Phyio: Chap. 62- General Principles of GI Function- Motility, Nervous Control, and Blood Circulation
1. General Principles of GI Motility
a. Physiologic Anatomy of GI wall
1. From outer to inward: serosa, longitude smooth muscle layer, circular smooth muscle layer,
submucosa, mucosa
2. Mucosal muscle lies in deep layers of mucosa in some parts
b. Gastrointestinal Smooth Muscle Functions as a Syncytium
i. SM fibers arranged in 1000 parallel fibers
ii. 200-500 micrometers in length
iii. 2-10 micrometer in diameter
iv. Either extend longitudinally or in circular pattern around gut
v. Gap junction connect fibers together easily allowing electrical signals to transmit= contraction
vi. Forms latticework of many contact points between each fiber= syncytium
c. Electrical Activity of GI Smooth Muscle
i. Slow waves
1. Rhythm of contraction determined by “slow waves”
2. Do NOT have regular action potentials
3. Instead they vary in their resting membrane potential intensity and frequency
4. Intensity and frequency in:
a. Body of stomach- 3/min.
b. Duodenum- 12/min.
c. Terminal ileum- 8-9/min.
5. Cause of slow waves and varying resting potential voltages is unknown
6. Thought to be caused by “interstitial cells of Cajal”- electrical pacemakers of intestine
7. Slow waves require “spike potentials” in order to produce action potential
ii. Spike Potentials
1. True action potentials that occur at around -40millivolts
2. Higher the slow wave potential the greater the frequency of spike potentials
3. Spike potentials last much longer than normal neural impulses because:
a. Calcium-sodium channels have influx of calcium and sodium
b. Much slower to open and close= longer lasting potentials
c. Large increase of calcium into muscle fiber accounts for contraction
d. Changes in voltage of Resting Membrane Potential
i. Factors that affect depolarization (make it more excitable):
1. Stretching of muscle
2. Stimulation of acetylcholine release from parasympathetic fibers
3. Stimulation by specific GI hormones
ii. Factors that hyperpolarize membrane (make it less excitable):
1. Norepinephrine/epinephrine on membrane
2. Stimulation of sympathetic nerves that secrete mostly norepinephrine at their endings
e. Calcium ions and Muscle Contraction
i. Smooth muscle contraction occurs due to calcium moving into muscle fiber
ii. Calcium ions acting through calmodulin control mechanism activate myosin filaments
1. = attraction between myosin and actin= contraction
iii. Slow waves do not cause calcium to enter smooth muscle fibers= no contraction
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f.
Tonic Contraction of Some GI smooth muscle
i. Some smooth muscle exhibits tonic contraction instead of or along with rhythmical contractions
ii. Not associated with slow waves
iii. Can last several minutes to hours, and can increase and decrease in intensity
iv. Greater the frequency= greater the contraction
v. Sometimes caused by hormones or other factors, or continuous entry of calcium into cell
2. Neural Control of GI Function- Enteric Nervous System
a. GI tract’s nervous system- enteric nervous system
i. Found within gut lining from esophagus down to anus
ii. It controls GI movements and secretions
iii. 2 plexuses
1. Myenteric plexus (aka: auerbach’s plexus)- outer between longitudinal and circular muscle
layers
a. It controls:
i. Controls GI movements
ii. Increases tone of gut wall
iii. Increased intentsity of rhythmical contractions
iv. Increased rate of contractions
v. Increased velocity of contraction
vi. Inhibitory plexus- Inhibits pyloric sphincter, ileocecal valve
2. Submucosal plexus (aka: Meissner’s plexus)- lies in submucosa
a. It controls:
i. GI secretion and local blood flow
ii. Controls inner wall of each section of intestine
iii. Local secretion, absorption, contraction of submucosal muscle
iv. Sympathetic and parasympathetic systems connect to both plexuses
v. Sensory nerve endings send afferent fibers to both plexuses as well as to:
1. Prevertebral ganglia of sympathetic n. system
2. Spinal cord
3. Vagus n. all the way to brain stem
b. Types of Neurotransmitters Secreted by Enteric Neurons
i. Different types of neurotransmitters:
1. Acetylcholine
a. Excites GI activity
2. Norepinephrine
a. Inhibits GI activity
b. Secreted by adrenal medulla into blood
3. ATP
4. Serotonin
5. Dopamine
6. Cholecystokinin
7. Substance P
8. Vasoactive intestinal polypeptide
9. Somatostatin
10. Leu-enkephalin
11. Met-enkephalin
12. Bombesin
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c. Autonomic control of GI Tract
d. Parasympathetic Stimulation Increases Activity of the Enteric Nervous System
i. Supply to gut divided into :
1. Cranial division
a. Cranial parasympathetic nerves almost entirely in vagus nerve
b. Innervate esophagus, stomach, pancreas, intestines
2. Sacral division
a. Sacral parasympathetics originate in S2-S4 through pelvic nerves
b. Innervates distal lg intestine down to anus
ii. Sigmoidal, rectal, and anal regions better supplied with parasymp fibers than other areas
1. Function to execute defecation reflexes
iii. Postganglionic neurons of GI parasympathetic mostly in myenteric and submucosal plexuses
1. Causes increase in activity of entire enteric system= enhanced GI function
e. Sympathetic stimulation usually inhibits GI tract activity
i. T5-L2 control sympathetic of GI system
ii. Most that innervate gut are part of sympathetic chain and lie lateral to spinal cord
1. Pass through celiac ganglia, or mesenteric ganglia
iii. Norepinephrine largely inhibits effects of neurons in enteric nervous system
iv. Norepinephrine slightly inhibits intestinal tract smooth muscle (except mucosal muscle which it
excites)
v. Stong stimulation can actually block movement of food through GI tract
f.
Afferent Sensory nerve Fibers from the Gut
i. Afferent sensory fibers can be stimulated by
1. Irritation of gut mucosa
2. Excessive distention of gut
3. Presence of specific chemical substance in gut
ii. Causes excitation or inhibition of intestinal movements and secretions
iii. Much of vagus nerve (80%) is afferent sensory- takes signals back to brain and initiates vagal reflex
g. Gastrointestinal Reflexes
i. Autonomics of enteric nervous system and connections to sympathetic and parasympathetic cause:
1. Reflexes that are integrated entirely within the gut wall enteric nervous system
a. Includes reflexes to control secretion, peristalsis, mixing, inhibition
2. Reflexes from gut to prevertebral sympathetic ganglia and then back to GI tract
a. Transmits signals long distances to other parts of GI tract
b. Gastrocolic reflex- signals from stomach to colon for evacuation
c. Enterogastric reflex- colon & small intestine to inhibit stomach motility & secretion
d. Colonileal reflex- from colon to inhibit emptying of ileal contents into colon
3. Reflexes form gut to spinal cord or brain stem and back to GI tract
a. Reflexes from stomach and duodenum to brain and back to stomach by vagus n.
i. Control secretory activity and gastric motor activity
b. Pain reflexes cause general inhibition of entire GI tract
c. Defecation reflex from colon and rectum to spinal cord and back to produce
contractions for defecation (defecation reflex)
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h. Hormonal Control of GI Motility
3. Functional types of Movements in GI Tract
a. 2 types:
i. Propulsive (peristalsis)
1. Movement of bolus forward in intestinal tract
2. Ring of muscle around lumen that constricts and then moves it forward
3. Stimulus for peristalsis= distention of gut
a. Other stimulants: chemical/ physical irritants, strong parasympathetic innervations
4. Effectual peristalsis requires active myenteric plexus
5. Peristalsis occurs in the direction towards the anus
a. It is thought that myenteric plexus is polar toward the anus so it goes that way
6. Peristaltic reflex and the “law of the Gut”
a. Movement or peristaltic movements toward anus- myenteric reflex or peristaltic
reflex
ii. Mixing Movement
1. Local intermittent constrictive contractions occur in “chopping/ shearing” motion
2. This churns the feces rather than moves it down the line
4. GI Blood flow- “Splanchnic Circulation”
a. Includes blood flow from gut, spleen, pancreas, and liver
b. Blood from the gut, spleen, and pancreas pass into liver by way of portal vein through sinusoids and into
hepatic sinuses out of liver
c. Nonfat- water soluble nutrients absorbed in gut are transported in portal vein to liver sinusoids
i. Reticuloendothelial cells and principle parenchymal cells of liver (hepatic cells) absorb and
temporarily store ½-3/4 of the nutrients
ii. Chemical processing takes place in liver
iii. Most fats absorbed form GI tract are not carried in portal blood but are instead absorbed into
intestinal lymphocytes and then to circulating blood by thoracic duct (bypassing liver)
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d. Anatomy of GI blood supply
i. General arterial supply- superior mesenteric & inferior mesenteric arteries supplying walls of small
and large intestine by arching arterial system
ii. Upon entering gut arteries branch into smaller arteries in all directions
iii. Small arteries penetrate intestinal wall and spread along muscle bundles, intestinal villi, and
submucosal vessels beneath epithelium (for absorption)
e. Possible Causes of Increased Blood Flow During GI Activity
i. Several vasodilator substances released during digestive process (from mucosa)
1. Most are peptide hormones (CCK, vasoactive intestinal peptide, gastrin, secretin)
ii. Some GI glands release into gut wall 2 kinins: (kallidin, & bradykinin)
1. These are powerful vasodilators and may also cause secretion
iii. Decreased oxygen concentration in gut wall increases intestinal blood flow 50-100%
1. Increased metabolic rate during activity lowers O2 concentration= vasodilation
2. Also leads to increase in adenosine (vasodilator)
5. “Countercurrent” Blood Flow in Villi
a. Arterial flow into villus and veous flow out of villus are in opposite direction
b. They are in close proximity to eachother
c. Blood oxygen diffuses out of arterioles and into adjacent venules
d. Countercurrent moves to villi (similar to vasarecta of kidney medulla)
e. Normally shunting from arterioles directly to venules is NOT harmful
i. In some pathology where blood flow is lost or deficient=tips or whole villi die ischemic death
ii. This leads to diminished GI absorption of nutrients
6. Nervous control of GI Blood Flow
a. Parasympathetic stimulation to stomach and lower colon increases blood flow and glandular secretion
b. Sympathetic stimulation causes vasoconstriction of arterioles= reduced blood flow
i. Autoregulatory escape- vasodilation will soon follow sympathetic stimulation that is illicited by
ischemic override effects
7. Importance of Nervous Depression of GI Blood Flow When Other Parts of Body Need Extra Blood Flow
a. Sympathetic can shut off blood flow during heavy exercise and shunt that blood to places it is needed
b. In circulatory shock the same thing happens so more blood can go to heart and brain
c. Vasoconstriction of intestinal & mesenteric veins can displace lots of blood to other parts of body that need
it most (200-400mL)
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