PHASES
* The primary cephalic phase (central) involves a
reflex where
the C.N.S.
participates.
- The sight, smell or taste of food excites
secretion of
gastric juice
through impulses along the vagus nerve.
- This mechanism is also brought into action by
a fall of
blood
glucose.
- This gastric juice is rich in acid and
pepsin.
* The secondary phase is initiated by the presence
of food in
the stomach.
- This reflex is stimulated by the distension
of the stomach
and certain
chemical substances (peptones, amino acids,
caffeine
etc.)
- This juice secreted is rich in acid.
The transmitter in both these reflexes is acetylcholine,
this
local reflex in secondary gastric phase can be prevented
by local
anaesthetic application to the antral mucosa.
This action is through histamine and is executed through
H2
receptors and is not affected by antihistamine
* The third phase
is hormonal by the liberation of a polypeptide
gastrin from
antral mucosa.The normal plasma levels of
gastrin are 30-60 pg/ml, after feeding they increase
to 200-
400 pg/ml
Gastrin Release
The
G cells in the antrum synthesize the peptide gastrin. The release of gastrin is
stimulated by intraluminal amino acids as well as di- and tripeptides. The most
powerful amino acids are aromatic: tryptophane and phenylalanine. Antral
distention also causes the release of gastrin.
During the cephalic phase of acid secretion, stimulated by the
senses (sight, smell, and taste) gastrin is released into the systemic
circulation through a long neural network involving the vagal nucleus in the
thalamus. The neural transmitter for this is the gastrin-releasing peptide
(GRP) released from the postganglionic neurouns terminating on the G cell.
There are also D cells in the antrum, that contain
somatostatin. Somatostatin acts as a paracrine agent to inhibit the release of
gastrin, when the antral lumen is acidified, serving as a negative feedback mechanism
to inhibit the release of gastrin. There are some data suggesting that the
colonization of the antrum by Helicobacter pylori is associated with increased
rate of acid secretion in some patients. One of the mechanisms suggested is
related to the ability of H pylori to interfere with this negative feedback
mechanism.
There is some evidence that colonistion of antral mucosa
by H pylori inhibits release of somatotstatin thus blocking the negative feed
back, these patients have hyper gastrinemia and huperacidity.
- Gastrin is also
produced by pancreatic tumors and the high
levels thus
produced give rise to Zollinger-Ellison Syndrome
leading to
peptic ulceration.
HISTAMINE
It seems that Gastrin response of the gastric mucosa is
also
mediated through the release of histamine in the vicinity
of
parietal cells.
This action of histamine is executed through H2 receptors
and is
not affected by antihistamines.
GASTRIN INHIBITORS
* Gastric
inhibitory peptide (GIP) released from duodenum.
Its initial peak
is stimulated by blood glucose and later
sustained
release is evoked by fat in the lumen of duodenum.
* Vasoactive
intestinal peptide (VIP) is present in the entire
gastrointestinal
tract.
It inhibits
gastric secretion.
This hormone
also stimulates secretion of water and
electrolyte by
the pancreas.
Certain
intestinal tumours secreting this hormone cause watery
diarrhoea and
hypokalemia.
* Glucagon
secreted by cells of the islets of Langerhans in the
pancreas, inhibits
gastric secretion and motility of the
gastrointestinal
tract.
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