Normal Bowel Rectosphincteric Reflex

FIGURE 12 Mass movement. (A) Colon before entry of barium sulfate. (B) Barium enters proximal ascending colon, showing haustra. (C) As more barium enters, the haustra disappear from a portion of the ascending and transverse colons, and a contraction begins in this area. (D) The contraction has moved a portion of the barium into the caudad transverse colon. (E) Haustra return.

exposing them to absorptive surfaces. These contractions last from 12-60 seconds and generate intraluminal pressures between 10 and 50 mm Hg. These segmental contractions are believed to be partly responsible for the formation of haustra.

Approximately one to three times a day, peristaltic contractions move significant amounts of material caud-ally from one region of the colon to another. At the start of a so-called mass movement, segmentation ceases and haustrations disappear from the segment of bowel involved (Fig. 12). Contents are moved in a narrow tubular length of bowel at least 20 cm long. One mass movement may transport contents from the transverse to the sigmoid colon or rectum. After the mass movement, haustrations reappear and segmentation begins.

Motility of the Descending and Sigmoid Colon

Most absorption of water and electrolytes occurs in the proximal colon, so that material present in the distal colon is in a semisolid state. Even so, the primary form of motility is nonpropulsive segmentation. This activity produces a certain amount of resistance, which retards movement of material into the rectum. Net caudad movement of contents in this region also occurs by mass movements that propel fecal contents into the rectum.

Motility of the Rectum and Anal Canal

The rectum has more segmental contractions than the sigmoid colon. Therefore, unless filled by a mass movement, it is kept empty or nearly so by retrograde movement of contents into the sigmoid colon. This accounts for the retention and subsequent absorption of suppositories. As fecal material is forced into the rectum, the rectum contracts and the internal anal sphincter relaxes (Fig. 13). Normally, the anal canal is closed by contraction of the internal sphincter. The relaxation of the internal anal sphincter after contraction of the rectum is the rectosphincteric reflex. Filling the rectum to about 25% of capacity produces an urge to defecate. Defecation is prevented by the external anal sphincter, which is normally in a state of tonic contraction maintained by reflex activation through dorsal roots in the sacral segments. In paraplegics lacking this tonic contraction, the rectosphincteric reflex results in defecation. In the normal individual, if defecation is not convenient, the external sphincter remains closed, the receptors in the rectum accommodate to the distension stimulus, the internal sphincter regains its tone (Fig. 13), and the urge to defecate subsides.

If the rectosphincteric reflex occurs under convenient circumstances, defecation may occur through a series of acts that are both involuntary and voluntary. The external anal sphincter is relaxed voluntarily, and the

Clinical Note

Increased or decreased time of passage or transit of material through the colon can lead to the common symptoms of constipation or diarrhea. Delayed transit and constipation are primarily dietary in origin and can be corrected by the addition of fiber or bulk to the diet. Increased speed of transit may result in diarrhea, although diarrhea can be the result of many diseases or conditions unrelated to colonic motility.

Alterations in colonic motility and in transit are frequently caused by emotional factors and are indicative of the strong influence the higher centers of the CNS have on motility. The final effects of stress on colonic motility vary greatly from individual to individual. Most students are familiar with diarrhea previous to an important examination. The severity of the problem is usually related inversely to how well the student knows the material to be covered by the test. Prolonged, extreme responses of anger, anxiety, hostility, or resentment may result in irritable bowel syndrome. In these individuals constipation may alternate with diarrhea, and abdominal pain or cramping and flatulence are often present as well.

Time

FIGURE 13 Pressures recorded within the rectum and the internal and external anal sphincters. As contents distend the rectum, the pressure increases passively; if sufficient, active contraction increases pressure further. This is accompanied by relaxation of the internal anal sphincter and contraction of the external anal sphincter. As contents continue to enter the rectum, the pressure in the internal anal sphincter decreases and the pressure in the external sphincter increases.

Time

FIGURE 13 Pressures recorded within the rectum and the internal and external anal sphincters. As contents distend the rectum, the pressure increases passively; if sufficient, active contraction increases pressure further. This is accompanied by relaxation of the internal anal sphincter and contraction of the external anal sphincter. As contents continue to enter the rectum, the pressure in the internal anal sphincter decreases and the pressure in the external sphincter increases.

longitudinal muscles of the rectum and distal colon contract. This shortens the rectum and straightens the angle between the rectum and sigmoid colon, facilitating the passage of feces. This plus the resulting increase in pressure is often sufficient for evacuation. The process, however, is enhanced by inspiration and contraction of the chest muscles against a closed glottis and full lungs. This raises both intrathoracic and intra-abdominal pressures. Contraction of the abdominal muscles increases pressure further. Intra-abdominal pressures may increase to as much as 100-200 mm Hg. The pelvic floor—which supports the abdominal contents—relaxes during defecation, allowing the increased pressure to force the floor downward, which straightens the rectum.

The hemodynamic consequences of the pressure changes involved in defecation are substantial. There is an abrupt rise in arterial pressure as the increased intrathoracic pressure is transmitted across the wall of the heart and aorta. The large veins in the thorax collapse, stopping venous return and causing peripheral venous pressure to rise. Together, these events result in decreased stroke volume and cardiac output and a resultant drop in systemic arterial pressure. In a normal individual, these events are of no consequence, but death can result from cerebral vascular accidents caused by increased intracranial pressures produced while straining to defecate.

Control of Large Intestinal Motility

The resting tone of the ileocecal sphincter is primarily myogenous, that is, a property of the smooth muscle cells themselves. Relaxation of the sphincter in response to distension of the ileum and its contraction after distension of the proximal colon are neural reflexes. These are probably mediated entirely by the enteric nerves. Shortly after a meal, the ileum contracts and the sphincter relaxes, resulting in the propulsion of ileal contents into the colon. This is referred to as the gastroileal reflex, and appears to be mediated by the extrinsic autonomic nerves. There is some evidence that digestive hormones may also be involved.

As is the case with the stomach and small intestine, the membrane potential of the smooth muscle cells of

Clinical Note

The major advance, during the past 10 years or so, in our understanding of the control of gastrointestinal motility has been the appreciation of the role played by the interstitial cells of Cajal (ICCs). However, in addition to being responsible for generating the pacemaker potentials of the various tissues (as outlined in this chapter), strong evidence is accumulating that defects in these cells may be the cause of a variety of human motility disorders. ICCs express a novel protein, and antibodies to this protein have allowed clinicians to evaluate ICC function in a variety of conditions. These studies have shown that ICCs are reduced in number in pseudoobstruction, achalasia, ulcerative colitis, Chaga's disease, diabetes, and slow transit constipation. Investigators are using animal models of various genetic mutations to determine whether changes in ICCs are the causes or the results of these conditions.

the colon and rectum fluctuates. Again, this fluctuation is initiated in the interstitial cells of Cajal. Spike potentials have also been recorded from the slow, wavelike depolarizations. Although these events initiate contractions, they are more irregular than those of the small intestine, and their correlation with contractile events is not totally understood.

Enteric or intrinsic nerves play a major role in colonic motility, for haustrations and mass movements occur in the absence of extrinsic innervation. The major effect of the enteric nerves is inhibitory, because interruption of their influence results in tonic contraction. This inhibition of contraction is probably mediated by VIP and nitric oxide. In megacolon or Hirschsprung's disease, the ganglion cells are absent from a segment of colon and the tissue concentration of VIP is extremely low. This results in constriction and loss of coordinated movements in the affected segment. Colonic contents accumulate proximal to the constriction, and the colon becomes grossly distended and hyperplastic. This condition is therefore the colonic correlate of esophageal achalasia. Surgical removal of the aganglionic segment usually restores normal function. Defecation is controlled by both extrinsic and intrinsic nerves. Activity within the spinal cord reinforces the rectosphincteric reflex, which is primarily under control of the intrinsic nerves. The sensation of distension and the voluntary control of the external anal sphincter are mediated by nerves within the spinal cord to the cerebral cortex.

Suggested Readings

Conklin JL, Christensen J. Motor functions of the pharynx and esophagus. In Johnson LR, ed., Physiology of the GI tract, 3rd ed. New York: Raven Press, 1994, pp 903-928. Christensen J. Motility of the colon. In Johnson LR, ed., Physiology of the GI tract, 3rd ed. New York: Raven Press, 1994, pp 991-1024. Makhlouf GM. Neuromuscular function of the small intestine. In Johnson LR, ed., Physiology of the GI tract, 3rd ed. New York: Raven Press, 1994, pp 977-990. Mayer EA. The physiology of gastric storage and emptying. In Johnson, LR, ed., Physiology of the GI tract, 3rd ed. New York: Raven Press, 1994, pp 977-990. Sanders KM, Ordog T, Ward SM. Physiology and pathophysiology of the interstitial cells of Cajal: From bench to bedside. Am J Physiol Gastrointest Liver Physiol 2002; 282:G747-G756.

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  • Crispus
    What is rectosphincteric reflex?
    5 months ago

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