Describe the contractions of the orad and caudad regions of the stomach.
Explain the regulation of the contractile activity of the stomach, including the role of slow waves.
List the components of the gastric contents that affect the rate of gastric emptying.
Understand the role of duodenal receptors in the regulation of gastric emptying.
Describe the changes in motility that regulate gastric emptying.
Describe the disorders that may result in an impairment of gastric emptying.
Motility of the stomach and upper small intestine is organized to accomplish the orderly emptying of contents into the duodenum in the presence of ingested material of variable quantity and composition. Accommodation and temporary storage of ingested material result from receptive relaxation of the orad stomach (see Chapter 3 ). Emptying, which also requires mixing ingested material with gastric juice and reducing the particle size of any solids that have been swallowed, results from integrated contractions of the orad stomach, caudad stomach, pylorus, and duodenum.
Gastric contractions result from activity of smooth muscle cells that are arranged in three layers: an outer longitudinal layer, a middle circular layer, and an inner oblique layer. The longitudinal layer is absent on the anterior and posterior surfaces of the stomach. The circular layer is the most prominent and is present in all areas of the stomach except the paraesophageal region. The oblique layer , the least complete, is formed from two bands of muscle lying on the anterior and posterior surfaces. These two bands meet at the gastroesophageal sphincter and fan out to fuse with the circular muscle layer in the caudad part of the stomach. Both the circular and the longitudinal muscle layers increase in thickness toward the duodenum.
The stomach is richly innervated with both intrinsic and extrinsic nerves. The intrinsic nerves lie in various plexuses, the most prominent being the myenteric plexus, which lies in a three-dimensional matrix between the longitudinal and circular muscle layers and throughout the circular muscle layer. The myenteric plexus receives nerve endings from other intrinsic plexuses, as well as from extrinsic nerves. Axons from neurons within the myenteric plexus synapse with the muscle fibers and with glandular cells of the stomach. Extrinsically the stomach is innervated by branches of the vagus nerves and by fibers originating in the celiac plexus of the sympathetic nervous system.
The pylorus , or gastroduodenal junction, is characterized by a thickening of the circular muscle layer of the distal antrum. Separating this bundle of muscle from the duodenum is a connective tissue septum; however, some of the longitudinal muscle fibers pass from the antrum to connect with muscle cells of the duodenum. The pylorus is richly innervated with both extrinsic and intrinsic nerves, and nerve endings within the thickened circular muscle layer are abundant. Many of these endings contain neuropeptides, especially enkephalin, and many produce and release nitric oxide (NO).
The anatomy of the proximal duodenum is similar to that of the rest of the intestine (described in Chapter 5 ). A significant difference is the larger number of intrinsic nerves present in this area compared with the rest of the small bowel. These nerves may be involved in the regulation of gastric emptying (described in a later section).
In addition to the muscle cells and nerves, interstitial cells of Cajal (ICCs) also are prominent in all regions and appear to play a prominent role in regulating motility. Many ICCs form gap junctions with smooth muscle cells, whereas others appear to create a bridge between nerve endings and smooth muscle cells.
Contractions of the Orad Region of the Stomach
As detailed in the previous chapter, the predominant motor activity of the orad region of the stomach is the accommodation of ingested material. The musculature of the orad stomach is thin, contractions are weak, and during the remainder of the digestive state, pressures are essentially equal to intraabdominal pressure, with superimposed tonic pressure changes. These pressure changes are predominantly of low amplitude and have durations of 1 minute or more. The contractions that produce these pressure changes reduce the size of the stomach as the stomach empties. These tonic contractions result in accommodation of the remaining gastric contents and propulsion of those contents into the caudad stomach. A consequence of this minimal contractile activity is that little mixing of ingested contents occurs in the orad stomach. Contents often remain in relatively undisturbed layers for an hour or more after eating. As a result, salivary amylase (see Chapter 7 ), which is inactivated by gastric acid, can digest a significant portion of the starch present in a meal. Little is known about the regulation of contractions in the orad stomach during digestion. Both gastrin and cholecystokinin (CCK) decrease contractions and increase gastric distensibility. However, only the effect of CCK appears to be physiologic.
Contractions of the Caudad Region of the Stomach
In the fasted state, the stomach is mostly quiescent. After eating, phasic contractions of variable intensity occur almost continuously. Contractions normally begin in the midstomach and move toward the gastroduodenal junction ( Fig. 4.1 ). Thus the primary contractile event is a peristaltic contraction . As contractions approach the gastroduodenal junction, they increase in both force and velocity. At any one locus of the human stomach, the duration of each contraction ranges between 2 and 20 seconds, and the maximum frequency is approximately three contractions per minute. Between contractions, pressures in the caudad region are near intraabdominal levels.
Contractions of the caudad region of the stomach serve to both mix and propel gastric contents. Once a contraction begins in the midportion of the stomach, gastric contents are propelled toward the gastroduodenal junction ( Fig. 4.2A ). As the contraction approaches the gastroduodenal junction, some contents are evacuated into the duodenum ( Fig. 4.2B ). However, because the peristaltic wave increases in velocity as it approaches the junction, the contraction overtakes the gastric contents. Once this occurs, most of the contents are propelled back into the main body of the stomach ( Fig. 4.2C ), where they remain until the next contraction sequence ( Fig. 4.2D ). This propulsion back into the stomach has been termed retropulsion. Retropulsion causes a thorough mixing of the gastric contents and mechanically reduces the size of solid particles. (See videos: www.wzw.tum.de/humanbiology/motvid01/movie_11_1mot01.wmv; www.wzw.tum.de/humanbiology/motvid01/movie_13_1mot01.wmv ; accessed March 2018).
Contractions of the caudad area of the stomach are controlled by interactions among smooth muscle cells and ICCs, as well as by nervous and humoral elements. Smooth muscle cells in this area have a membrane potential that fluctuates rhythmically with cyclic depolarizations and repolarizations. These fluctuations are called slow waves (also referred to as basic electric rhythm, pacesetter potentials, and control activity ). Slow waves have two components: an initial upstroke potential and a secondary plateau potential. In the stomach, slow waves can initiate significant contractions; thus some investigators refer to them as action potentials. However, slow waves are always present, regardless of the presence or absence of contractions. Their frequency is constant, and humans have approximately 3 cycles/minute (cpm). When slow waves are recorded from multiple sites between the midstomach and the gastroduodenal junction, they have the same frequency at all sites ( Fig. 4.3 ). However, slow waves do not occur simultaneously at all points along the stomach. Rather, a phase lag occurs; thus they seem to pass from an area in the midstomach toward the gastroduodenal junction. This phase lag between slow waves at equidistant points lessens as the gastroduodenal junction is neared. The frequency and velocity of the peristaltic waves are therefore controlled by the frequency and velocity of spread of the slow wave.