Oesophagus And Stomach
It is possible to swallow food and drink and for it to enter the stomach
while standing on one’s head or
experiencing zero gravity. A ring of skeletal muscle called the upper
oesophageal sphincter usually closes the pharyngeal end of the oesophagus.
During the oesophageal phase of swallowing, this sphincter is relaxed,
allowing the bolus of food to pass through it. Immediately afterwards, the
sphincter closes. Once in the oesophagus, the bolus is propelled the 25 cm
(approximately) to the stomach by a process called peristalsis, a
coordinated wave of relaxation in front of the bolus and contraction behind the
bolus of the circular and longitudinal muscle layers of the oesophagus, forcing
the food into the stomach in about 5 s. Before the bolus enters the stomach, it
passes through another sphincter, the lower oesophageal sphincter,
formed from a ring of smooth muscle which relaxes as the peristaltic wave
reaches it. The swallowing centres in the medulla produce a sequence of
events that lead to both efferent activity to somatic nerves (innervating
skeletal muscle) and autonomic nerves (innervating smooth muscle). This
sequence of events is influenced by afferent receptors in the oesophagus wall
sending impulses back to the medulla. The sphincters and the peristaltic waves
are principally controlled by activity in the vagus nerve and aided by a
high degree of coordination of the activity within the enteric nerve
plexuses within the tract itself.
Once the bolus of food passes
through the lower oesophageal sphincter, it enters the stomach (Fig.
38a). The main functions of the stomach are to store food
temporarily (as it can be ingested more rapidly than it can be digested) to
chemically and mechanically digest food using acids, enzymes and
movements, to regulate the release of the resulting chyme into
the small intestine, and to secrete a substance called intrinsic factor which
is essential for the absorption of vitamin B12. The stomach lies immediately
below the diaphragm and, like the rest of the gastrointestinal tract, it has
longitudinal and circular muscle layers and nerve plexuses in its walls;
however, within the mucosa are specialized secretory cells that line the
gastric glands or pits (Fig. 38b). When empty, the stomach has a volume of
approximately 50 mL; however, when fully distended, its volume can be as much
as 4 L. Proteins in the food are broken down into polypeptides in
the stomach by enzymes called pepsins. These enzymes are produced in an inactive
form called pepsinogens by the chief cells in the gastric mucosa,
and are converted into active pepsins by the acid environment in the stomach
(Fig. 38c). The acid in the stomach is hydrochloric acid and is produced
by a specialized group of cells called parietal cells. The stomach can
secrete as much as 2 L of acid per day, and the concentration of H+ ions in the
stomach is estimated to be about 1 million times higher than that in the blood.
This concentration of H+ ions requires a very efficient exchange of
intracellular H+ for extracellular K+ using energy provided by the breakdown of
adenosine triphosphate (ATP). This is achieved using a protein known as the proton
pump or the H+–K+ ATPase protein (Fig. 38d).
The gastric mucosa does not digest
itself because it is protected by an alkaline, mucin-rich fluid secreted
by the gastric glands, which acts as a mucosal barrier by bathing the gastric
epithelial cells. In addition,
local mediators, such as prostaglandins, are released when the mucosa is irritated, and these increase the
thickness of the mucous layer and stimulate the production of bicarbonate
which neutralizes the acid.
Control of gastric secretions
Gastric secretions occur in
basically three phases: cephalic, gastric and intestinal (Fig.
38e). The cephalic phase is brought about by the sight, smell,
taste and mastication of food. At this stage, there is no food in
the stomach and acid secretion is stimulated by the activation of the vagus and
its actions on the enteric plexus. Postganglionic parasympathetic
fibres in the myenteric plexus cause the release of acetylcholine
(ACh) and stimulate the release of gastric juices from the gastric
glands. Vagal stimulation also causes the release of a hormone called gastrin
from cells in the antrum of the stomach called G-cells. Gastrin is
secreted into the bloodstream and, when it reaches the gastric glands, it
stimulates the release of acid and pepsinogens. Both vagal
activity and gastrin also stimulate the release of histamine from mast
cells, which, in turn, acts on parietal cells to produce more acid.
When food arrives in the stomach,
it stimulates the gastric phase of secretion of acid, pepsinogen
and mucus. The main stimuli for this phase are the distension of
the stomach and the chemical composition of the food. Mechanoreceptors
in the stomach wall are stretched and set up local myenteric reflexes and also
longer vagovagal reflexes. Both cause the release of ACh which
stimulates the release of gastrin, histamine and, in turn, acid,
enzymes and mucus. Stimulation of the vagus also releases
a specific peptide, gastrin-releasing peptide (GRP), which mainly
acts directly on the G-cells to release gastrin. Whole proteins
do not affect gastric secretions directly, but their break- down products, such
as peptides and free amino acids, do so by directly
stimulating gastrin secretion. A low pH (more acid) in the stomach inhibits
gastrin secretion; therefore, when the stomach is empty or after food has
entered it and acid has been secreted for some time, there is an inhibition of
acid production. However, when food first enters the stomach, the pH rises (less
acid) and this leads to a release of the inhibition and causes a maximum
secretion of gastrin. Thus, gastric acid secretion is self-regulating.
The gastric phase normally
lasts for about 3 h and the food in the stomach is converted into a sludge-like
material called chyme. The chyme enters the first part of the
small intestine, the duodenum, through the pyloric sphincter. The
presence of chyme in the pyloric antrum distends it and causes antral
contractions and opening of the sphincter. The rate at which the stomach
empties depends on the volume in the antrum and the fall in the pH of the
chyme, both leading to an increase in emptying. However, distension of
the duodenum, the presence of fats and a decrease in pH in the
duodenal lumen all cause an inhibition of gastric emptying. This
mechanism leads to a precise supply of chyme to the intestines at a rate
appropriate for it to be digested properly. (For a description of the intestinal phase of gastric secretion, see
Chapter 39.)
