Checked by Dr. Gwirtz
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 1 of 7
GI Motility, Part II
I.
Introduction—Review
 What is the major neurotransmitter secreted by the parasympathetics? ACh
 What is its affect on the gut? Increased motility & secretions?
 Sympathetic nerves—norepinephrine; decreased motility; major effect at
sphincters—constriction
 Neurotransmitter causing sphincter relaxation—NO, VIP (vasoactive inhibitory
peptide) secreted by parasympathetic myenteric nerves
 What is the myenteric plexus? Where located? What does it do?
 Submucosal plexus?
 What’s an electrical slow wave? Slow electrical fluctuations in the smooth
membrane electrical potentials.
o Electrical slow waves do not cause smooth muscle contractions; Ca2+ entry
into smooth muscle causes contractions.
o Can have a contraction without an action potential by exposing smooth
muscle to a hormone or paracrine agent that depolarizes cell. This opens
Ca2+ channels and causes a small contraction. Now expose it to more
gastrin or stimulate the myenteric nerves to release ACh (both depolarize the
cell), and it can now reach threshold for an action potential, primarily found
on the peaks of slow waves.
o A greater number of action potentials bring increasingly more Ca2+ into the
cell causing contractions with greater force. If you increase the # of action
potentials, can NOT increase the # of contractions.
o Rate of the slow wave is determined by the rate of depolarization of
pacemaker cells, interstitial cells of Tehal in stomach, duodenum, small
intestine. Rate of slow wave determines the number of contractions. Rate
of slow wave: 3/min in stomach, 12/min in upper duodenum and decreases
as move the length of the gut.
Action potential threshold
Ca2+ channel threshold
mV
Slow wave


How does information move between smooth muscle cells since they are not all
innervated? Gap junctions and mechanical connections between cells
Mixing vs peristaltic contractions:
o Mixing contractions—little contractions that dig into chyme to break it up.
Stimulus: distention, presence of food rubbing against the epithelial cells
Rate in the stomach: 3/min In small intestine: 12/min Slow wave rate
determines the rate of contraction.
Checked by Dr. Gwirtz
II.
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 2 of 7
o Peristaltic contraction—stimulus: presence of food; distention. This leads
to a reflex requiring myteric and parasympathetic nerves and the central
nervous system. There’s a contraction (circular muscle contracts,
longitudinal muscle relaxes) behind a bolus of food and receptor
relaxation (circular muscle relaxes, longitudinal muscle contracts) in
front of the bolus. The contraction moves down the gut.
 What is a primary peristaltic contraction? Location? Cause? Upper esophagus,
stimulated by food touching the pharyngeal receptors initiating the swallowing
reflex.
 What initiates a secondary contraction? Food stuck somewhere in the smooth
muscle section of the esophagus.
 Substances causing the lower esophageal sphincter to relax: NO, fats,
peppermint, caffeine, nicotine, alcohol, antacids, nitrates, anticholinergic drugs,
progesterone, valsalva maneuver, carbohydrates
 Note: the tape stopped recording at this point. The rest of the lecture followed
the power points closely. I had written most everything else down and have
included it in the scribe.
 Name a swallowing disorder: achlasia—atony, no peristalsis; food stays in the
esophagus; lower esophageal sphincter won’t relax. Pressure = 0 in the body;
pressure is high in the LES and normal in the UES
Stomach
 Body: has thin walls; location of most of the gastric secretory glands; mainly
has mixing contractions
 Antrum: thick walls; peristaltic contractions that push chyme (a liquid of
particles <2mm in diameter) against the pyloric sphincter. If the chyme is the
right consistency and a contraction occurs at the right time, the chyme is pushed
through the pyloric sphincter.
A. Functions of the Stomach
 Store large quantities of food
 Mix food with gastric secretions until it forms a semifluid mixture, called
chyme
 Slow emptying of the chyme into the small intestine at a rate suitable for
proper digestion and absorption
 Dilutes or concentrates fluids so that they are the same concentration as
the body fluids before reaching the intestine
 Forms intrinsic factor which is necessary for Vitamin Bl2 absorption
B. Receptive relaxation of the Stomach
 Ability of the stomach to accommodate a large volume meal with only a
small increase in intraluminal pressure. Function of all hollow organs due to
vagal nerve mediated response and the ability of smooth muscles to slide on
each other.
 Vagal fibers innervate intrinsic nerves to cause receptive relaxation via a
transmitter (VIP or NO)
 Vagotomy greatly diminishes receptive relaxation
Checked by Dr. Gwirtz
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 3 of 7
C. Motility in the stomach
 [Electrical] Slow waves - 3 per min (Basic Electrical Rhythm) spontaneous fluctuations of membrane potential; ongoing waves
 Mixing waves - weak contractions which move toward antrum; mix food
with gastric secretions
 Peristaltic constriction rings - force antral contents under pressure toward
pylorus
D. Emptying of the Stomach
 Promoted by intense peristaltic contractions of the stomach antrum.
Increased intragastric pressure forces material across the pyloric sphincter.
 Opposed by varying degrees of resistance to the passage of chyme through
the pyloric sphincter—influenced by nervous and humoral signals from the
stomach and duodenum. These decrease the force of contractions and
decrease emptying of the stomach.
 Begins 30-60 min after eating; complete within 4-4 1/2 hr after eating
E. Factors Promoting Gastric Emptying
 Promoted by factors which cause antral pressure > duodenal pressure
 Interdigestive Phase: Motilin released into bloodstream, mediates IMMC—
housekeeping functions. ↑ motilin in stomach and small intestine →
peristaltic contraction sweeps through the gut from stomach to small
intestine emptying them to prepare for the next meal.
 Cephalic Phase—thinking about eating, smelling, seeing, chewing food:
o Vagal Reflexes (direct)—before swallowing
o Vagal stimulated release of gastrin from G-cells. Motility and secretions
are vagally mediated. Vagus releases ACh, which depolarizes smooth
muscle → ↑ force of contraction → ↑ gut motility
o Cephalic phase abolished by atropine or by cutting the vegus nerve.
 Gastric Phase:
o Mediated by stretch—stimulates mechanoreceptors
o Vagal Reflexes (ACh)— ↑ contractility
o Myenteric Reflexes—local reflexes
o Gastrin (release stimulated by food and vagal reflexes)
o Partial Gastrectomy—lopping off part of the stomach decreases its
volume and causes it to empty faster.
F. Factors Which Delay Gastric Emptying
 See figure in power points for flow chart
o There’s an error: Gastrin promotes emptying!!
o Stomach secretes acid, mixes with food stuffs → small intestine → acid
receptors → secretin release into blood → reaches targets in stomach →
hyperpolarizes cells → decreases contractions in stomach and gastric
emptying, decreases releases from g- and parietal cells
o Proteins and amino acids → CCK and GIP release → stomach → cells
hyperpolarized → decreases contractions in stomach and gastric
emptying
Checked by Dr. Gwirtz
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 4 of 7
o G cells in small intestine secrete an intestinal gastrin which causes
contraction of pyloric sphincter (delaying emptying) but also increases
gastric motility (which will promote gastric emptying).
o Release of an unknown hormone occurs in response to food and
distention of the stomach and duodenum.
 Intestinal Phase:
o Duodenal distension—myenteric nerve feedback
o Duodenal irritation—myenteric nerve feedback
o CCK (fats, proteins, amino acids)—hyperpolarize stomach
o Gastrin ( via ↑ pyloric tone)
o Secretin (acid, osmolality of lumen of stomach)
o GIP (fat)
o VIP (distension)—paracrine factor of duodenum, decreases activity of
all smooth muscles
o Enterogastric Reflexes (local myenteric, sympathetic, vagal, hormonal)
o Diabetes mellitus (autonomic neuropathy)
o Surgical vagotomy (gastroparesis)
G. Gastric Emptying Rates
 Liquids (2-3 min) faster than solids (15 min)
 Small particles > larger
 Easily fragmented food (noodles > meat)
 Large, heavy persons faster than non-obese (greater pressure gradient)
 Inverse with caloric content, not meal weight (noncaloric liquids such as
water empty first)
 Post-gastrectomy (resection), solids empty faster than before (8O% of
contents in 10 min) due to the smaller stomach volume
 CHO > protein > fat
CHO empty quickly; proteins trigger release of
CCK and GIP to decrease the force of contractions and inhibit stomach
release; fats float on top of the chyme and are the last to empty—cause a
strong secretion of CCK
 Neutral acid
 Isotonic > hypo- or hypertonic—cause release of secretin—feeds back to
stomach delaying release of contents
 For the graph: liquid glucose empties quickly. If liver is eaten, it takes
longer to empty because it’s full of fat which causes the release of CCK. If
spheres are ingested, they stay in the stomach because they’re too large to fit
through the pyloric sphincter.
H. Case Study: Dumping Syndrome
1. Case Study
A 72 yr old man complains of tiredness, long standing symptoms of
dizziness, sweating, and palpitations after meals. Had a partial gastrecomy 8
years earlier. Has become forgetful and forgets to take his medications, vit
B12 injections. Has megoloblastic (pernicious) anemia (because he’s not
getting his B12 injections) and mild metabolic acidosis, iron deficiency.
Checked by Dr. Gwirtz
III.
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 5 of 7
Explained by the effects of the gastrectomy. Dumping syndrome explains
dizziness, sweating, and palpitations.
2. Dumping Syndrome
After gastrectomy, hypertonic/osmotic food empties (dumps) directly into
duodenum/jejunum without mixing with gastric secretions. So, it’s not
diluted and the small intesting doesn’t like anything that’s not isoosmotic.
– nausea, epigastric pain,  BP, sweating, vertigo, fainting
– due to hypertonic chyme being dumped rapidly into duodenum or jejunum
– fluid moves from blood stream into intestinal lumen to dilute contents 
 BV (can lose lots of blood volume trying to dilute the contents)  
BP  sympathetic reflex—baroreflex (↑ HR, force of contractility,
sweating, causes orthostatic hypotenion due to  BP; stuff sitting in
duodenum causes nausea)
– Prevent this by eating lots of small meals several time/day
– Partial gastrectomy removes body of stomach, secretory cells—parietal
cells and intrinsic factor—can’t absorb Vit B12 without it
– acid (aids in iron absorption—changes it from Fe+3 to Fe+2)
– intrinsic factor (necessary for B12 absorption)
– pepsin (no real consequences; it’s the only enzyme that breaks down meat
fibers)—stomach is expendable
Small Intestine
A. Movements of the Small Intestine
1. Mixing or Segmentation Contractions
 Distention (stretch) initiates
 Purpose: Breaks up chyme to increase surface area to make it easier for
enzymes to digest
 Mixes chyme with secretions
 Rate related to electrical slow waves
 Myenteric plexus (myogenic)
2. Propulsive (Peristaltic) Contractions
 Distention (stretch) initiates
 Usually weak—die out after few cm, about 5cm
 Parasympathetic and myenteric nerves
 Influenced by nervous signals, hormonal factors
3. Law of the Intestine
 chyme moves analward
B. What increases small intestinal motility?
 ACh (vagal, myenteric)
 Gastrin
 CCK—fat triggers its release;  gastric motility
 Motilin—released during interdigestive period
 Distension (pressure)—open Ca2+ channels with a stretch
Checked by Dr. Gwirtz
GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 6 of 7
 Hyperthyroid— ↑ metabolism of all cells
 Fever
 Hyperglycemia
 Intense irritation—can be caused by bacteria, toxins, viruses
 An overabundance of intestinal motility causes diarrhea
C. What decreases small intestinal motility?
 Norepi (sympathetic)
 Epinephrine
 VIP—inhibits smooth muscle
 GIP
 Secretin
 NO
 Glucagon—released in gut in response to different food substances
 Opioids
 Over-distension—blockage, build-up of gas
 Hypothyroid
 Hypoglycemia
 Malabsorption syndrome
 Trauma
 1 big problem after surgery is the lack of peristaltic contractions which
decrease gut motility (response to anesthesia). Patients complain of a
bloated abdomen because gas builds up in the small intestine and colon
causing discomfort.
D. Peristaltic Rush
 Also called Power Propulsion
 Stimulus: intense irritation of intestinal mucosa e.g., severe infectious
diarrhea, parasites, enterotoxins, ionizing radiation, application of vinegar to
mucosa—anything irritating
 Initiated by extrinsic nervous reflexes to autonomic nervous system
ganglia and to brainstem and back to the gut
 Enhanced by myenteric plexus reflexes
 Strong, long-lasting giant migrating contractions which travel long distances
in small intestine
 Begins in duodenum, moves length of gut and Sweeps contents into colon
→ diarrhea
E. Interdigestive Migrating Myoelectric Complex System
 Bursts of rhythmic contractions occur in cycles during the fasting state (2-4
hr after a meal), lasting 5-10 min followed by a quiet period.
 Recurs every 1.5 - 2 hrs and is related to the release of motilin. Occurs
when the stomach is empty
 Active region slowly passes down length of the gut: starts in gastric antrum
and progress to ileum (ileocecal valve)
 Related to hormone-like substance motilin
Checked by Dr. Gwirtz

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GI #15
Wed, 02/19/03, 10am
Dr. Gwirtz
Jennifer Uxer for Michelle Steiner
Page 7 of 7
Stops with feeding—with the 1st swallow
Housekeeping function - keeps lumen cleared out during interdigestive
period.
 Stops immediately with feeding.salivary glands secrete at basal rate to
moisten oral cavity & keep it clean
 UES and LES constricted.
 Gastric juice produced at low level (stomach contains low volume of highly
acidic fluid). There’s also a low rate of bicarbonate formation.
F. Other Events Occurring During Interdigestive Phase of Digestion
 IMMC
 Pancreas produces low HCO3, low enzyme juice at minimal rate
 Concentration of bile salts in portal venous blood low
 Rate of hepatic bile salt synthesis is high
 Rate of hepatic salt secretion low