Effect of Agonist and Antagonist on the Uterine Contraction of a Rat

8/10/2019 Effect of Agonist and Antagonist on the Uterine Contraction of a Rat

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Effect of Agonist and Antagonist on the Uterine Contraction of a Rat

Julio Francisco, Chris Grant, Chessie Cales and, Nora Abbas

Dr. Turingan

Mammalian Physiology

October 8, 2013

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Normal

Contraction 2

2.1 0.12 0.34 0.11 225.49 2

Normal

Contraction 3

1.84 0.16 0.31 0.21 225.9 2

Normal Average 1.93 0.12 0.307 0.173 225.65 22

Oxytocin 1 2.966 0.14 0.24 0.19

Oxytocin 2 2.571 0.07 0.89 0.49

Oxytocin 3 3.219 0.06 0.5 0.36

Oxytocin

Average

2.919 0.09 0.543 0.347

Atropine-Acetylc

holine 1

2.69 0.1 0.27 0.17

Atropine-Acetylc

holine 2

2.51 0.16 0.33 0.17

Atropine-Acetylc

holine 3

2.81 0.15 0.37 0.22

Atropine-Acetylc

holine Average

2.67 0.137 0.323 0.187

Epinephrine 1 3.36 0.22 0.28 0.14

Epinephrine 2 1.87 0.05 0.16 0.11

Epinephrine 3 2.115 0.12 0.14 0.04

Epinephrine

Average

2.448 0.13 0.193 0.0967

Table 1. The Contraction Amplitude, Contraction Time, Relaxation Time, Contraction Period

and Uterine Tone of Uterine Tissue Exposed to Different Agonists and Antagonists.

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Figure 1. Effect of different drug treatments on the Mean Contraction Amplitude (g) of the

Female Rodent Uterine.

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Figure 2. Effect of Different Drug Treatment on the Mean Contraction Time (sec) of Rodent

Uterine.

Figure 3. Effect of Different Treatments on the Mean Contraction Period (sec) on Rodent

Uterine.

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Figure 4. Effect of Different Drug Treatments on the Mean Relaxation Time (sec) on the Uterus

of a Rodent.

Discussion:

The menstrual cycle is a sequence in which the inner glandular membrane of the uterus

called the endometrium is shed, regrown, proliferated, and shed again (Endometrium, 1999).

The menstrual cycle begins with menarche and end with menopause, in which the cycle takes

about 28 days for changes to occur (Menstrual cycle, 2012 Scogna, 2004). The menstrual

cycle is divided into three phases: the menstrual phase, proliferative phase, and secretory (or

progestational) phase (Sherwood, 2012).

The menstrual phase is characterized by a period of bleeding. In this phase, progesterone

and estrogen level drop depriving the uterine lining of its hormonal support. The drop of ovarian

hormone level releases the hormone, prostaglandin, which causes vasoconstriction of

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endometrial vessels. As a result of the vasoconstriction, the endometrial blood supply is

disrupted, and thus, oxygen supply is also tempered, causing the death of the endometrial.

Furthermore, the proliferative phase is period in which the endometrial starts

self-repairing and proliferation of the epithelial cells, glands, and blood vessels of the

endometrial, all of which is influenced by the increase level of estrogen.

Subsequently, the secretory phase occurs after the development of the ovum, a period

called ovulation (Ovulation, 2010). During the secretory phase, the corpus luteum (CL)

secretes the hormones progesterone and estrogen. Both hormones cause the endometrium to

develop into a vascularized, glycogen-filled tissue. Progesterone also stimulates the glands to

secrete substances to maintain the endometrium from breaking down. If fertilization does not

occur, CL will stink and progesterone level will drop, at approximately 22 to 28 days. As a

result, the endometrium will degenerate and a new follicular phase (the stage of mature follicular

development) and menstrual phase begin again.

Menstruation, also occurring during menstrual cycle, is a monthly period that starts at age

11 to 15 until a female reaches menopause. During this period, women experience vaginal

bleeding, abdominal or pelvic cramping, lower back pain, bloating and sore breasts, food

cravings, mood swings and irritability, headache, and fatigue (U.S. National Library of Medicine

[NLM], 2013). Not to mention, menstruation is the stage in which there is an increase of the

hormone, prostaglandins. Prostaglandin is associated with uterine contractions and cramps. As

prostaglandins level increases, the stronger the contractions and more intense cramps occur

(Scogna, 2004).

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Lastly, the cession of estrogen and progesterone production occurs during menopause,

which affects women around age 45. For some women, three consecutive months of absence of

menstruation is an indicator of menopause (Nelson, 2008). Some of the symptoms of menopause

include hot flashes, night sweats, sleeping problems, vaginal dryness, mood swings, trouble

focusing, hair loss, and facial hair growth. People affect with menopause often seek treatment

such as hormonal therapy, alternative drug treatments, and lifestyle changes (NLM, 2013).

With this information in mind, we investigate the effect of different drug treatments on an

isolated uterine of the rat. As previously mention, we used the four different stimulants: normal,

oxytocin, atropine-acetylcholine combination, and epinephrine. We hypothesized the following:

1. There is no difference between the four different treatments and contraction amplitude.

Alternatively, one should also consider that there is a different between the four different

treatments and contraction amplitude.

2. There is no different between the treatments and contraction time. Our alternate hypothesis

that there is different between the treatments and contraction time.

3. There is no difference between the four different treatments and contraction period.

Alternatively, there is a difference between the four different treatments and contraction

period.

4. There is no difference between the four different treatments and relaxation time. Our

alternative hypothesis is that there is a difference between the four different treatments and

relaxation time.

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To predict the effect of the four various treatments on the values of the contraction

amplitude, contraction time, contraction period, and relaxation time, one must understand the

nature of the drugs and its effect on the uterine.

First, oxytocin, produced by the pituitary gland, is known to stimulate uterine contraction.

Oxytocin is also used to assist in labor and childbirth (Oxytocin, 2010). Next, atropine is a

competitive antagonist for the parasympathetic nervous system (PNS) action (Atropine, 2010),

in which the PNS consist of the smooth muscle, cardiac muscle, and gonads. As one should

know, the uterine is composed of smooth muscle. Therefore, atropine is expected to inhibit the

action of the uterine. Furthermore, acetylcholine is a neurotransmitter that is release in the

synaptic gap at the neuromuscular junction or between neurons to cause nerve impulses at the

motor end plate of a muscle fiber or postsynaptic terminal. Lastly, epinephrine (also known as

the adrenaline) is a hormone secreted by the adrenal medulla that responsible for the preparing

the body for physiologic emergency, and elevates heart pressure and heart rate (Kemppainen &

Li, 2012). Nobly, the epinephrine binds to beta-adrenergic receptors to cause the relaxation of

smooth muscle (Labscribe).

Based on the nature of the drug compounds, one can expect the oxytocin to increase the

values of contraction amplitude, contraction time, contraction period, and relaxation time due to

the fact that oxytocin causes uterine contractions. Furthermore, atropine would cause a larger

value. This is due to the atropine proclivity to cause the smooth muscle to relax, and thus, cause

a prolonged in time of uterine contraction and increase the values of the contraction amplitude,

contraction time, contraction period, and relaxation time. However, this experiment called for an

atropine-acetylcholine combination. No further research can be found on the effect of adding

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atropine and then acetylcholine to the rodent uterine. On the other hand, one can predict that

value for the combination will be lesser than the normal due to the fact that atropine is a

competitive antagonist.

Additionally, one can assume that adding epinephrine would cause the values to be

higher than the normal. This could be explained by epinephrine ability to relax the smooth

muscle, and therefore, prolonging the time for contraction. .

After conducting the experiment, we discovered the following:

1. Our result supports the null hypothesis that there is no difference between the contraction

amplitude and the treatments used (F=2.709, df=3, p=0.115).

2. The result supports that there is no difference between the different drug treatments and

the contraction time (F=0.431, df=3, p=0.737).

3. The data supports the null hypothesis there is no difference between the four treatment

groups and contraction period (F=2.205,df=3, p=0.165).

4. Our result reject the null hypothesis, and therefore, accepts our alternative hypothesis that

there is a difference between the drug treatments and relaxation time (F=4.541, df=3,

p=0.039).

These finding is evident as one can see from Figures 1 to 4. There was no significant

difference between the drug treatments and the values of the contraction amplitude,

contraction time, and contraction period. However, there was a significant difference

between the treatment and the mean relaxation time. Oxytocin has the highest mean value, of

0.347 sec. The second highest was atropine-acetylcholine combination with a value of 0.187

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sec, leading to a significant difference of 0.160 sec. Therefore, we had to reject our null

hypothesized and accept the alternative hypothesis.

All and all, we cultured an understanding of the menstrual cycle and recognized the

nature of the drugs. We also supported that there is no difference between the drug treatments

and the values of the contraction amplitude, contraction time, and the contraction period.

However, we did reveal that there is a difference in the treatment group and the relaxation

time.

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References:

Acetylcholine. (2009).In The Penguin Dictionary of Science. Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/penguinscience/acetylcholin

Atropine. (2010).In Black's Medical Dictionary, 42nd Edition. Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/blackmed/atropine

Endometrium. (1999).In Macmillan Dictionary of Toxicology. Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/mactox/endometrium

Kemppainen, R., & Li, C.H. (2012) Epinephrine. InAccessScience. Retrieved from

http://www.accessscience.com.portal.lib.fit.edu/content/Epinephrine/238400.

LabScribe Manual, Experiment AM-4: Uterine Motility.

Menstrual cycle. (2012).In Mosby's Dictionary of Medicine, Nursing, & Health Professions.

Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/ehsmosbymed/menstrual_cycle.

Nelson, H. D. (2008). Menopause. The Lancet, 371. Retrieved from

http://www.sciencedirect.com.portal.lib.fit.edu/science/article/pii/S0140673608603463?n

p=y.

Ovulation. (2010).In Black's Medical Dictionary, 42nd Edition. Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/blackmed/ovulation

Oxytocin. (2010).In Black's Medical Dictionary, 42nd Edition. Retrieved from

http://www.credoreference.com.portal.lib.fit.edu/entry/blackmed/oxytocin.

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Scogna, K. (2004). Menstrual Cycle.In The Gale Encyclopedia of Science. Retieved from

http://go.galegroup.com/ps/i.do?id=GALE%7CCX3418501432&v=2.1&u=d0_mlpbcls&

it=r&p=GVRL&sw=w&asid=7fcacfdc9608585f317b2ace7eb24bc6.

Sherwood, Lauralee. (2012).Fundamentals of Human Physiology. 4th ed. Belmont, CA:

Brooks/Cole Cengage Learning.

U.S. National Library of Medicine. (2013). Menopause. Retrieved from

http://www.nlm.nih.gov/medlineplus/menopause.html.

U.S. National Library of Medicine. (2013). Menstruation. Retrieved from

http://www.nlm.nih.gov/medlineplus/menstruation.html.

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Effect of Agonist and Antagonist on the Uterine Contraction of a Rat