Physiology of the healthy gastrointestinal tract

The physiology of normal intestinal function is complex, and a grasp of the basic principles of intestinal motility is invaluable to an understanding of gut motor dysfunction.

There are many determinants of gut motility (Quig.ley.J996). An intricate and interrelated neural network invests all layers of the bowel wall and responds to stimuli originating locally, in the autonomic nervous system, and in the brain. Disturbances at all levels can upset motility. The intrinsic nervous system of the bowel comprises Meissner's submucosal plexus investing the muscularis mucosae, Auerbach's myenteric plexus running between the longitudinal and circular muscular fibers, and a fine subserosal plexus running with the external longitudinal muscle fibers. The external nervous system is divided into two autonomic components: sympathetic activity which is generally adrenergic and inhibitory, and parasympathetic activity which is cholinergic and excitatory. Responding to distension through mechanoreceptors, and to other disturbances through chemoreceptors, efferents arising in the thoracolumbar splanchnic nerves act to inhibit motility through release of norepinepherine (noradrenaline). Circulating catecholamines do not appear to impair gut motility.

All portions of the small bowel maintain an intrinsic electrical control activity capable of prompting peristalsis. Electrical control activity frequency declines gradually along the bowel length. As the duodenum maintains the fastest and therefore overriding rate, it serves as the pacemaker for peristalsis. The gut behaves differently in fed and fasted (interdigestive) states. Migrating motor complexes are phasic peristaltic contractions occurring in 90- to 120-min cycles to clear the fasted small bowel of a regular build-up of enteric residue, desquamated cells, and bacteria. Slower more irregular contractions emerge postprandially to facilitate mixing and absorption. Such contractions are an intrinsic phenomenon and occur independent of vagal regulation. Giant migrating complexes are large-amplitude long-duration contractions which move enteric contents distally en masse and propagate uninterrupted to the ileocolic junction. Erythromycin enhances this activity. These more intense contractions may stimulate nociceptors causing intermittent crampy pain, particularly where obstruction is present. Migrating clustered contractions lasting 1 to 3 min are thought to occur randomly over short segments (10-30 cm) of small bowel to assist with postprandial clearance. These contractions increase in the early phase of small bowel obstruction. Neurohormonal reflexes involving vagal innervation and hormones such as motilin co-ordinate postprandial activity with the rest of the gut. Emesis occurs when retrograde giant complexes originating in the mid small bowel return intestinal contents to the stomach for expulsion. The colon manifests broad peristaltic activity based largely on migrating motor complex and giant migrating complex contractions ( Sarna 1993).

The colon is extremely efficient in absorbing the 1.5 liters of water, sodium, potassium, and bile salts entering the cecum daily. When excess bile salts are delivered to the colon, as may occur in short gut or dysfunctional bowel syndromes, a secretory diarrhea results.

Although less rigidly regulated than cerebral or renal blood flow, there is significant autoregulation of intestinal perfusion such that gut oxygen uptake is maintained despite pressure fluctuations as great as 50 mmHg. Significant hypotension or hypoxia provokes a fall in vascular resistance and capillary recruitment that helps protect the gut from ischemia.

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