The rate at which the stomach empties is regulated by signals from both the stomach and the duodenum. However, the duodenum provides by far the more potent of the signals, controlling the emptying of chyme into the duodenum at a rate no greater than the rate at which the chyme can be digested and absorbed in the small intestine.
Gastric Factors That Promote Emptying
Effect of Gastric Food Volume on Rate of Emptying. Increased food volume in the stomach promotes increased emptying from the stomach. However, this increased emptying does not occur for the reasons that one would expect. It is not increased storage pressure of the food in the stomach that causes the increased emptying because, in the usual normal range of volume, the increase in volume does not increase the pressure much. How ever, stretching of the stomach wall does elicit local myenteric reflexes in the wall that greatly accentuate activity of the pyloric pump and at the same time inhibit the pylorus.
Effect of the Hormone Gastrin on Stomach Emptying. In Chapter 65, we discuss how stretching of the stomach wall and the presence of certain types of foods in the stomach—particularly digestive products of meat—elicit release of the hormone gastrin from the G cells of the antral mucosa. This has potent effects to cause secretion of highly acidic gastric juice by the stomach glands. Gastrin also has mild to moderate stimulatory effects on motor functions in the body of the stomach. Most important, it seems to enhance the activity of the pyloric pump. Thus, gastrin likely promotes stomach emptying.
Powerful Duodenal Factors That Inhibit Stomach Emptying
Inhibitory Effect of Enterogastric Nervous Reflexes From the Duodenum. When food enters the duodenum, multiple nervous reflexes are initiated from the duodenal wall. These reflexes pass back to the stomach to slow or even stop stomach emptying if the volume of chyme in the duodenum becomes too much. These reflexes are mediated by three routes: (1) directly from the duodenum to the stomach through the enteric nervous system in the gut wall, (2) through extrinsic nerves that go to the prevertebral sympathetic ganglia and then back through inhibitory sympathetic nerve fibers to the stomach, and (3) probably to a slight extent through the vagus nerves all the way to the brain stem, where they inhibit the normal excitatory signals transmit ted to the stomach through the vagi. All these parallel reflexes have two effects on stomach emptying: First, they strongly inhibit the “pyloric pump” propulsive contractions, and second, they increase the tone of the pyloric sphincter.
The types of factors that are continually monitored in the duodenum and can initiate enterogastric inhibitory reflexes include the following:
1. Distention of the duodenum
2. The presence of any irritation of the duodenal mucosa
3. Acidity of the duodenal chyme
4. Osmolality of the chyme
5. The presence of certain breakdown products in the chyme, especially breakdown products of proteins and, perhaps to a lesser extent, of fats
The enterogastric inhibitory reflexes are especially sensitive to the presence of irritants and acids in the duodenal chyme, and they often become strongly activated within as little as 30 seconds. For instance, whenever the pH of the chyme in the duodenum falls below about 3.5 to 4, the reflexes frequently block further release of acidic stomach contents into the duodenum until the duodenal chyme can be neutralized by pancreatic and other secretions.
Breakdown products of protein digestion also elicit inhibitory enterogastric reflexes; by slowing the rate of stomach emptying, sufficient time is ensured for adequate protein digestion in the duodenum and small intestine.
Finally, either hypotonic fluids or, especially, hyper tonic fluids elicit the inhibitory reflexes. Thus, flow of nonisotonic fluids into the small intestine at too rapid a rate is prevented, thereby also preventing rapid changes in electrolyte concentrations in the wholebody extracellular fluid during absorption of the intestinal contents.
Hormonal Feedback From the Duodenum Inhibits Gastric Emptying—Role of Fats and the Hormone Cholecystokinin. Hormones released from the upper intestine also inhibit stomach emptying. The stimulus for releasing these inhibitory hormones is mainly fats entering the duodenum, although other types of foods can increase the hormones to a lesser degree.
Upon entering the duodenum, the fats extract several different hormones from the duodenal and jejunal epithelium, either by binding with “receptors” on the epithelial cells or in some other way. In turn, the hormones are carried by way of the blood to the stomach, where they inhibit the pyloric pump and at the same time increase the strength of contraction of the pyloric sphincter. These effects are important because fats are much slower to be digested than most other foods.
Precisely which hormones cause the hormonal feedback inhibition of the stomach is not fully clear. The most potent of these hormones appears to be cholecystokinin (CCK), which is released from the mucosa of the jejunum in response to fatty substances in the chyme. This hormone acts as an inhibitor to block increased stomach motility caused by gastrin.
Other possible inhibitors of stomach emptying are the hormones secretin and glucose-dependent insulinotropic peptide, also called gastric inhibitory peptide (GIP). Secretin is released mainly from the duodenal mucosa in response to gastric acid passed from the stomach through the pylorus. GIP has a general but weak effect of decreasing gastrointestinal motility.
GIP is released from the upper small intestine mainly in response to fat in the chyme, but to a lesser extent in response to carbohydrates as well. Although GIP inhibits gastric motility under some conditions, its main effect at physiological concentrations is probably mainly to stimulate secretion of insulin by the pancreas.
These hormones are discussed at greater length else where in this text, especially in Chapter 65 in relation to control of gallbladder emptying and control of the rate of pancreatic secretion.
In summary, hormones, especially CCK, can inhibit gastric emptying when excess quantities of chyme, especially acidic or fatty chyme, enter the duodenum from the stomach.
Summary of the Control of Stomach Emptying
Emptying of the stomach is controlled only to a moderate degree by stomach factors such as the degree of filling in the stomach and the excitatory effect of gastrin on stomach peristalsis. Probably the more important control of stomach emptying resides in inhibitory feedback signals from the duodenum, including both enterogastric inhibitory nervous feedback reflexes and hormonal feedback by CCK. These feedback inhibitory mechanisms work together to slow the rate of emptying when (1) too much chyme is already in the small intestine or (2) the chyme is excessively acidic, contains too much unprocessed protein or fat, is hypotonic or hypertonic, or is irritating. In this way, the rate of stomach emptying is limited to the amount of chyme that the small intestine can process.
