Motility of the gastrointestinal tract

GI motility is a function of circular and longitudinal smooth muscle also called tunica muscularis present in the walls of hollow GI organs. The muscles in the proximal two-thirds of the oesophagus and in the external anal sphincter are skeletal, the rest of the tunica muscularis contains smooth muscle cells. Gap junctions are present between the smooth muscle cells that facilitates coordination of contractions. The interstitial cells of Cajal are believed to be the source of spontaneous electrical impulses which then spreads to the adjoining smooth muscles. In a sense, cells of Cajal act like pacemakers of the GIT. This spontaneous electrical activity does not need neuronal input and leads to slow waves. Activation of Ca2±activated Cl− channels in cells of Cajal generates inward currents, producing slow waves. Slow waves conduct to smooth muscle cells, producing cycles of depolarization that can activate Ca2+ channels and lead to coupling of slow waves to smooth muscle contractions. The frequency of slow waves varies from 3 in the stomach to 12 in the duodenum. The GIT exhibits both tonic (sustained) and phasic (transient) contractions.

Excitation–contraction coupling occurs by calcium entry via L-type calcium channels causing depolarization which is followed by opening of T-type calcium channels that lead to calcium influx into the cell. Ca2+ binding to calmodulin activates myosin light chain kinase. Subsequent phosphorylation of myosin initiates cross-bridge cycling. Myosin phosphatase dephosphorylates myosin to relax muscles, and a process known as Ca2+ sensitization regulates the activity of the phosphatase. Other channels called TRP or transient receptor potential channels are voltage independent and nonselective for the cations. Hormones and vagal stimulation can open some other nonselective cation channels also leading to depolarization. Repolarization is by the opening of K+ channels. The intracellular Ca2+ levels in turn regulate the activity of all other channels.

Enteric neurons regulate the peristaltic reflex, segmentation movements, tonic contractions and control of sphincters. ACh acting on M2 and M3 receptors and substance P and neurokinin A acting on NK-1 and NK-2 receptors are excitatory to GIT. Nitric oxide (NO) is inhibitory. It activates guanylate cyclase leading to rise in intracellular cGMP, activation of protein kinase G, activation of K+ channels and decreased Ca2+ sensitivity.

Spontaneous pacemaker activity in the stomach, small intestine and colon (electrical slow waves) organizes contractile patterns into phasic contractions that are the basis for peristaltic or segmental motility patterns. Basal slow wave activity generates low amplitude contractions, and inhibitory or excitatory neural inputs modulate the amplitude of contractions during each cycle.

Deglutition or Swallowing: Swallowing has three phases—preparatory, transfer, and transport phases—that follow each other in a sequence. The preparatory phase includes conscious effort to ingest food and reflexes in the oral cavity that help the preparation of the bolus to be swallowed. The transfer phase involves reflex activities in the oral and pharyngeal passages. The transport phase includes transport of the swallowed food bolus through the esophagus into the stomach.

Anatomically, swallowing has been divided into three phases: oral, pharyngeal, and esophageal. The oral phase includes preparatory as well as early transfer phases. The oral preparatory phase includes chewing, the mixing of the food with saliva; and the formation of a bolus of suitable size and consistency. As the bolus enters the esophagus, the esophagus, including the lower esophageal sphincter (LES), relaxes to receive the bolus. The act of swallowing has voluntary and involuntary components. The preparatory/oral phase is voluntary, whereas the pharyngeal and esophageal phases are mediated by an involuntary reflex called the swallowing reflex.

The muscles of the oral cavity and tongue are voluntary and striated, of the pharynx and cervical esophagus are specialized and striated, and of the thoracic esophagus and LES are smooth. In addition, the sphincter muscles of the UES and LES are specialized and exhibit tonic contractions. The striated muscles of the oral cavity, pharynx, and cervical esophagus are innervated by lower motor neurons that are carried in cranial nerves, including the vagus. Lower motor neurons are excitatory in nature and excite striated muscles by releasing ACh at the motor end plates. The smooth muscles of thoracic esophagus and LES are innervated by the vagus and myenteric plexus. Moreover, the autonomic innervation has both an excitatory pathway and a parallel inhibitory pathway. Ach is excitatory while NO and VIP are inhibitory.

The swallowing center is located in the brainstem. The swallowing center innervates the motor nuclei of cranial nerves. Pharyngeal and esophageal peristalsis mediated by the swallowing reflex is known as primary peristalsis.

The nucleus of the solitary tract sends fibers to the nucleus ambiguus of the vagus. Primary peristaltic movements are mediated by the premotor neurons in solitary tract, which send projections to the caudal and rostral parts of the dorsal motor nucleus of vagus. The caudal part of the dorsal motor nucleus of vagus contains neurons of the inhibitory pathway to the esophagus, whereas the rostral part houses the excitatory pathway neurons to the esophagus. The inhibitory pathway neurons are activated first, this results in inhibition of all ongoing activity in the esophagus and relaxation of the LES. This is followed by sequential activation of neurons to distal areas of the esophagus. Afferents in the superior laryngeal nerves are important stimulators of the swallowing reflex.

Esophageal peristalsis that occurs in the thoracic esophagus without the associated pharyngeal contraction is known as secondary peristalsis. Its physiologic role is to clear the esophagus of food residues and refluxed materials by moving them to the stomach. Secondary peristalsis, which is elicited by esophageal distention, is executed entirely by a local intramural reflex. Transient LES relaxation, in which the LES may relax without associated peristaltic contraction reflex has been implicated as an important mechanism of gastroesophageal reflux.

Small intestinal motility: Chyme is the semi-digested food that passes from the stomach into the duodenum. The small intestine exhibits two types of contractions - segmentation and peristaltic contractions. Segmentation contractions lead to mixing of chyme with pancreatic enzymes and secretions. Peristaltic contractions help in movement of chyme along the small intestine. ACh and substance P stimulates movement while VIP and NO cause relaxation. Sympathetic stimulation inhibits movement.

Large intestinal motility: Segmental contractions of the large intestine lead to haustra formation. Contraction of the ileocecal sphincter prevents reflux of contents into the ileum. Mass movements of the colon help to move colonic contents over the colon and towards the rectum. They occur 1-3 times per day. In the gastrocolic reflex, distension of the stomach leads to increased mass movements.