Smooth muscles of the small intestine undergo spontaneous oscillations of membrane potential; these cyclic changes are termed pacesetter potentials or electrical control activity. Each segment of intestine has a characteristic frequency of pacesetter potentials; it is highest proximally, and it decreases progressively to ileum. In intact intestine, higher-frequency pacesetter potentials can drive adjacent distal intestine so that both segments have the same frequency (said to be phase-locked). In humans, the duodenum determines the frequency of pacesetter potentials for the entire small intestine.
As pacesetter potentials spread distally, they bring the onset of action potentials and muscular contractions into phase. One type of muscular contraction (nonpropagating, or stationary) causes segmentation, which mixes chyme with digestive juices, repeatedly exposes the mixture to the absorptive surface, and moves chyme slowly in an aboral direction. Another type of muscular contraction (propagating) is peristaltic. Normal peristalsis is a short, weak propulsive movement that travels at about 1 cm/s for a distance of 10–15 cm before subsiding. Mean transit time for a solid meal is 4 hours from mouth to colon.
The enteric nervous system is a regulator of all aspects of motility of the small intestine. The two types of nerve plexuses in the enteric nervous system are the myenteric plexus, mainly responsible for control of peristaltic activity, and the submucosal plexus, which regulates secretion and absorption. The enteric nervous system contains four types of neurons: motor, secretory, sensory, and interneurons. Neurotransmitters include cholinergic, adrenergic, serotonergic, and peptidergic substances. Among the numerous peptides secreted in the enteric nervous system are cholecystokinin, vasoactive intestinal peptide, somatostatin, neurotensin, enkephalin, galanin, d substance P. In general, intestinal action potentials and muscular contractions are stimulated by substance P and galanin, and motility is inhibited by VIP, somatostatin, neurotensin, and enkephalin. Nitric oxide mediates neural inhibition.
Peristalsis is initiated by stretch of the intestinal wall by a food bolus, and a dual reflex is set in motion. The circular muscle orad to the bolus contracts; this reflex is mediated by enteric neurons with acetylcholine as neurotransmitter. Simultaneous relaxation of the intestinal circular muscle below is mediated by enteric neurons using VIP as the neurotransmitter.
The interdigestive migrating myoelectric complex originates every 11/2–2 hours in the stomach of fasting mammals. It is an aborally progressive front of action potentials and muscular contractions consisting of three successive phases:. The MMC progresses aborally until it reaches the colon, and then another burst of potentials and contractions begins proximally. The MMC has been called the “intestinal housekeeper” because it cleans up remnants of the preceding meal and gets rid of microorganisms that escaped destruction by gastric acid. The MMC is controlled by the nervous system; motilin and 5-hydroxytryptamine may play regulatory roles. The MMC is abolished by ingestion of food, and some features are altered by major abdominal operations or peritonitis.
Numerous peptides have been found to act in the brain to alter gastrointestinal motility. Hypothalamic hormones (eg, corticotropin-releasing factor and thyrotropin-releasing hormone), calcitonin, and nearly all of the nervous system neurotransmitters have central nervous system actions that affect motility, at least in animals. Exogenous opioids, including codeine and loperamide, exert antidiarrheal action by inhibition or disruption of the pattern of circular muscle contraction.
Paralytic (adynamic) ileus is routine after abdominal operations, and it also accompanies inflammatory conditions in the abdomen, intestinal ischemia, ureteral colic, pelvic fractures, and back injuries. Abdominal surgery abolishes gastrointestinal motility for a period of time that varies with the type of operation; the MMC returns within 3 hours after cholecystectomy, the small intestine recovers in 12–24 hours, and the colon may not regain normal motility until the sixth postoperative day. The manifestations of postoperative ileus do not correlate well with the myoelectric parameters, however, and the pathophysiology of ileus remains incompletely understood. Corticotropin-releasing factor may be an important mediator of postoperative ileus.
Orocecal transit time is an important indicator of small bowel function. Transit may be accelerated in patients with diarrhea and delayed in constipation; a variety of disease states are responsible. Orocecal transit time can be measured by the lactulose breath hydrogen test. An ingested solution of lactulose reaches the cecum in about 90 minutes; colonic fermentation of lactulose produces hydrogen, which is detected in the breath. Several techniques of gamma scintigraphy, including the use of isotopically labeled pellets, are alternative methods of estimating small bowel transit time.