Download Physiology Ch 62 p753-762 [4-25

Physiology Ch 62 p753-762
-Alimentary tract provides body with water, electrolytes, vitamins, and nutrients
-requires movement of food through tract, secretion of digestive juices and digestion of food,
absorption of water, vitamins and digestive products, circulation of blood through GI organs, and control
of all these systems by local, nervous and hormonal systems
Anatomy of GI Wall – Layers from outer surface to inward:
1. Serosa
2. Longitudinal smooth muscle
3. Circular smooth muscle
4. Submucosa
5. Mucosa
-GI smooth muscle acts as a syncytium
-each fiber is 200-500um in length and 2-10um in diameter
-extend longitudinally down length of GI tract in longitudinal smooth muscle
-extend around the gut in circular smooth muscle layer
-within each bundle, muscle fibers electrically connected by gap junctions that allow lowresistance movement of ions from one cell to the next
-can travel more rapidly down the length as opposed to sideways
-when an action potential is elicited anywhere within the muscle, it travels in all directions in the
muscle
-distance traveled depends on excitability of muscle, traveling only a few mm at a time
or down length of whole tract
-connections exist between longitudinal and circular muscle layers
-Smooth muscle of GI tract is always excited by continual, slow, intrinsic electrical activity along
membranes of muscle fibers
1. Slow Waves – GI contractions occur rhythmically, determined by slow waves
-not action potentials, but rather undulating changes in resting membrane potential
-varies between 5-15 mV and frequency ranges from 3-12/minute
-3/min in stomach, 12/min in duodenum, and 8-9/min in ileum
-cause of waves is thought to be interactions between smooth muscle cells and
interstitial cells of Cajal – believed to be pacemakers of smooth muscle cells
-do not cause contractions except maybe in the stomach, but instead excite intermittent
spike potentials, which can cause contractions
2. Spike Potentials – true action potentials occurring automatically when resting potential
depolarizes to -40mV from -50 or -60mV
-when slow waves become more positive than -40, spike potentials appear
-ranges between 1-10 spikes/second
-last 10-40x longer in GI muscle as action potentials in large nerve fibers and lasts as
long as 10-20ms
-unlike nerve fibers, spike potentials in GI originate from influx of Ca ions along with
smaller numbers of Na ions through calcium-sodium channels
-Calcium-sodium channels are much slower to open and close than rapid Na channels,
accounting for long duration of action potential
-influx of calcium plays special role in intestinal smooth muscle contraction
Changes in Voltage of Resting Membrane Potential – baseline voltage level of smooth muscle can also
change
-normal resting potential ~-56mV, multiple factors can change this
-when becoming less negative, muscle fibers become more excitable
-when becoming more negative (hyperpolarization), fibers become less excitable
-factors that depolarize membrane:
-muscle stretching, stimulation by acetylcholine from parasympathetic fibers, GI hormones
-factors that hyperpolarize the membrane:
-norepinephrine or epinephrine, stimulation by sympathetic fibers secreting norepinephrine
Calcium ions and Muscle Contraction – smooth muscle contracts in response to Ca influx
-act through calmodulin control, activate myosin filaments causing contractile forces
-slow waves do not cause Ca ions to enter, only Na ions. Therefore, slow waves do not cause muscle
contraction
-spike potentials cause Ca influx causing contraction
Tonic Contraction of some GI smooth muscle
-some smooth muscle exhibits tonic contraction, which is continuous contraction not associated with
basal rhythm of slow waves, which can last several minutes or hours
-sometimes caused by repetitive spike potentials, greater frequency = greater contraction
-can also be caused by hormones or other factors for depolarization
-can also be caused by continual influx of Ca ions not associated with changes in membrane potential
Neural Control of GI Function: Enteric Nervous System
-enteric nervous system is in wall of gut from esophagus to anuss
-100 million neurons in this system, controls GI movements and secretion
-composed of 2 plexuses:
1. Myenteric Plexus – between longitudinal and circular muscle layer (also called Auerbach’s
plexus)
-controls mainly GI movements
-linear chain of interconnecting neurons extends down entire length of GI tract
-controls muscle activity along length of gut, when stimulated, controls 4 things:
-increased tonic contraction
-increased intensity of rhythmical contractions
-increased rate of rhythmical contractions
-increased velocity of conduction of excitatory waves along gut wall causing
peristalsis
-contains some inhibitory neurons, secrete vasoactive intestinal polypeptide – an
inhibitory neurotransmitter for inhibiting sphincter muscles
2. Submucosal Plexus – inner plexus in the submucosa (also called Meissner’s plexus)
-controls mainly GI secretion and local blood flow
-inner wall function of each minute segment of intestine
-local secretion to a certain part of intestine via sensory signals
-local absorption
-contraction of submucosal muscle that causes degrees of infolding of GI mucosa
-both of these plexuses can act independent of parasympathetic or sympathetic innervation, but these
will greatly enhance or inhibit GI functions
-sensory nerve endings in GI epithelium send afferent fibers through plexuses to prevertebral ganglia,
spinal cord, and vagus nerves which can elicit local reflexes within gut wall
Types of Neurotransmitters Secreted by Enteric Neurons
-acetylcholine, norepinephrine, ATP, serotonin, dopamine, cholecystokinin, substance P,
vasoactive intestinal peptide, somatostatin, leu-enkephalin, met-enkephalin, and bombesin
-Acetylcholine most often excites GI activity
-Norepinephrine most often inhibits GI activity
Autonomic Control of GI Tract
-Parasympathetic innervation increases activity of enteric nervous system, which is divided into cranial
and sacral divisions (innervating most extensively near oral cavity and anus)
1. Cranial Parasympathetic – entirely in vagus nerves, innervate esophagus, stomach, and pancreas, less
to small intestine
2. Sacral Parasympathetic – originate ins 2nd, 3rd, and 4th sacral segments and pass through pelvic nerves
to distal half of large intestine all the way to anus
-sigmoid colon, rectum, and anal region better supplied with parasympathetics for defecation
-postganglionic neurons of GI parasympathetics are in myenteric and submucosal plexuses, which
enhances GI activities
Sympathetic innervation – inhibits GI activity
-originates in spinal cord between segments T5 and L2, preganglionic fibers enter sympathetic chains
and many pass through to outlying chains such as the celiac and mesenteric ganglia
-most post-sympathetic neuron bodies are in these ganglia
-innervate all of the GI tract instead of just oral cavity and anus, secrete norepinephrine
-inhibits activity of GI tract in 2 ways
1. slightly by direct secretion of norepinephrine on intestinal smooth muscle
2. more importantly, inhibitory effect of norepinephrine on entire enteric nervous system
-can block food moving through GI tract
Afferent Sensory Nerves from Gut – some have cell bodies in enteric nervous system and some in DRG
-can be stimulated by irritation of gut mucosa, excessive distention, presence of chemical substances in
got
-can cause excitation or inhibition of intestinal movements/secretion
-80% of nerve fibers in vagus nerve are afferent rather than efferent, controls vagal reflex to GI
Gastrointestinal Reflexes – 3 reflexes essential for GI control
1. Integrated entirely within gut wall – much of GI secretion, peristalsis, mixing contractions, local
inhibiting effects
2. Reflexes from gut to prevertebral sympathetic ganglia and back to GI tract – transmit signals
long distances to other areas of GI tract such as stomach to cause evacuation of colon
(gastrocolic reflex), signals from colon and small intestine to inhibit stomach motility and
secretion (enterogastric reflexes), and reflexes from colon to inhibit emptying of ileal contents
into colon (colonoileal reflex).
3. Reflexes from gut to spinal cord or brain stem and back to GI – include reflexes from
stomach/duodenum to brainstem and back to control gastric motor and secretory activity.
a. Also pain reflexes that cause general inhibition of entire GI tract
b. Defecation reflexes that travel from colon and rectum to spinal cord and back again to
produce powerful contractions required for defecation
Hormonal Control of GI Motility – GI hormones are released into portal circulation and exert physio
responses on target cells, persist even after all connections are severed
1. Gastrin – secreted by G cells of antrum of stomach in response to ingestion of meal/distention,
and gastrin releasing peptide (released by gastric mucosa after vagal stimulation)
a. Stimulate gastric acid secretion and growth of gastric mucosa
2. Cholecystokinin (CCK) – secreted by I cells in mucosa of duodenum and jejunum in response to
digestive products of fat, fatty acids, and monoglycerides
a. Contracts the gallbladder, expelling bile into small intestine (emulsify fatty acids)
b. inhibits stomach contraction
c. inhibits appetite
d. secretes pancreatic enzymes, pancreatic bicarbonate, and growth of exocrine pancreas
3. Secretin – secreted by S cells of mucosa of duodenum in response to acidic gastric juice
emptying into duodenum, promote pancreatic secretion of bicarbonate to neutralize acid
a. promotes pepsin secretion
b. biliary bicarb secretion
c. inhibits gastric acid secretion
4. Gastric Inhibitory Peptide – secreted by K cells of the upper small intestine in response to
protein, fat and carbs. Inhibits gastric motility
a. Stimulates insulin release (that’s why it is also known as glucose-dependent
insulinotropic peptide)
b. Inhibits gastric acid secretion
5. Motilin – Secreted by stomach and upper duodenum during fasting, which increases
gastrointestinal motility in response to fat, acid, and nerve stimulation
a. Released cyclically and stimulates waves of GI motility called interdigestive myoelectric
complexes that move through stomach and small intestine every 90 minutes
Functional Types of Movements – propulsive movements and mixing movements
1. Propulsive movements – cause food to move forward along tract at an appropriate rate to
accommodate digestion and absorption
-called peristalsis, where contractile ring appears around gut and moves forward
-inherent property of many syncytial smooth muscle tubes
-stimulation at any point in gut can cause the A-ring to appear and spread along tube
-usual stimulus for peristalsis is distention of gut, as well as parasympathetics and
chemicals
-occurs weakly if at all without a myenteric plexus, and blocked if person is treated with
atropine to paralyze cholinergic nerve endings of myenteric plexus
-is directional from mouth to anus, results from possibility that myenteric plexus is
polarized toward anal direction
-Peristaltic reflex (“law of the gut”) – when segment of gut is excited by distention,
peristalsis begins at orad side of distended segment and moves toward the distended
segment, pushing contents in anal direction 5-10cm before dying out
-gut sometimes relaxes downstream (called “receptive relaxation”)
-does not occur without the myenteric plexus
2. Mixing Movements – differ in different parts of tract, some areas peristalsis triggers movement
like near sphincter, when peristalsis can only churn food, at other places, local intermittent
constrictive contractions occur every few centimeters lasting 5-30 seconds, where new
constrictions occur to chop and shear contents.
Gastrointestinal Blood Flow – blood vessels of GI are part of more extensive system called splanchnic
circulation, includes blood flow through the gut itself plus blood flows through spleen, pancreas, and
liver
-blood from all GI, spleen and pancreas flows to liver through portal vein, passes through portal
sinusoids and leaves by hepatic veins to empty into the vena cava.
-reticuloendothelial cells in liver sinusoids remove bacteria and other particulate matter from blood so
that they don’t get transported to other areas of body
-nonfat, water-soluble nutrients absorbed from guy enter liver sinusoids as well.
-parenchymal cells of liver (hepatic cells) store 50-75% of all nutrients
-almost all fats do not go through portal system and instead are absorbed through intestinal wall into
lymphatics which drain into the thoracic duct bypassing the liver.
-blood flow in each area of GI is related to level of local activity. During absorption of nutrients, blood
flow in villi and adjacent submucosa is increased as much as 8-fold
-blood flow in muscle increases with motor activity of gut
Causes of increased blood flow during GI activity – vasodilator substances are released from mucosa of
tract during digestive processes, such as cholecystokinin, vasoactive intestinal peptide, gastrin, and
secretin
-GI glands release two kinins into gut wall: Kallidin and bradykinin – powerful vasodilatorsthat are
believed to cause much of the increased mucosal vasodilation that occurs along with secretion
-decreased oxygen concentration in gut wall can increase blood flow up to 100%, also increases
adenosine by 4-fold, which is a vasodilator
Countercurrent Blood Flow in the Villi – arterial blood flow into villus is right next to venous drainage,
and as much as 80% of arterial blood drains directly into veins before ever reaching the tip of the villus,
making it not available for local metabolic functions of villi
-not harmful to villi, but in disease conditions in which blood flow to got becomes stopped, villus can
suffer ischemic death
Nervous Control of Gastrointestinal Blood Flow – parasympathetic nerves going to stomach and lower
colon increases blood flow at the same time as glandular secretion (nerve second to gland)
-sympathetic stimulation however has a direct affect to cause vasoconstriction of arterioles with greatly
diminished blood flow
-after a few minutes, blood flow returns to normal via a mechanism called autoregulatory
escape – where local metabolic vasodilator mechanisms are elicited by ischemia to override
sympathetic vasoconstriction
-major value of sympathetic vasoconstriction is that it allows shutoff of GI and other splanchnic blood
flow during heavy exercise, when skeletal muscle needs the blood, and also in circulatory shock when
brain and heart need the blood
-sympathetic stimulation also vasoconstricts big vessels such as intestinal and mesenteric veins,
shunting blood to other parts of body to sustain general circulation