Welcome. This is our last lecture on the GI tract.
Today, we want to talk about motility and how we move materials through the GI
tract. So if you recall, we've been talking
about the, the gastrointestinal tract or GI tract as a processing plant where we
start in the mouth and we digest the materials in the next compartment, which
is in the stomach and in the small intestines.
And then, move materials into the lower portion of the intestine where we're
absorbing most of our fluids and our nutrients.
And then, move into the, to the colon where the large intestinal region, where
we are absorbing a lot of the fluids. And so, this, this is a unidirectional
movement through the tract. And what's important is we have a timed
event. So that there are sufficient amounts of
time for digestion to occur, and for reabsorb, for absorption to occur before
the materials then exit from the body as the feces, fecal material.
A motility then is going to govern this time, this timing as we're moving along
the, the tube. So let's consider the first, the general
anatomy of the tube. As you recall from our first lecture that
in, of this particular series that we have, on the outer most aspect of the
gastrointestinal tract or tube, we have two layers of smooth muscle and that's
what's shown here. The smooth muscle is said to be in the
muscularis externa. The muscularis externa has these two
layers the inner most layer is circumferential around the lumen of the
tube and the outermost layer is longitudinally-oriented along the long
axis of the tube. When we contract this, the circular
muscle, the circular layer or the inner layer, if that contacts, it will make the
lumen of the tubes smaller, and if it relaxes, then the lumen of the tube
increases. In contrast, when we contract, when we
contract the outermost layer, as we as we contract the outermost layer, the tube
will shorten, and it will shorten in regions or segments along the tube.
The from the time that we enter into the esophagus to the time that we leave the
tube, most of the, of this muscle is going to be smooth muscle.
It starts in the in the lower 1 3rd of the esophagus and moves all the way
through to to the end of the large intestine.
This is all smooth muscle, and the smooth muscle is the signal, signal unit type
smooth muscle, where all of the cells are going to be connected to one another
through gap junctions, so they're electrically coupled cells.
[COUGH] Excuse me. The activity of the two layers of muscle
have to be coordinated and this coordination is done by a local nervous
system which is called the enteric system enteric nervous system, and that is what
shown here. So, the enteric nervous system is located
between the two muscle layers. The enteric nervous system effectively
governs the mortality along the tract independent of the central nervous
system. The central nervous system can modulate
this activity through other branches of the autonomic nervous system and that is
the parasympathetic and the sympathetic nervous system.
Now, the, there's another factor that we have to consider when we talking about
motility of the smooth muscle through this tract.
And that is, is that there is located within the tract, within the, within the
fundic region of the stomach, within the small intestine and within the large
intestine specialized smooth muscle cells which are called pacemakers.
And like all pacemakers, they have an unstable resting membrane potential and
that's what's shown here. So in our top image, we have the cells
are slowly depolarizing. And then they repolarize, and then again,
slowly repolarize. As the cells are slowly repolarizing,
depolarizing and repolarizing, they're generating what is called the electrical
slow-waves. These electrical slow-waves then bring
the resting membrane potential of the smooth muscle cells of these pacemaker
cells close to threshold, and at that point, we can initiate an action
potential. And if the action potential is initiated,
it means we've reached the voltage at which the voltage gated calcium channels
open. The voltage gated calcium channels open,
calcium enters the cells, and action potential is generated.
To repolarize the cells, we then close the voltage-gated calcium channels and
open a voltage-gated potassium channel, and that then repolarizes the cells.
It, within this, the intestines, that is, within the small intestine and the large
intestine, every every one of these slow-waves, electrical slow-waves is not
associated with an action potential. Only those that reach threshold and will
generate will generate the action potential.
But those that generate the action potential will be followed by a
contraction. So, wherever we have an action potential
generated, there would be a contraction of the smooth muscle.
Within the stomach, this is not true. So within the stomach, as we have these
rhythmic slow-waves, the rhythmic slow-waves actually can give rise to a
contraction. So within the stomach, you don't have to
generate an action potential, but the threshold of the slow-wave is associated
with, with contraction. There's one other thing about these
slow-waves, and that is that the slow-wave determines the frequency of the
action potential, and therefore, the frequencies of the contraction, but then
the slow-waves can be modulated. That is the pacemaker cells.
Can, their timing can be modulated by the sympathetic system and by the
parasympathetic, parasympathetic system. The sympathetic nervous system will cause
a hyperpolarization of these cells and move this and move this resting membrane
potential of the pacemaker cell further from threshold.
This simply means that it takes a longer time for the cells to be able to reach
threshold, and eventually, to fire off an action potential.
So the sympathetic nervous system then delays the, the ability of the cell to
reach, to reach a threshold and to generate an action potential, and
therefore, delays contraction. The converse is true of the
parasympathetic system. The parasympathetic system moves the
resting membrane potential towards threshold, so it's fast, the cells reach
threshold at a faster pace. And by reaching threshold at a faster
pace, they can then generate an action potential and, and contraction, so we can
speed up contractions by having input from the parasympathetic system.
Now, what kinds of motility are we actually talking about?
So, in the fed, in the fed state, you have two types of motility.
The motility that we're going to talk about first is called segmentation or
this is a mixing type of motility. In segmentation, we have a neighboring
two neighboring regions of the, of the tract, where the first is relaxed, and we
have a food bolus within that region. And the second is contracted and has no
food within the region. The first will contract and the second
relaxes, and that moves the food bolus, then to the second contract, second
chamber. And then, as the, as the second chamber
contracts, the first then open, relaxes again, and so we have this sloshing of
material back and forth. This kind of movement or segmentation or
mixing movement is very critical for mixing the materials the food substances
with the enzymes and with the buffers, and all of the secretions that we have
added to the lumens of the tract. In addition to that, it's also mixing the
material with the surfaces of the epithelial cells that are lining this
track and, and enhancing the absorption of the nutrients that we, that we have
generated. So, the smooth, the small amino acids,
the small sugars, and so forth are now being delivered to the surfaces of these
cells, and they can then be absorbed by these cells.