Download Motor function( peristalsis or motility)

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Lec.2
17 March 2016 2014
Dr Baybeen Alselevany
GIT
Objectives:
 Motor function( peristalsis or motility)
 Blood supply (splanchnic circulation)
Motor function: Peristalsis
The motor functions of digestive system are of two basic types:
1. Propulsive Movements
2. Mixing movements
1. Propulsive Movements: Peristalsis
Peristalsis is an inherent property of many syncytial smooth muscle
tubes. Propulsive movements which cause food to move forward
along the tract at an appropriate rate to accommodate digestion and
absorption. The total time that is takes food to travel the length of the
digestive system is usually 24-36 hours.
 . Peristalsis is a reflex response that is initiated when the gut wall
is stretched by the contents of the lumen, and it occurs in all parts
of the gastrointestinal tract from the esophagus to the rectum.
The stretch initiates a circular contraction behind the stimulus and
an area of relaxation (receptive relaxation) in front of it. There are
other stimuli that can initiate peristalsis such as chemical or
physical irritation of the epithelial lining in the gut .Also strong
parasympathetic excitation to the gut will elicit strong peristalsis by
releasing ACH. Peristalsis is greatly depressed or completely
blocked in the entire gut when a person is treated with atropine to
paralyze the cholinergic nerve ending of the myenteric plexus
therefore effectual peristalsis requires an active myenteric plexus .
Peristaltic activity can be increased or decreased by the
autonomic input to the gut, but its occurrence is independent of
the extrinsic innervation
2. Mixing Movement: Is a local intermittent constrictive contraction
that occurs every few centimeters in the gut wall. The main function of
these mixing contractions is to mix the food with digestive secretion and
to help break it into smaller pieces. Segmentation contractions are
example of mixing contraction that occurs in the small intestine.
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Gastrointestinal Blood Flow—“Splanchnic Circulation”
The blood vessels of GIT are part of a more extensive system called
the Splanchnic Circulation., It includes the blood flow through the gut
itself plus blood flows through the spleen, pancreas, and liver.
Blood drains from gut, spleen and pancreas via Hepatic Portal veins to
liver and from the liver through hepatic veins to the inferior vena cava.
The viscera and liver receive about 80% of cardiac output. This flow of
blood through the liver before it empties in to the vena cava, allows the
reticuloendothelial (REC) cells that line the liver sinusoids to remove
bacteria and other matter that might enter the blood from the GIT thus
preventing direct transport of potentially harmful agent into the remainder
of the body. Carbohydrate, and proteins (non -fat water – soluble
nutrients) absorbed from the gut, are transport in the portal venous blood
to the same liver sinusoids, while all of the fats absorbed from the GIT
are not carried in the portal blood but instead are absorbed into the
intestinal lymphatic and then conducted by way of the thoracic duct to the
systemic circulation blood by passing the liver.
Effect of GIT Activity and Metabolic Factors on GI Blood Flow
Under normal condition the blood flow in GIT is directly relative to the
level of local activity. After a meal the motor activity (peristalsis)
& secretary activity and absorptive activity all increase ; likewise the
blood flow increases but then decreases back to the resting level over
another 2-4 hours. The possible causes of the increased blood flow during
GI activity are due to. First, several vasodilator substances are released
from the mucosa of the intestinal tract during the digestive process. Most
of these are peptide hormones, including cholecystokinin (CCK), gastrin,
secretin and vasoactive intestinal peptide (VIP). Second, some of the
gastrointestinal glands also release into the gut wall kinins, kallidin and
bradykinin, at the same time that they secrete their secretions into the
lumen. These are powerful vasodilators that are believed to cause much
of the increased mucosal vasodilation. Third. Decreased O2
concentration (hypoxia) in the gut can increase intestinal blood flow at
least 50-100%. Hypoxia can also lead to an increase in adenosine, a wellknown vasodilator that could be responsible for much of the increased
flow.
Nervous Control of Gastrointestinal Blood Flow
Parasympathetic Stimulation: Stimulation of the parasympathetic
nerves going to the stomach and lower colon increases local blood flow at
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the same time that it increases glandular secretion. Sympathetic
stimulation, by contrast, has a direct effect on essentially all the
gastrointestinal tract to cause intense vasoconstriction of the arterioles
with greatly decreased blood flow. After a few minutes of this
vasoconstriction, the flow often returns almost to normal by means of a
mechanism called “autoregulatory escape.” That is, the local metabolic
vasodilator mechanisms that are elicited by ischemia become prepotent
over the sympathetic vasoconstriction and, therefore, redilate the
arterioles, thus causing return of necessary nutrient blood flow to the GI
glands and muscle.
Importance of Nervous Depression of Gastrointestinal Blood
Flow When Other Parts of the Body Need Extra Blood Flow.
A major value of sympathetic vasoconstriction in the gut is that it allows
shut-off of gastrointestinal and other splanchnic blood flow for short
periods of time during heavy exercise, when increased flow is needed by
the skeletal muscle and heart. Also, in circulatory shock, when all the
body’s vital tissues are in danger of cellular death for lack of blood
flow—especially the brain and the heart—sympathetic stimulation can
decrease splanchnic blood flow to very little for many hours.
"Countercurrent” Blood Flow in the Villi.
The arterial flow into the villus and the venous flow out of the villus are
in directions opposite to each other, and that the vessels lie in close
apposition to each other. Because of this vascular arrangement, much of
the blood oxygen diffuses out of the arterioles directly into the adjacent
venules without ever being carried in the blood to the tips of the villi.
As much as 80 per cent of the oxygen may take this short-circuits route
and therefore not be available for local metabolic functions of the villi.
The reader will recognize that this type of countercurrent mechanism
in the villi is analogous to the countercurrent mechanism in the vasa
recta of the kidney medulla.
Under normal conditions, this shunting of oxygen from the arterioles to
the venules is not harmful to the villi, but in disease conditions in which
blood flow to the gut becomes greatly curtailed, such as in circulatory
shock, the oxygen deficit in the tips of the villi can become so great that
the villus tip or even the whole villus suffers ischemic death and can
disintegrate. Therefore, for this reason and others, in many
gastrointestinal diseases the villi become seriously blunted, leading to
greatly diminished intestinal absorptive capacity.
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L ec.3
17 April. 2016
Hormonal control of GIT
Objective
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Gastrin
Cholecystokinin
Secretin
gastrin releasing peptide
Gastric inhibitory peptide
Vasoactive intestinal peptide
motilin
There are More than 15 types of hormone-secreting entero-endocrine
cells have been identified in the mucosa of the stomach, small intestine,
and colon. Many of these secrete only one hormone and are identified
by letters (G cells, S cells –cells, etc.).. Gastrointestinal hormones are
biologically active polypeptides. They also enter the circulation and play
a role in the regulation of gastrointestinal secretion and motility.
1. Gastrin
1. Gastrin is secreted by the “G” cells of the antrum of the stomach in
response to stimuli associated with ingestion of a meal, such as distention
of the stomach, the products of proteins, and gastrin releasing peptide
(GRP).GRP is released by vagal nerve endings to G- cells. Gastrin
functions :
(a) Stimulation of gastric acid secretion (b) stimulation of growth of the
gastric mucosa.
2. Cholecystokinin (CCK)
Is produced by I -cells in the duodenum and upper jejunum
1- Strongly contracts the gallbladder and allow release of bile into the
small intestine where the bile in turn plays important roles in emulsifying
fatty substances, allowing them to be digested and absorbed..
2. Causing secretion of pancreatic juice rich in enzymes. .
3- Relaxes sphincter of Oddi.
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4. Fatty acids are the main stimuli for the release of CCK.
3. Secretin
Secreted by S-cells in the duodenal mucosa.
1-acts to promote secretion of bicarbonate from pancreas and gallbladder
which in turn neutralize the gastric acid in the small intestine.
3. Stimuli that increase secretin secretion is gastric acidic juice emptying
into the duodenum from stomach.
4. Gastrin Releasing Peptide (GRP)
1. Secreted by the postganglionic vagal nerve ending to G-cells that
release hormone gastrin rather than acetylcholine (Ach), So atropine does
not inhibit the gastrin release in response to a meal test in humans.
2. Increase release of the hormone gastrin .
5. Gastric Inhibitory polypeptide (GIP)
1. GIP in secreted by K- cells in small intestine
2. Stimulate insulin secretion and it is called glucose – dependent
insulintropic polypeptide
3. Inhibit gastric motility and secretion.
6. Vasoactive Intestinal Peptide (VIP)
1. secreted from duodenal mucosa.
2- Inhibit gastric acid and gastrin secretion
3- sphincters dilatation.
7. Motilin
1. secreted by the upper duodenum during fasting.
2. Its function to increase gastrointestinal motility every 90 minutes in a
fasted person.