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Discussion

The purpose of
this lab was to observe and measure the effects of epinephrine, methacholine,
ADP and Ca2+-free Ringer-Tyrode’s solution on the motility of a small intestine
segment. This lab gives an overview of the mechanisms involved in intestinal
motility. The different substances used in each trial mimic different
mechanisms that involve parasympathetic and sympathetic activity as well as
illustrate the importance of calcium in smooth muscle contraction.  While doing this lab, we directly applied the
substances to the small intestine segment and observed the response using the
BioPac system.

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Before the
addition of epinephrine, we observed the normal activity of the intestinal
segment while it was submerged in normal Ringer-Tyrode’s solution; this
solution contains calcium ions. All the controls. for the different trails, were
measured the same way. The extracellular calcium ions available allowed the
regular contraction of the intestinal segment, creating slow waves. Once
epinephrine was added, we observed a significant decrease in tension and wave
amplitude, while frequency had a small increase. These results agree with our
hypothesis, except for the slight increase in frequency which we concluded was
not significant and believed this was due to the pacemaking activity of ICC which
was not affected by the addition of epinephrine. According to Munro’s paper,
adrenaline (epinephrine), has an inhibitory effect on the tone of the smooth
muscle cells of the small intestine (Munro, 1953). We expected epinephrine to
mimic sympathetic activity on the intestinal segment, since epinephrine is an
adrenergic agonist. Epinephrine acts on GPCR which activates adenyl cyclase as
second messenger which later activate MLC phosphatase. MLC phosphatase
dephosphorylates MLC, causing a decrease in cross-binding of the thick and thin
filaments. This chain of reactions results in a decrease in smooth muscle
tension, but does not influence frequency sine ICC are not affected by
epinephrine. In figure 1, we can observe an 80.82% change from normal tension
to a suppressed tension caused by epinephrine; this a significant decrease that
illustrates sympathetic activity, which suppresses GI activity. It is believed
that the effect of epinephrine can fully abolish the tension produced in the
smooth muscle (Munro, 1953), but since we treated the intestinal segment with
only three drops of epinephrine, we believe that the dosage was not enough to
produce a complete suppression of tension production; our results after the addition
of epinephrine did not reach 0 at any point.

On the other hand,
when the intestinal segment was treated with methacholine we observed an
increase in tension and wave amplitude. In figure 2, we observe a dramatic
increase in tension and amplitude, as expected, while there was a slight
increase in frequency. These results mimic parasympathetic activity,
specifically the effects of acetylcholine on smooth muscle. Parasympathetic
activity stimulates muscle contraction, increasing muscle tension (Sherwood,
2016). The chain reaction initiated by acetylcholine on smooth muscle in the
gut ultimately activates MLC kinase which increases cross-binding of the thin
and tick filaments, increasing smooth muscle tension. Methacholine uses
acetylcholine’ pathway to produce this effect on smooth muscle since it is a
cholinergic agonist. Cholinergic agents produce tonic and phasic contractions
on longitudinal and circular smooth muscle respectively (Nowak et al. 1985).
This 51.29% change in tension from control to methacholine addition,
illustrates parasympathetic activity effect on small intestine, which increases
GI motility.

In trial 3, we
treated the intestinal segment with ADP, a purinergic agent. In figure 3 we
observed similar results to the epinephrine trial (figure 1), where there was a
decrease in both tension and wave amplitude. There was a slight increase in
frequency, but since the increase was not significant we concluded it was
caused by a system’s error in the Biopac system. These results agree with our
hypothesis. The decrease in tension is explained by the effect ADP has on
smooth muscle. This purinergic agent also activates IP3 pathway, just like
acetylcholine does (parasympathetic activity), but unlike acetylcholine
receptor, purinergic receptors are very localized and produce “calcium sparks”
which activate potassium channels, and lead to potassium efflux and
hyperpolarization of the cell. These receptors do not allow enough calcium to
enter the cell to overpower the potassium influx (Bournstein). On the contrary
muscarinic Ach receptors does allow more calcium influx, which leads to
depolarization. ADP mechanism is believed to be an alternate pathway of
sympathetic activity with the use of norepinephrine (Bournstein). Therefore,
the hyperpolarization caused by ADP decreases smooth muscle tension, leading to
the results observed in figure 3. Purinergic agents signaling is an
understudied topic, although it is believed to play signaling roles in the GI
track and its motility, the physiological conditions in which they act are not
fully understood (Bournstein, 2008).

In trial 4, we
looked at the differences found on intestinal motility when the intestinal segment
was moved from a rich calcium environment to a free calcium environment. In
figure 4, we observe there was a dramatic decrease in tension and wave
amplitude when the intestinal segment was moved from normal Ringer’s solution
to calcium-free Ringer’s solution. In addition, we observed a dramatic
decreased in frequency. These results agreed with our hypothesis. The key
factor in the explanation for these results is extracellular calcium, since extracellular
calcium is needed for smooth muscle contraction. Extracellular calcium is
necessary for smooth muscle contraction, since smooth muscle has a poorly
developed sarcoplasmic reticulum so it depends on extracellular calcium for
cross-bridge cycling between thin and thick filaments, and the depolarization
of the cell (Giraldi et al, 2015). The lack of calcium, once the segment was
submerged in calcium-free solution, decreased the tension created in the smooth
muscle of the intestinal segment since there was a decrease in cross-bridge
activity. Although there was a big decrease in tension, 82.82% change, tension
was not completely suppressed, meaning tension was never zero, we believe that
this is due to the small calcium storage in the SR, and still such calcium
allowed the production of tension to some extent. The interstitial cells of
Cajal (ICC) in the smooth muscle are also affected by external calcium
availability. These pacemaker cells act on the frequency of the contraction (Sherwood,
2016), once extracellular calcium was removed, we observed a significant
decrease in frequency, 50.79% change, as it can be observed in figure 4. The
slow waves or BER created by ICC, rely on calcium for their normal rhythmicity,
approximately 12 cycles per minute (Kito et al., 2015). Once voltage gated
channels open, there is a calcium influx which rises calcium concentration
inside the cell until it creates an action potential spike; with the absence of
extracellular calcium this mechanism does not occur as frequently, since the AP
threshold is not reached. In this trial, unlike the previous three trials,
frequency was affected, since this time the peacemaking activity was affected.
Adrenegic, cholinergic and purinergic agents do not influence ICC, as long as extracellular
calcium is available, ICC keeps its normal rhythmicity.

The experiments
done in this lab illustrate different mechanisms and pathways that have
different effects on intestinal motility.

 

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