The gastrocolic reflex is a physiological reflex that controls the motility of the lower gastrointestinal tract following a meal. As a result of the gastrocolic reflex, the colon has increased motility in response to the stretch of the stomach with the ingestion of food. The gastrocolic reflex allows room for the consumption of more food via control over peristalsis and movement of ingested food distally toward the rectum. Myoelectric recordings demonstrate the reflex in the large intestine that shows a spike in electrical activity within minutes of food consumption. The gastrocolic reflex initiates and controls migrating motor complexes throughout the colon. These motor complexes act cyclically during the digestion process and can be broken up into four phases.
The control of these phases is multifactorial, involving neurological, mechanical, and paracrine mediators. Several neuropeptides are suspected mediators of the reflex, including cholecystokinin, serotonin, neurotensin, and gastrin. Three centers of control have been identified and studied and include myogenic control, hormonal control, and neural control. The sigmoid colon is the region most affected during the phasic response of digestion, which consists of cyclical periods of contraction followed by relaxation to propel food distally toward the rectum. These contractions are generated in the myenteric plexus and accomplished by the muscularis externa — the gastrocolic reflex results in the urge to defecate after a meal. When food enters the rectum and drives pressures up, the gastrocolic reflex stimulates expulsion of the contents of the rectum via defecation.
Alteration in the gastrocolic reflex has been a suspected etiology in patients with irritable bowel syndrome (IBS). Patients with IBS have demonstrated a stronger colonic response to the gastrocolic reflex. These patients may experience a strong urge to defecate following ingestion of a meal and may experience symptoms like abdominal distension, flatulence, pain, and tenesmus. Furthermore, alternations in the gut microbiome can cause a downstream effect that alters the enteroendocrine cells' ability to sense and carry out paracrine functions, thus indirectly affecting the motility of the colon.
Profound gastrocolic reflex has been implicated in the idiopathic variant of dumping syndrome (DS). Although abdominal pain is present in both DS and IBS, systemic signs including palpitations, hypotension, dizziness, diaphoresis often accompany DS. Another key difference in the presentation of DS is that they often present with protein-calorie malnutrition due to increased excess nutritional loss in diarrhea.
Both IBS and DS are caused by profound gastrocolic reflex, whereas poor gastrocolic reflex results in constipation. Neuronal dysfunction may lead to impaired gastrocolic reflex and poor gut motility. Diabetic patients with neuropathy often have gastroparesis resulting in delayed gastric emptying and also impaired gastrocolic reflex leading to constipation.
The cellular makeup of the gastrocolic reflex is multisystemic and includes cell bodies from the nervous, endocrine, and gastrointestinal systems. The primary mediators are neurons of the autonomic nervous system, neurons of the myenteric (Auerbach’s) plexus, interstitial cells of Cajal, and enteroendocrine cells that line the GI tract.
Sympathetic nerve fibers contribute an inhibitory effect on the colon, while parasympathetic nerve fibers contribute a stimulatory effect. The nerve supply to the colon is broken up between midgut and hindgut derived structures. Structures derived from the midgut include the ascending colon and proximal two-thirds of the transverse colon. These midgut derived structures receive their sympathetic supply from nerves that originate from the superior mesenteric plexus and their parasympathetic supply via the vagus nerve. Structures derived from the hindgut include the distal one-third of the transverse colon, the descending colon, and the sigmoid colon. These structures receive their sympathetic innervation from the inferior mesenteric plexus and parasympathetic innervation via pelvic splanchnic nerves.
Located in between the inner and outer layers of the muscularis externa, the myenteric plexus generates and helps coordinate gut motility. A sensory component of the myenteric plexus has been identified, and this is thought to help with coordination and the propagation of migrating motor complexes. The myenteric plexus propels a food bolus distally by contracting the radius of the lumen of the bowel and extending the length of the bowel. The cell bodies of nerves located in the myenteric plexus communicate using gap junctions with both an excitatory component, as well as an inhibitory component.
Interstitial cells of Cajal are located between smooth muscle cells and nerve endings throughout the GI tract and are responsible for the inherent pacemaker activity of the GI system. These cell bodies interact with smooth muscle cells to transduce contributions from the enteric motor neurons and turn these signals into the stimulus needed for phasic smooth muscle cells to propel the food bolus distally.
Enteroendocrine cells (EECs) are cells derived from endoderm epithelial cells that are abundant throughout the GI tract. These cells form the largest endocrine organ in the body and are responsible for many tasks, including GI secretion and motility. These cells function via endocrine and paracrine roles. They sense the contents of the lumen of the bowel and excrete neuropeptides that can act on distal organs or even act on cells nearby, including neurons of the enteric nervous system that control motility. Research has shown that EECs can act directly on cells of the enteric nervous system to help initiate and propagate the proper physiological response.
The vagus nerve derives from two separate origins depending on functionality. The motor aspect of the nerve derives from the basal plate of the medulla oblongata, and the sensory aspect arises from the neural crest. The neurons of the enteric nervous system derive from neural crest cells that migrate to occupy the GI tract. Interstitial cells of Cajal appear to arise from mesenchymal precursor cells. Enteroendocrine cells that are responsible for the management of GI hormones arise from pluripotent intestinal stem cells. These stem cells are present within intestinal crypts. Smooth muscles of the colon derive from mesoderm.
The gastrocolic reflex is multisystemic in origin. The reflex involves the autonomic nervous system, the enteric nervous system, and cells of the GI tract that regulate endocrine functions. Signals from the central nervous system communicate with the enteric nervous system and vice versa controlling peristalsis. The enteric nervous system proves to be paramount and is demonstrated by the morbid effects of enteric nervous system neuropathies; this is in contrast with the importance of vagal and sympathetic inputs, which have shown not to carry as much of an effect if these connections become interrupted.
The gastrocolic reflex is essentially the colonic response to food ingestion. Through a series of coordinated signals via the enteric nervous system and neuropeptides, the colon is stimulated via muscarinic pathways to contract, resulting in colonic migratory motor complexes or high amplitude propagating contractions (HAPCs) which usually occur in bursts and often after food intake. These colonic contractions following meal consumption help propel the food bolus toward the rectum for defecation. Neuropeptides like serotonin, gastrin, cholecystokinin, and prostaglandin E1 all have all implications as mediators of the response. According to a study enrolling “twenty-nine healthy volunteers with a colonoscopically positioned multi-lumen manometric probe and low-compliance infusion system,” the motor activity of the large bowel was significantly increased following consumption of a meal. This study also showed that the right colon and transverse colon showed a much faster, stronger increase in motor activity when compared to a slower, steadier increase in distal segments.
When food gets introduced into the stomach, a coordinated response via stretch receptors, neuropeptides, and the enteric nervous system activate the gastrocolic reflex, which in turn increases the motility in the colon to make room for more food. Migrating motor complexes induce food bolus movement through slow waves and faster segments of increased electrical activity, know as spike waves; this is very similar to how the stomach and small intestine move food. The large bowel also employs stronger, more frequent contractions known as mass movements in response to signals from mechanical stretch receptors in the stomach and the products of digestion in the small intestine. The enteric nervous system controls these mass movements and is most active in the transverse and left colon, which helps move food toward the rectum for defecation, which is the reason behind the urge to defecate following ingestion of a meal.
A colon transit study may be employed to test for the functionality of the gastrocolic reflex. The gold standard for measuring colon transit time utilizes a radiopaque indicator that is easy to do and relatively low cost. The only downside to this test is that it subjects the patient undergoing radiation exposure. Another test utilized is radionuclide scintigraphy. This is done using a labeled radioisotope and viewed through a specialized camera. The patient swallows a labeled radioisotope, and it gets followed throughout transit through the GI tract; this approach exposes a lesser degree of radiation. Both of these transit studies are usually for research purposes and less often used in clinical practice. Colonic manometry and bead expulsion are more frequently used to assess the contractility and motility of the colon. Colonic manometry is a more common modality in children with colonic dysmotility, encopresis, and abdominal pain. They record various colonic motor contractions and guide the further courses of treatment, including the need for surgical interventions. Lastly, a test that uses wireless motility capsules has been considered.
Patients that have irritable bowel syndrome have been shown to have a heightened gastrocolic response to ingested food. A common symptom of patients with IBS is the urge to defecate following a meal and the relief of symptoms like tenesmus, distension, and abdominal pain following defecation. This phenomenon is believed to be due to, in part, a heightened gastrocolic response. As discussed previously, any impairment of the neural or the hormonal mechanisms leading to decreased or absent gastrocolic reflux will result in decreased colonic transit of fecal matter and will lead to functional constipation. This presentation is more prevalent in older patients with spinal cord problems, and also diabetic neuropathy patients with gastroparesis.
The gastrocolic reflex has correlations with the pathogenesis of irritable bowel syndrome. The act of food consumption can provoke an overreaction of the gastrocolic response due to heightened visceral sensitivity seen in IBS patients, resulting in abdominal pain, constipation, diarrhea, bloating, and tenesmus. It is also a known fact that ondansetron decreases the tonic response to stretch, giving evidence toward its use in providing relief for patients with IBS. Commonly prescribed medications to treat overreactive gastrocolic response include antispasmodics, tricyclic antidepressants, and SSRIs. Antibiotics and probiotics have also been utilized to restore normal colonic flora, which in turn helps regulate the response of integral components of the reflex.
The gastrocolic reflex is most active during morning time and immediately after meals. Using this physiological reflex to our advantage helps treat constipation. For both children and geriatric patients with constipation, using the toilet immediately after having breakfast and establishing a daily routine helps to improve constipation. The use of stimulant laxatives like sennosides or bisacodyl will augment the gastrocolic reflex and helps in improved colonic contractions and defecation.
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