Gastric Motility
Functions of gastric motility
1. Store food
2. Gradually release it into small intestine
3. Mix food with gastric secretions
Food Storage in the Stomach
Stomach can enlarge as food enters, but intragastric pressure is
nearly constant at volumes below 1 liter (for most of us). This is
called receptive relaxation. At higher volumes, intragastric
pressure increases dramatically.
Mechanism: Smooth muscle can change length over a wide range
with little change in resting tension. In the stomach, this occurs
via a reflex mediated by the vagus nerve.
Mixing and Propulsion of Gastric Contents
When stomach isn’t empty, peristalsis occurs in stomach.
Gastric peristalsis begins in fundus, travels to antrum. Antral
muscle is thicker than elsewhere, so antral contractions are
stronger.
Lumen in peristaltic wave is pretty big, so mixing occurs as content
moves in both directions. Since gastroduodenal sphincter is
normally partly open, each peristaltic wave pushes some gastric
content into duodenum (first segment of small intestine). This is
the mechanism of stomach emptying
The greater the volume in the stomach, the more frequent the
peristaltic waves. Thus, the rate of stomach emptying is related to
the amount in the stomach.
Control of Gastric Peristalsis
Local, as described. There are also neural and humoral controls.
Distension activates stretch receptors in gastric wall. This initiates
short and long reflexes that increase gastric motility
Partially digested protein causes release of the hormone, gastrin,
from G-cells in the antrum. Gastrin is secreted into circulation,
reaches gastric muscle cells and stimulates gastric peristalsis.
Duodenal cells secrete hormones in response to fat and acidity.
They reach the stomach via the circulation and inhibit gastric
peristalsis. There are also neural reflexes originating in the
duodenum that inhibit gastric peristalsis. Some involve the little
brain, some involve the CNS
Why does a high fat meal increase alcohol tolerance?
Gastric Secretion
There are 1-2 liters of saliva per day; the stomach secretes 2-3
liters/day. That’s about 4 liters/day, not counting what we ingest.
Three kinds of gastric glands secrete into the lumen
1. Mucus, secreted by mucous cells (= mucous neck cells)
2. Pepsinogen, a protease precursor secreted by chief cells
3. HCl, secreted by parietal cells
Parietal cells secrete 300 mOsm HCl (pH = 1-2). This acidifies lumen,
converting pepsinogen into pepsin and providing the low pH at
which pepsin works best, breaks down ingested connective tissue,
and is bactericidal.
Gastric pH falls from 7.8 to 4 within 20 minutes of eating. Gastrin
(secreted by G-cells in response to partially digested protein in
stomach) stimulates gastric motility and HCl secretion.
Control of Gastric HCl Secretion
1. Cephalic phase: Sight or smell of food, food in the mouth,
activate conditioned reflexes that elicit HCl secretion before
food enters stomach. Efferent arm of the reflex is vagal
stimulation of parietal cells and submucosal plexus, which then
stimulates G-cells.
2. Gastric phase: Partially digested protein in stomach stimulates
parietal and G-cells via submucosal plexus. Gastric distension
stimulates G-cells via submucosal plexus. Low pH in stomach
inhibits G-cells
3. Intestinal phase: Same systems in duodenum that inhibit
gastric motility also inhibit gastric secretion of HCl
Gastric Secretion of Pepsinogen
Chief cells secrete pepsinogen, precursor of the only gastric
enzyme, pepsin (a protease). Conversion of pepsinogen to pepsin
is initiated by acidity in stomach, then by pepsin itself.
Optimum for protein digestion by pepsin is pH 2 to 3; intragastric
pH is maintained around that level.
Protein digestion is quite incomplete in stomach, although some
proteins is digested to amino acids.
In addition to protein being partly digested in stomach, there is
some starch hydrolysis from swallowed salivary amylase. It
doesn’t work below pH 4, so gastric starch digestion only occurs
during first 20 minutes or so of a meal. On the other hand, salivary
amylase digests more starch in the stomach than in the mouth.
Absorption in the Stomach
There’s no active reabsorption in the stomach, although a few
things can diffuse into the circulation across the stomach wall.
Most notable is alcohol. More about this soon.
Pancreatic Secretion of Sodium Bicarbonate
“Pancreas” = exocrine pancreas. Endocrine pancreas will come later.
Pancreatic cells are arranged in clusters called acini; they’re acinar
cells. They secrete into ducts that empty into pancreatic duct, which
leads to the proximal end of the duodenum.
Pancreatic secretions are alkaline (iso-osmotic sodium bicarbonate
solutions), and neutralize gastric acid. The alkalinity also provides
optimal pH for the many digestive enzymes secreted by acinar cells.
For anyone interested, the chemistry of bicarbonate secretion is
described in Sherwood. It’s similar to the one by which parietal cells
secrete HCl, but in the opposite direction.
Net effect of gastric secretion of HCl and pancreatic secretion of
sodium bicarbonate is that plasma pH is unaffected.
Pancreatic Secretion of Digestive Enzymes
There are pancreatic enzymes that can digest every digestible thing
we eat. Pancreatic proteases (trypsin, chymotrypsin,
aminopeptidase, carboxypeptidase, and a few others) are secreted
as inactive precursors (“proenzymes”).
Enterokinase is a protease secreted into the duodenal lumen by
glands in the submucosa. It converts trypsinogen to trypsin.
Trypsin converts more trypsinogen to trypsin, also converts the
other protease proenzymes to active forms.
Pancreatic amylase hydrolyzes starch (and starch partly digested by
salivary amylase) into disaccharides – molecules consisting of two
simple sugar molecules joined together.
Pancreatic lipases digest various kinds of lipids. Triglycerides, the
most common dietary fats, are digested into free fatty acids and
glycerol.
Pancreatic nucleases digest RNA and DNA.
Control of Pancreatic Secretion
Mainly via hormones secreted into circulation by cells of
duodenum.
Secretin, secreted in response to acidity in duodenum, elicits
bicarbonate secretion by pancreas
Cholecystokinin (= CCK) is secreted in response to partially digested
protein and fat. It stimulates enzyme secretion by pancreas.
Hepatic Secretion
Liver secretes bile. Important thing in bile is bile salts, which are
detergents. They reduce surface tension at oil/water interfaces,
reducing the size of fat droplets (that’s what the detergent you use
to wash dishes does).
Reducing size of fat droplets increases surface-to-volume ratio of
fat. Lipases act only on the surfaces of fat droplets, so this greatly
increases rate of fat digestion.
Bile is more or less continuously produced. It flows into
gallbladder, where it’s stored. Gallbladder vigorously reabsorbs Na,
water follows osmotically. This concentrates bile.
CCK (secreted into bloodstream by duodenal cells in response to fat
and partially digested protein) stimulates gallbladder contraction.
This forces bile into duodenum.
Enterohepatic Circulation
Bile salts adhere to intestinal fat droplets. As fats are digested and
absorbed, bile salts end up in lumen of intestine.
Ileum (distal fourth of small intestine) has active transport systems
that reabsorb bile salts, so very little is lost in feces. Splanchnic
circulation takes them straight back to the liver. They’re removed
from the circulation by liver, secreted into bile again.
The cycle of secretion by the liver and reabsorption from
circulation by the liver is called enterohepatic circulation.
Regulation of Hepatic Secretion
Most hepatic secretion is bile salts that were reabsorbed from the
ileum. They are actively transported from the hepatic cells into the
bile ducts; water follows osmotically. Since the transport rate
depends on bile salt concentration in liver, the most bile is secreted
when the most bile salts are being reabsorbed.
Thus, bile secretion is highest during digestion of a meal, lowest
during fasting. This is why people without gallbladders do OK – the
surgery that removes the gallbladder re-routes the bile from the
liver straight to the duodenum.
People without gallbladders don’t do so well with high fat meals
because they can’t accelerate delivery of concentrated bile to
duodenum. Having a high fat meal causes fatty diarrhea for them.
They rarely do it more than once.