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PHGY210: MAMMALIAN PHYSIOLOGY II
Lecture25:
March 8th 2010
THE DIGESTIVE SYSTEM
Gut regulatory peptides  Gut peptides are a number of peptide agents that are released
from endocrine cells in the mucosa of the stomach and the small intestine by nervous,
chemical and mechanical stimulation, coincident with the intake of food. They are
released into the portal circulation, and then they pass through the liver to the heart, and
back to the digestive system to regulate its movements and secretion.
Thus, GIT regulation involves short enteric (intramural) reflexes that are essential and the
digestive system would fail if these were destroyed. It also involves long extrinsic (ANS)
reflexes that are modulatory only. Hormonal factors also modulate enteric reflexes.
3 activities:
1. MOTILITY  muscular activity  propulsion and physical breakdown
Propulsion (flow) down the GIT depends on the gradients of pressure and the variations
in resistance.
 The gradients of pressure are used to set up propulsions and involve coordinated
contractions of muscular elements in the walls of the GIT. There are two types of
contraction:
o Segmentation – this divides the tube into segments and is analogous to
kneading dough.
o Peristalsis – this is a propagated wave of contraction that is analogous to
squeezing toothpaste out of a tube.
 The variations in resistance: there is normally little to no resistance.
There are three phases of deglutination (swallowing): the oral, pharangeal and
esophageal phases. Deglutination is accomplished though a complex series of highly
coordinated muscular movements aimed at building up pressure, temporarily sealing off
of compartments to prevent dissipation of pressure and decreasing resistance.
a) The oral phase of deglutition – this involves transport from the anterior mouth to the
pharynx. This phase is under voluntary control. Food becomes a bolus and is rolled to the
posterior portion of the mouth. As soon as the bolus goes to the pharynx – we enter the
pharyngeal phase. Thus the oral phase involves a series of reflexes coordinated in the
deglutition centre in the medulla oblongata. However, all the movements of the tongue,
cheeks etc… are under involuntary control in the medulla – reflex control. The voluntary
portion originates from the cortex.
b) The pharyngeal phase – this is where the respiratory and digestive tracts cross. This is
under involuntary control and involves a series of protective reflexes, initiated by
stimulation of afferent fibres in the pharynx, as organized in the Deglutition Centre. To
swallow safely and get the bolus to the esophagus and not the trachea, all the openings to
the nose, mouth and larynx close to prevent misdirection of the bolus. At the same time,
respiration is briefly inhibited  apnea. As well, in the transfer to the esophagus, as the
pharyngeal muscles contract, the upper esophageal sphincter (UES) relaxes.
Deglutition reflexes are integrated n the medullary centre. Pharyngeal receptors
send out afferents to the deglutition centre that sends efferent outputs that effectuate
protective reactions like deglutition apnea, contraction of the pharyngeal constrictor
muscles and relaxation of the UES.
Closure of the UES occurs from impulses originated in the CNS and mediated by
the vagus nerve that releases Ach onto nicotinic receptors on the cricopharyngeus
muscle (a striated muscle with a neuromuscular junction). These receptors can be blocked
by curare. Relaxation is controlled by the cessation of impulses from the vagus so the
muscle receives no stimulation and it will relax.
In summary, the pharyngeal phase is under involuntary control, is rapid (takes
only about 1/5th of a second) so we aren’t aware of apnea, and is “Stereotyped” – once
the pharangeal receptors are stimulated, the entire sequence of events occurs. This is a
temporospatial coordination.
c) The esophageal phase – this is a strongly muscular organ. The body of the esophagus
lies within the thoracic cavity. The pressure in the intrathoracic cavity is subatmospheric.
Since the pressure in the pharynx is equal to atmospheric pressure, the UES must contrict
so that air and saliva are not sucked into the esophagus. As well, the intragastric pressure
is positive so without the lower esophageal sphyncter, gasses would always be going
back into the esophagus.
The entire esophagus is innervated via the vagus nerve. Impulses are sent to the
striated cricopharyngeus muscle. As well, impulses from the vagus nerve are sent to the
enteric neurons in the smooth muscle. Here, the parasympathetic preganglionic fibers
stimulate the release of Ach onto muscarinic Ach receptors or onto NANC inhibitory
neurons.
Peristalsis – a wave of contraction moving over the wall of the organ, narrowing the
lumen and setting up a gradient of pressure favoring aboral (away from the mouth)
movement. Each time we swallow, a single primary peristaltic wave is generated. It
takes 8-10 seconds to be propagated the length of the esophagus. Thus, primary
peristalsis is part of the deglutition reflexes. Pharyngeal receptors send afferents to the
deglutition centre that sents out vagal somatic fibers to the striated regions. These fire
sequentially distally to proximal. The deglutition centre also activates the vagus
autonomic fibers that stimulate enteric nerves around at the same time as the striated
muscle is activated but there is a pre-programmed delay with which the enteric neurons
respond.
Thus, when you cut the vagus at the upper portion, there is no primary peristaltic
wave. However, if it is cut lower down, the somatic system is still intact and there are
some autonomic fibers left uncut. This is enough activation to activate sequential ganglia.
Thus, the peristaltic wave is propagated. This results in a smoothly propagated
contraction. Thus, the vagus is essential for initiating peristalsis in the proximal
esophagus. Continuation and propagation in the distal esophagus requires intactness of
the ENS.
The primary peristaltic wave carries the bolus to the esophagus but if the bolus is
too large or too sticky, it will be constricted in the esophagus. Local distension initiates a
secondary peristaltic wave that may be mediated by enteric reflexes or by long vagal
reflexes. Several secondary peristaltic waves may be generated until the bolus has been
displaced.