STOMACH

ANATOMY
 The stomach is readily recognizable as the asymmetrical, pearshaped, most proximal abdominal
organ of the digestive tract
 parts
cardia The part of the stomach attached to the esophagus. Just proximal to the cardia at the
gastroesophageal (GE) junction is the anatomically indistinct but physiologically
demonstrable lower esophageal sphincter. At the distal end, the readily apparent pyloric
sphincter connects the stomach to the proximal duodenum. The stomach is relatively fixed at
these points, but the large midportion is quite mobile with the shorter lesser curvature on
the right and the longer greater curvature on the left.
o fundus The superior-most part of the stomach which is the distensible bounded superiorly
by the diaphragm and laterally by the spleen. The angle of His is where the fundus meets the
left side of the GE junction. Generally, the inferior extent of the fundus is considered to be the
horizontal plane of the GE junction, where the body (corpus) of the stomach begins.
o It is usually full of gas
o Significance
 To identify the side (right or left) of the body in a plain X-ray
abdomen.
 In achalasia cardia, fundic air bubble is absent.
 Fundic 'Wrap' is used in hiatus hernia.
 GISTs (gastroinstestinal stromal tumours) are common in fundus.
o The body of the stomach contains most of the parietal (oxyntic) cells, some of which are also
present in the cardia and fundus.
o Significance
 Ability to have a large meal is due to receptive relaxation of the
body of the stomach.
 Greater curvature is located at the level of umbilicus. Classical
gastrojejunostomy (GJ) , anterior or posterior, involves using body
of the stomach.
o
o Antrum At the angularis, incisura the lesser curvature turns rather abruptly to the right,
marking the anatomic beginning of the antrum, which comprises the distal 25% to 30% of
the stomach.
o Significance
 Pyloric antrum is a common site for gastritis , ulcer and carcinoma.
 Incompetence of pyloric sphincter results in severe duodenogastric
reflux.
 The organs that commonly abut the stomach are the liver, colon, spleen, pancreas, and occasionally
the kidney. The left lateral segment of the liver usually covers a large part of the anterior stomach.
 Inferiorly, the stomach is attached to the transverse colon by the gastrocolic omentum. The lesser
curvature is tethered to the liver by the hepatogastric ligament, also referred to as the lesser
omentum or pars flaccida.
 Posterior to the stomach is the lesser omental bursa and the pancreas.


Arterial and Venous Blood Supply

It is mainly supplied by coeliac trunk and its branches:
 1. Left gastric artery is a direct branch of coeliac trunk. It ascends up to
oesophageal hiatus and turns to the right along the lesser curvature of stomach.
It branches and anastomoses with branches of right gastric artery and supplies
anterior and posterior wall of the stomach. The consistently largest artery to the stomach
is the left gastric artery
1. Right gastric artery is a branch of hepatic artery which comes from coeliac
trunk. ft also supplies lesser curvature and body of stomach, along with left
gastric artery.
2. Left gastroepiploic artery arises from splenic artery and supplies greater
curvature of stomach and anastomoses with right gastroepiploic artery.
3. Right gastroepiploic artery is a branch of gastroduodenal artery, which is a
branch of hepatic artery. The second largest artery to the stomach is the right gastroepiploic
4. Short gastric arteries are the branches of splenic artery. They supply the
fundus of the stomach. They are also called vasa braevia.
Venous drainage
 Veins run with the corresponding arteries.
 Right and left gastric veins drain into the portal vein directly.
 Right gastroepiploic vein joins superior mesenteric vein.
 Left gastroepiploic vein and vasa braevia join splenic vein
 Prepyloric vein of Mayo is a useful guide to the junction between stomach and
duodenum

The richness of the gastric blood supply and the extensiveness of the anastomotic connections have some
important clinical implications, such as:
a) At least two of the four named gastric arteries may be occluded or ligated with impunity.
b) Following radical subtotal gastrectomy during which the right and left gastric arteries and
both gastroepiploic arteries are all ligated, the gastric remnant is adequately supplied by
short gastric arteries as long as the splenic artery is patent and intact;
c) Angiographic control of gastric bleeding from deep ulcer or tumor often requires
embolization of more than one feeding artery;
d) Because of the rich venous interconnections in the stomach, a distal splenorenal shunt,
which connects the distal end of the divided splenic vein to the side of the left renal vein, can
effectively decompress esophagogastric varices in patients with portal hypertension.
Lymphatic Drainage
 Generally speaking, the gastric lymphatics parallel the blood vessels.
 The cardia and medial half of the corpus commonly drain to nodes along the left gastric and celiac
axis.
 The lesser curvature side of the antrum usually drains to the right gastric and pyloric nodes,
 while the greater curvature half of the distal stomach drains to the nodes along the right
gastroepiploic chain.
 The proximal greater curvature side of the stomach usually drains into nodes along the left
gastroepiploic or splenic hilum.
 The nodes along both the greater and lesser curvature commonly drain into the celiac nodal basin.
There is a rich anastomotic network of lymphatics that drain the stomach,boften in a somewhat
unpredictable fashion. Thus, a tumor arising in the distal stomach may give rise to positive lymph
nodes in the splenic hilum.
 The rich intramural plexus of lymphatics and veins accounts for the fact that there can be
microscopic evidence of malignant cells in the gastric wall at a resectionvmargin that is several
centimeters away from palpable malignant tumor. It also helps explain the not infrequent
finding of positive lymph nodes which may be many centimeters away from the
primary tumor, with closer nodes that remain negative.
Innervation
  The vagus nerves provide the extrinsic parasympathetic innervations to the stomach, and
acetylcholine is the most important neurotransmitter.
 From the vagal nucleus in the floor of the fourth cerebral ventricle, the vagus traverses
the neck in the carotid sheath and enters the mediastinum, where it gives off the
recurrent laryngeal nerve and divides into several branches around the esophagus. These
branches come together again above the esophageal hiatus and form the left (anterior)
and right (posterior) vagal trunks (mnemonic LARP). Near the GE junction the anterior
vagus sends a branch (or branches) to the liver in the gastrohepatic ligament, and
continues along the lesser curvature as the anterior nerve of Latarjet (Fig. 26-5).
Similarly, the posterior vagus sends branches to the celiac plexus and continues along the
posterior lesser curvature.
 Vagal fibers originating in the brain synapse with neurons in Auerbach’s myenteric plexus
and Meissner’s submucosal plexus. In the stomach the vagus nerves affect secretion
(including acid), motor function, and mucosal bloodflow and cytoprotection. They also
play a role in appetite control and perhaps even mucosal immunity and inflammation
 The extrinsic sympathetic nerve supply to the stomach originates at spinal levels T5
through T10 and travels in the splanchnic nerves to the celiac ganglion. Postganglionic
sympathetic nerves then travel from the celiac ganglion to the stomach along the blood
vessels.
 Neurons in the myenteric and submucosal plexuses constitute the intrinsic nervous
system of the stomach. There may be more intrinsic gastric neurons than extrinsic
neurons, but theirfunction is poorly understood.

Histology
 There are four distinct layers of the gastric wall: mucosa, submucosa, muscularis propria,
and serosa .
 mucosa, which is lined with columnar epithelial cells of various types. Beneath the
basement membrane of the epithelial cells is the lamina propria, which contains
connective tissue, blood vessels, nerve fibers, and inflammatory cells. Beneath the lamina
propria is a thin muscle layer called the muscularis mucosa, the deep boundary of the
mucosal layer of the gut. The epithelium, lamina propria, and muscularis mucosa
constitute the mucosa.14
 The gastric glands are lined with different types of epithelial cells,.
o Throughout the stomach, the carpet consists primarily of mucus-secreting
surface epithelial cells (SECs) that the cytoplasmic tubulovesicles fuse with the
membrane of the secretory canaliculus
o Progenitor cells at the base of the glands differentiate and replenish sloughed
cells on a regular basis.
o Parietal cells These are in the body (acid-secreting portion) of the
stomach and line the gastric crypts, being more abundant distally. They are
responsible for the production of hydrogen ions to form hydrochloric acid. The
hydrogen ions are actively secreted by the proton pump, a hydrogen–
potassium-ATPase (Sachs), which exchanges intraluminal potassium for
hydrogen ions. The potassium ions enter the lumen of the crypts passively,
but the hydrogen ions are pumped against an immense concentration
gradient (1 000 000:1).
o Arguably, parietal cells produce the only truly essential substance made by the
stomach (i.e., intrinsic factor).
o Chief cells These lie principally proximally in the gastric crypts and
produce pepsinogen. Two forms of pepsinogen are described: pepsinogen I
and pepsinogen II. Both are produced by the chief cell, but pepsinogen I is
produced only in the stomach. The ratio between pepsinogens I and II in the
serum decreases with gastric atrophy. Pepsinogen is activated in the stomach
to produce the digestive protease, pepsin.
 o Endocrine cells The stomach has numerous endocrine cells, which are
critical to its function.
o In the gastric antrum, the mucosa contains G cells, which produce gastrin.
o Throughout the body of the stomach, enterochromaffin-like (ECL) cells are
abundant and produce histamine, a key factor in driving gastric acid
secretion.
o In addition, there are large numbers of somatostatin-producing D cells
throughout the stomach, and somatostatin has a negative regulatory role.
 Histologic analysis suggests that in the normal stomach, 13% of the epithelial cells are
oxyntic (parietal) cells, 44% are chief (zymogenic) cells, 40% are mucous cells, and 3%
are endocrine cells. In general, the antrum produces gastrin but not acid, and the
proximal stomach produces acid but not gastrin. The border between the corpus and
antrum migrates proximally with age (especially on the lesser curvature side of the
stomach).
 submucosa, which is rich in branching blood vessels, lymphatics, collagen, various
inflammatory cells, and nerve fibers and ganglion cells of Meissner’s autonomic
submucosal plexus. The collagen-rich submucosa gives strength to GI anastomoses
 The mucosa andsubmucosa are folded into the grossly visible gastric rugae, which tend to
flatten out as the stomach becomes distended.
 muscularis propria ( muscularis externa), which consists of an incomplete inner
oblique layer, a complete middle circular layer (continuous with the esophageal circular
muscle and the circular muscle of the pylorus), and a complete outer longitudinal layer
(continuous with the longitudinal layer of the esophagus and duodenum). Within the
muscularis propria is the rich network of autonomic ganglia and nerves that make up
Auerbach’s myenteric plexus. Specialized pacemaker cells, the interstitial cells of Cajal
(ICC), also are present.
The serosa, also known as the visceral peritoneum. This layer provides significant
tensile strength to gastric anastomoses. When tumors originating in the mucosa penetrate and
breach the serosa, microscopic or gross
peritoneal metastases are common, presumably from shedding of tumor cells that would not
have occurred if the serosa had not been penetrated. In this way, the serosa may be thought of
as an outer envelope of the stomach.
PHYSIOLOGY
The stomach stores food and facilitates digestion through a
variety of secretory and motor functions. Important secretory
functions include the production of acid, pepsin, intrinsic factor,
mucus, and a variety of GI hormones. Important motor functions
include food storage (receptive relaxation and accommodation),
grinding and mixing, controlled emptying of ingested
food, and periodic interprandial “housekeeping.”
Acid Secretion
Hydrochloric acid in the stomach hastens both the physical and
(with pepsin) the biochemical breakdown of ingested food. In
an acidic environment, pepsin and acid facilitate proteolysis.
Gastric acid also inhibits the proliferation of ingested pathogens,
which protects against both infectious gastroenteritis and
intestinal bacterial overgrowth. Long-term acid suppression
with proton pump inhibitors (PPIs) has been associated with an
increased risk of community acquired Clostridium difficile colitis
and other gastroenteritis, presumably because of the absence
of this protective germicidal barrier.18,19
Parietal Cell. The parietal cell is stimulated to secrete acid
(Fig. 26-12) when one or more of three membrane receptor types
is stimulated by acetylcholine (from vagal nerve fibers), gastrin
(from D cells), or histamine (from ECL cells).7,20,21 The enzyme
H/K-ATPase is the proton pump. It is stored within the intracellular
tubulovesicles and is the final common pathway for gastric

acid secretion. When the parietal cell is stimulated, there is a

cytoskeletal rearrangement and fusion of the tubulovesicles with
the apical membrane of the secretory canaliculus. The heterodimer
assembly of the enzyme subunits into the microvilli of the
secretory canaliculus results in acid secretion, with extracellular
potassium being exchanged for cytosolic hydrogen. Although
electro-neutral, this is an energy requiring process because the
hydrogen is secreted against a gradient of at least 1 million-fold,
which explains why the parietal cell is packed with energy producing
mitochondria. During acid production, potassium and

chloride are also secreted into the apical secretory canaliculus

through separate channels, providing potassium to exchange for
Hvia the H/K-ATPase, and chloride to accompany the secreted
hydrogen. At the basolateral membrane, the combined activity of
various cotransporters and ion exchangers accomplishes intracellular
pH regulation and electrolyte homeostasis.20
The normal human stomach contains approximately 1 billion
parietal cells, and total gastric acid production is proportional to
parietal cell mass. The potent acid-suppressing PPI drugs irreversibly
interfere with the function of the H/K-ATPase molecule.

These agents must be incorporated into the activated enzyme to

be effective, and thus work best when taken before or during a
meal (when the parietal cell is stimulated). When PPI therapy
is stopped, acid secretory capability gradually returns (within
days) as new H/K-ATPase is synthesized.
Gastrin, acetylcholine, and histamine stimulate the parietal
cell to secrete hydrochloric acid (see Fig. 26-12). Gastrin binds
to type B cholecystokinin (CCK) receptors, and acetylcholine
binds to M3 muscarinic receptors. Both stimulate phospholipase
C via a G-protein–linked mechanism leading to increased
production of inositol trisphosphate from membrane bound
phospholipids. Inositol trisphosphate stimulates the release of
calcium from intracellular stores, which leads to activation of

protein kinases and activation of H/K-ATPase. Histamine

binds to the histamine 2 (H2) receptor, which stimulates adenylatecyclase,
also via a G-protein–linked mechanism. Activation
of adenylatecyclase results in an increase in intracellular cyclic
adenosine monophosphate which activates protein kinases,
leading to increased levels of phosphoproteins and activation of
the proton pump. Somatostatin from mucosal D cells binds to
membrane receptors and inhibits the activation of adenylatecyclase
through an inhibitory G protein.
Physiologic Acid Secretion. Food ingestion is the physiologic
stimulus for acid secretion (Fig. 26-13). The acid secretory
response that occurs after a meal is traditionally described
in three phases: cephalic, gastric, and intestinal.22,23 The cephalic
or vagal phase begins with the thought, sight, smell, and/or taste
of food. These stimuli activate several cortical and hypothalamic
sites (e.g., tractus solitarius, dorsal motor nucleus, and
dorsal vagal complex), and signals are transmitted to the stomach
by the vagal nerves. Acetylcholine is released, leading to
stimulation of ECL cells and parietal cells. Although the acid
secreted per unit of time in the cephalic phase is greater than
in the other two phases, the cephalic phase is shorter. Thus,
the cephalic phase accounts for no more than 30% of total acid
secretion in response to a meal. Sham feeding (chewing and
spitting) stimulates gastric acid secretion only via the cephalic
phase, and results in acid secretion that is about half of that seen
in response to IV pentagastrin or histamine.
When food reaches the stomach, the gastric phase of
acid secretion begins. This phase lasts until the stomach is
empty, and accounts for about 60% of the total acid secretion
in response to a meal. The gastric phase of acid secretion has
several components. Amino acids and small peptides directly
stimulate antral G cells to secrete gastrin, which is carried in the
bloodstream to the parietal cells and stimulates acid secretion in
an endocrine fashion. In addition, proximal gastric distention

INTRODUCTION
The function of the stomach is to act as a reservoir for ingested
food. It also serves to break down foodstuffs mechanically and
commence the processes of digestion before these products
are passed on into the duodenum.
GROSS ANATOMY OF THE
STOMACH AND DUODENUM
Blood supply
Arteries
The stomach has an arterial supply on both lesser and greater
curves (Figure 63.1). On the lesser curve, the left gastric
artery, a branch of the coeliac axis, forms an anastomotic
arcade with the right gastric artery, which arises from the
common hepatic artery. Branches of the left gastric artery pass
up towards the cardia. The gastroduodenal artery, which is
also a branch of the hepatic artery, passes behind the first part
of the duodenum, highly relevant with respect to the bleeding
duodenal ulcer. Here it divides into the superior pancreaticoduodenal
artery and the right gastroepiploic artery. The
superior pancreaticoduodenal artery supplies the duodenum
and pancreatic head, and forms an anastomosis with the
inferior pancreaticoduodenal artery, a branch of the superior
mesenteric artery. The right gastroepiploic artery runs along
the greater curvature of the stomach, eventually forming an
anastomosis with the left gastroepiploic artery, a branch of
the splenic artery. This vascular arcade, important for the
construction of the gastric conduit in oesophageal resection,
is often variably incomplete. The fundus of the stomach is
supplied
by the vasa brevia (or short gastric arteries), which
arise from near the termination of the splenic artery.
Veins
In general, the veins are equivalent to the arteries, those
along the lesser curve ending in the portal vein and those on
the greater curve joining via the splenic vein. On the lesser
curve, the coronary vein is particularly important. It runs up
the lesser curve towards the oesophagus and then passes left
to right to join the portal vein. This vein becomes markedly
dilated in portal hypertension.

Lymphatics
The lymphatics of the stomach are of considerable importance
in the surgery of gastric cancer and are therefore described in
detail in that section.
Nerves
As with the entire gastrointestinal tract, the stomach and
duodenum possess both intrinsic and extrinsic nerve supplies.
The intrinsic nerves exist principally in two plexuses, the
myenteric plexus of Auerbach and the submucosal plexus of
Meissner. Compared with the rest of the gut, the submucosal
plexus of the stomach contains relatively few ganglionic cells,
as does the myenteric plexus in the fundus. However, in the
antrum the ganglia of the myenteric plexus are well developed.
The extrinsic supply is derived mainly from the vagus
nerves (CN XI), fibres of which originate in the brainstem.
The vagal plexus around the oesophagus condenses into bundles
that pass through the oesophageal hiatus (Figure 63.2),
the posterior bundle being usually identifiable as a large nerve
trunk. Vagal fibres are both afferent (sensory) and efferent.
The efferent fibres are involved in the receptive relaxation of
the stomach and the stimulation of gastric motility, as well as
having the well-known secretory function. The sympathetic
supply is derived mainly from the coeliac ganglia.
MICROSCOPIC ANATOMY
OF THE STOMACH AND
DUODENUM
The gastric epithelial cells are mucus producing and are
turned over rapidly. In the pyloric part of the stomach, and
also the duodenum, mucus-secreting glands are found. Most
of the specialised cells of the stomach (parietal and chief
cells) are found in the gastric crypts (Figure 63.3). The stomach
also has numerous endocrine cells.

Duodenum
The duodenum is lined by a mucus-secreting columnar epithelium.
In addition, Brunner’s glands lie beneath the mucosa
and are similar to the pyloric glands in the pyloric part of the
stomach. Endocrine cells in the duodenum produce cholecystokinin
and secretin.
PHYSIOLOGY OF THE STOMACH
AND DUODENUM
The stomach mechanically breaks up ingested food and,
together with the actions of acid and pepsin, forms chyme
that passes into the duodenum. In contrast with the acidic
environment of the stomach, the environment of the duodenum
is alkaline, due to the secretion of bicarbonate ions
from both the pancreas and the duodenum. This neutralises
the acid chyme and adjusts the luminal osmolarity to

approximately
that of plasma. Endocrine cells in the duodenum
produce cholecystokinin, which stimulates the pancreas
to produce trypsin and the gall bladder to contract. Secretin
is also produced by the endocrine cells of the duodenum. This
hormone inhibits gastric acid secretion and promotes production
of bicarbonate by the pancreas.

Gastric acid secretion

The secretion of gastric acid and pepsin tends to run in parallel,
although the understanding of the mechanisms of gastric acid
secretion is considerably greater than that of pepsin. Numerous
factors are involved to some degree in the production of
gastric acid. These include neurotransmitters, neuropeptides
and peptide hormones. This complexity need not detract from
the fact that there are basic principles that are relatively easily
understood (Figure 63.4). Hydrogen ions are produced by the
parietal cell by the proton pump. Although numerous factors
can act on the parietal cell, the most important of these is histamine,
which acts via the H2-receptor. Histamine is produced,
in turn, by the ECL cells of the stomach and acts in a paracrine
(local) fashion on the parietal cells. These relationships
explain why proton pump inhibitors can abolish gastric acid
secretion, as they act on the final common pathway – hydrogen
ion secretion. H2-receptor antagonists have profound effects
on gastric acid secretion, but this is not insurmountable (Figure
63.4). The ECL cell produces histamine in response to a
number of stimuli that include the vagus nerve and gastrin.
Gastrin is released by the G cells in response to the presence
of the food in the stomach. The production of gastrin is inhibited
by acid, creating a negative feedback loop. Various other
peptides, including secretin, inhibit gastric acid secretion.
Classically, three phases of gastric secretion are described.
The cephalic phase is mediated by vagal activity, secondary
to sensory arousal as first demonstrated by Pavlov. The gastric
phase is a response to food within the stomach, which is
mediated principally, but not exclusively, by gastrin. In the
intestinal phase, the presence of chyme in the duodenum and
small bowel inhibits gastric emptying, and the acidification

of the duodenum leads to the production of secretin, which

inhibits gastric acid secretion, along with numerous other
peptides originating from the gut. The stomach also possesses
somatostatin-containing D cells. Somatostatin is released in
response to a number of factors including acidification. This
peptide acts probably on the G cell, the ECL cell and the
parietal cell itself to inhibit the production of acid.
Gastric mucus and the gastric
mucosal barrier
The gastric mucous layer is essential to the integrity of the gastric
mucosa. It is a viscid layer of mucopolysaccharides produced
by the mucus-producing cells of the stomach and the
pyloric glands. Gastric mucus is an important physiological
barrier to protect the gastric mucosa from mechanical damage,
and also the effects of acid and pepsin. Its considerable buffering
capacity is enhanced by the presence of bicarbonate ions
within the mucus. Many factors can lead to the breakdown of
this gastric mucous barrier. These include bile, non-steroidal
anti-inflammatory drugs (NSAIDs), alcohol, trauma and
shock. Tonometry studies have shown that, of the entire gastrointestinal
tract, the stomach is the most sensitive to ischaemia
following a hypovolaemic insult and also the slowest to
recover. This may explain the high incidence of stress ulceration
in the stomach.
Peptides and neuropeptides in the
stomach and duodenum
As with most of the gastrointestinal tract, the endocrine
cells of the stomach produce peptide hormones and neurotransmitters.
Previously, nerves and endocrine cells were
considered distinct in terms of their products. However, it is
increasingly realised that there is enormous overlap within
these systems. Many peptides recognised as hormones may also
be produced by neurones, hence the term neuropeptides. The
term ‘messenger’ can be used to describe all such products.
There are three conventional modes of action that overlap.
1 Endocrine. The messenger is secreted into the circulation,
where it affects tissues that may be remote from the site of
origin (Bayliss and Starling).
2 Paracrine. Messengers are produced locally and have local
effects on tissues. Neurones and endocrine cells both act
in this way.
3 Neurocrine (classical neurotransmitter). Messengers are
produced by the neurone via the synaptic knob and pass
across the synaptic cleft to the target.
Many peptide hormones act on the intrinsic nerve plexus
of the gut (see later) and influence motility. Similarly, neuropeptides
may influence the structure and function of the
mucosa. Some of these peptides, neuropeptides and neurotransmitters
are shown in Table 63.1. The stomach is vital
in the regulation of appetite and weight control via a combination
of mechanical and hormonal mechanisms; these are
discussed further in following chapters.
Gastroduodenal motor activity
The motility of the entire gastrointestinal tract is modulated
to a large degree by its intrinsic nervous system. Critical in
this process is the migrating motor complex (MMC). In the
fasted state, and after food has cleared, in the small bowel
there is a period of quiescence lasting in the region of 40 minutes
(phase I). There follows a series of waves of electrical and
motor activity, also lasting for about 40 minutes, propagated
from the fundus of the stomach in a caudal direction at a rate
of about three per minute (phase II). These pass as far the
pylorus, but not beyond. Duodenal slow waves are generated
in the duodenum at a rate of about 10 per minute, which carry
down the small bowel. The amplitude of these contractions
increases to a maximum in phase III, which lasts for about 10
minutes. This 90-minute cycle of activity is then repeated.
From the duodenum, the MMC moves distally at 5–10 cm/
min, reaching the terminal ileum after 1.5 hours.
Following a meal, the stomach exhibits receptive relaxation,
which lasts for a few seconds. Following this, adaptive
relaxation occurs, which allows the proximal stomach to act as
a reservoir. Most of the peristaltic activity is found in the distal
stomach (the antral mill) and the proximal stomach demonstrates
only tonic activity. The pylorus, which is most commonly
open, contracts with the peristaltic wave and allows
only a few millilitres of chyme through at a time. The antral
contraction against the closed sphincter is important in the
milling activity of the stomach. Although the duodenum is
capable of generating 10 waves per minute, after a meal it only
contracts after an antral wave reaches the pylorus. The coordination
of the motility of the antrum, pylorus and duodenum

means that only small quantities of food reach the small bowel
at a time. It is important to consider that this control of gastric
emptying can be abolished after gastric surgery leading to
significant symptoms (discussed in later sections). Motility is
influenced by numerous factors, including mechanical stimulation
and neuronal and endocrine influences (Table 63.1).