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FIGURE 8 Three sets of mechanical (g) and electrical (mV) tracings from the caudad region of the stomach. (A) Slow-wave depolarization of insufficient magnitude to cause contraction. (B) Increased depolarization results in contraction. (C) Electrical slow wave with multiple spike potentials and extended plateau produces a vigorous and extended contraction.

Although digestive events and the resulting neural and hormonal input to the stomach are not necessary for slow waves to occur, they markedly affect the amplitude of the slow waves and the degree of spiking on the plateau potential and, thus, the frequency of the contractions. These events have important regulatory effects on gastric motility. In general, vagal stimulation increases the force and frequency of contractions, whereas sympathetic stimulation decreases both of these parameters. Gastrin and motilin stimulates contractions, and secretin and gastric inhibitory peptide (GIP) decrease contractions. Motilin is responsible for the periodic contractions of the migrating motor complex during fasting. The physiologic significance of the gastric motor effects of gastrin, secretin, and GIP is doubtful.

Gastric Emptying

After a normal mixed meal, the stomach may contain 1500 mL of solids, ingested liquids, and gastric juice that take approximately 3 hr to empty into the duodenum. Gastric emptying is regulated by a variety of mechanisms to ensure that it occurs at a rate optimal for the digestion and absorption of nutrients and the neutralization of gastric contents. In general, the greater the volume, the more rapidly the contents empty. Liquids empty more rapidly than solids, and solids must be reduced in size to particles of 2 mm3 or less for emptying to occur. The regulation of emptying based on volume and particle size is, for the most part, intrinsic to the gastric smooth muscle itself.

The most rapidly emptying substance is isotonic saline. Both hypo- and hypertonic saline empty more slowly. The addition of calories, especially in the form of lipids, or acid further slows emptying. The receptors for these responses are located in the duodenal mucosa and are sensitive to changes in osmolarity, pH, or lipid content. Receptor activation triggers several neural and hormonally mediated mechanisms that inhibit gastric emptying. For example, fats release CCK, which physiologically inhibits emptying. Acid, when placed in the duodenum, inhibits motility and gastric emptying with a latent period as short as 20-40 sec, indicating that the inhibition is due to a neural reflex. This reflex appears to be entirely intrinsic, with information from the duodenal receptors to the gastric smooth muscle carried by the neurons of the intramural plexuses. Other hormones such as secretin and GIP also inhibit emptying, but do not appear to do so in physiologic concentrations. Much of the regulation of gastric emptying is mediated by as yet undefined pathways.

FIGURE 8 Three sets of mechanical (g) and electrical (mV) tracings from the caudad region of the stomach. (A) Slow-wave depolarization of insufficient magnitude to cause contraction. (B) Increased depolarization results in contraction. (C) Electrical slow wave with multiple spike potentials and extended plateau produces a vigorous and extended contraction.

Clinical Note

Most disorders of gastric motility result in abnormalities of gastric emptying. Impaired emptying produces symptoms of fullness, loss of appetite, nausea, and sometimes vomiting. Reduced emptying may be caused by obstruction of the gastroduodenal canal by peptic ulcers or cancer. Vagotomy, which may be performed to reduce acid secretion in patients with peptic ulcer disease, delays gastric emptying. This is usually prevented by a procedure called pyloroplasty, in which the surgeon cuts and weakens the muscle in the pyloric area. A rapid rate of gastric emptying may result in diarrhea due to the osmotic load placed in the small intestine during a given time period. Increased rates of gastric emptying are also associated with duodenal ulcer disease, indicating that the acid entering the intestine cannot be neutralized before it damages the duodenal mucosa.

Inhibition of gastric emptying results from a variety of changes in gastric and duodenal motility. These include increased distensibility of the orad stomach (this is the effect of CCK, for example), decreased frequency and force of peristaltic contractions in the caudad stomach, decreased diameter of the pylorus, and increased tone and, hence, pressure of the proximal duodenum. Although noticeable differences exist between the motility of the distal stomach and proximal duodenum, it is unclear whether a true sphincter exists at the pylorus. Some investigators have demonstrated a zone of increased pressure (indicative of a sphincter) between the human stomach and duodenum, but others have failed to do so. It is also uncertain whether a distinct anatomic ring of circular muscle exists between the two. However, recent studies have shown that the pylorus can contract independently and produce a large effect on gastric emptying.

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