (NO), vasoactive intestinal peptide (VIP), and possibly adenosine triphosphate (ATP) serve as major inhibitory mediators. Transmission between the pudendal nerves and the external anal sphincter is mediated by ACh.