Fig. 31.1 ). The primary functions of the large intestine are to digest and absorb components of the meal that cannot be digested or absorbed more proximally, reabsorb the remaining fluid that was used during movement of the meal along the GI tract, and store the waste products of the meal until they can conveniently be eliminated from the body. In fulfilling these functions, the large intestine uses characteristic motility patterns and expresses transport mechanisms that drive the absorption of fluid, electrolytes, and other solutes from the stool. The large intestine also contains a unique biological ecosystem known as the microbiota, consisting of many trillions of commensal bacteria and other microorganisms that engage in a lifelong symbiotic relationship with their human host. These microorganisms can metabolize components of the meal that are not digested by host enzymes and make their products available to the body via a process known as fermentation. Colonic bacteria also metabolize other endogenous substances such as bile acids and bilirubin, thereby influencing their disposition. There is emerging evidence that the colonic microbiota is critically involved in promoting development of the normal colonic epithelium and in stimulating its differentiated functions.
In addition the microbiota can detoxify xenobiotics (substances originating outside the body, such as drugs) and protect the colonic epithelium from infection by invasive pathogens. Finally, the colon is both the recipient and the source of signals that allow it to communicate with other GI segments to optimally integrate function. For example, when the stomach is filled with freshly masticated food, the presence of the meal triggers a long reflex arc that results in increased colonic motility (the gastrocolic reflex) and eventually evacuation of the colonic contents to make way for the residues of the next meal. Similarly the presence of luminal contents in the colon causes release of both endocrine and neurocrine mediators that slow propulsive motility and decrease electrolyte secretion in the small intestine. This negative feedback mechanism matches the rate of delivery of colonic contents to the segment’s capacity to process and absorb the useful components. Details of the signals that mediate this crosstalk between the colon and other components of the GI system are reviewed in the next section.
The colon is regulated primarily, though not exclusively, by neural pathways. Colonic motility is influenced by local reflexes that are generated by filling of the lumen, thereby initiating distention and the activation of stretch receptors. These regulatory pathways exclusively involve the enteric nervous system. Local reflexes triggered by distortion of the colonic epithelium and produced, for example, by passage of a bolus of fecal material stimulate short bursts of Cl− and fluid secretion mediated by 5-hydroxytryptamine (5-HT) from enteroendocrine cells and acetylcholine from enteric secretomotor nerves. On the other hand, colonic function and motility responses in particular are also regulated by long reflex arcs originating more proximally in the GI tract or in other body systems. One example is the gastrocolic reflex. Distention of the stomach activates a generalized increase in colonic motility and mass movement of fecal material, as described in more detail later. This reflex has both chemosensitive and mechanosensitive components at its site of origin and involves release of 5-HT and acetylcholine. Similarly the orthocolic reflex is activated on rising from bed and promotes a morning urge to defecate in many individuals.