Colonic Motility

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The colon functions to delay passage of luminal contents to allow for water absorption and for mixing of luminal contents with the mucosa, to store fecal matter prior to defecation, and, at the time of defecation, to propel contents forward.

The frequency and duration of propagative, high-pressure waves in the colon in part are determined by pressure exerted by intraluminal contents (mechanical) and the degree of stretch stimulation, the (chemical) composition of the contents, and other stimuli interacting with the colon.

The gastrocolic reflex, an anterograde postperis-taltic process, occurs following a meal, originating proximally and propagating anterograde. Both the caloric content and the fat composition of the meal influence colonic peristalsis. Gastric distention by food contents, water, or gas also has a stimulatory effect. Gastrointestinal hormones secreted in response to a meal, such as cholecystokinin, are thought to mediate peristaltic responses to a (fatty) meal. Irritant laxatives also stimulate peristalsis, even when administered rectally. Opiates are known to inhibit the ENS and, as a consequence, retard peristalsis. Colonic motility diminishes significantly during sleep, resuming upon awakening.

Motor activity varies by colonic region; in degree, frequency, amplitude, and velocity; in being propagative versus nonpropagative (the latter is more common in the distal colon); in relative distance of propagation; and in direction of propagation (ante-rograde versus retrograde, the latter most commonly seen in the proximal colon). Approximately one-third of these colonic peristaltic waves are propulsive, and those associated with propulsion of stool tend to be slower but greater in amplitude.

Defecation involves the integration of peristaltic activity in the majority of colonic regions, not exclusively to that solely in the anorectal region. In the predefecatory phase, approximately 1 h prior to actual defecation, the majority of the colon exhibits an increase in propulsive peristaltic waves, first in the proximal colon and then advancing distally.

The sensation of defecatory urge is not evident until approximately 15 minutes prior to defecation. At that time, there is a marked increase in propa-gative peristaltic activity, originating more distally in the colon. Each of these late propagative waves successively originates proximate to the preceding one with greater amplitude and presents over a greater distance of colonic length.

Stool contact with the receptors in the upper anal canal can effect relaxation of the inner anal sphincter. In addition, stretch receptor stimulation of the

Figure 5 Composition of feces (60-80 g/day).

Figure 5 Composition of feces (60-80 g/day).

rectal vault walls results in the urge to defecate. Failure of relaxation of the external anal sphincter (which is under voluntary control) results in retrograde passage of stool into the rectum, with subsequent diminishing of more proximal peristaltic propagative waves, thereby maintaining continence when immediate defecation is not desirable or convenient.

Evacuation of the rectum and defecation require correcting the angle of the anal canal in the anterior-posterior plane, which is accomplished by assuming a squatting position. Contraction of the abdominal musculature and of the diaphragm, with a relaxed pelvic floor, facilitates defecation, even in the absence of colonic peristalsis.

Stool size and consistency vary based on diet, water intake, and transit time, as well as bacterial content (a major component of stool). Higher water content tends to result in larger, softer stools. The more fusiform-shaped the stool is, the less likely that its passage is associated with straining. The transit time through the colon is inversely related to the stool's water content and, hence, its consistency (Figure 5).

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