SHINAL SHIWANI DEVI S11131664

BI309: COMPARATIVE ANIMAL PHYSIOLOGY TUESDAY (9-1PM)

TITLE: TOAD’S CARDIOVASCULAR PHYSIOLOGY

Objective

- To monitor the mechanical and electrical activity of the toad’s heart.

- To be able to dissect the toad for heart preparation
- Learn to perform in vivo preparation
- Observe how interventions such as temperature and chemical affect the way heart
performs.

Introduction

The cardiovascular system consists of the heart, blood vessels, and the approximately 5 liters of
blood that the blood vessels transport. Responsible for transporting oxygen, nutrients,
hormones, and cellular waste products throughout the body, the cardiovascular system is
powered by the body’s hardest-working organ — the heart, which is only about the size of a
closed fist. Even at rest, the average heart easily pumps over 5 liters of blood throughout the
body every minute .Unlike a human heart, the heart of the frog has three chambers, one
ventricle and two atria. Blood leaves the heart from the ventricle through a single truncus
arteriosus which is short and soon branches into two aortic arches which loop left and right and
dorsal to the heart to rejoin as a single aorta in the mid dorsal region of the body cavity (Ziser,
2014). Each aortic arch has a branch leading to the lungs and skin where oxygenation occurs.
Carotid arteries also branch off the aortic arches and supply the head region. Veins bring blood
to the left and right atria. Both atria then empty into the single ventricle. Blood from the
ventricle thus enters either the pulmonary or body circulation.

The purpose of this experiment is to monitor the activity of the toad’s heart as it was subjected
to various levels of temperature, stretch, and drug treatment. The drugs that was used in this
experiment was adrenaline, acetylchlorine and atrophine.

Materials and Method: as per lab handout

Results
Normal Tracing

normal graph
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(mV)

1
0
-1
-2
20 21 22 23 24 25
2

Heart beat rate (BPM)

7 beats = 5Seconds

X : 60 secs

X = 84 BPM

Duration of cardiac cycle

84BPM = 60 Sec

1BPM = X

X =0.71Sec
One beat-Cardiac Cycle

2 2/27/2018 10:47:10.846 AM
(mV)

1
0
-1
-2
21.3 21.4 21.5 21.6 21.7 21.8

VENTRICLE AND ATRIA CONTRACTION

A Auricular contraction (0.126 sec)

B Auricular relaxation (0.275 sec)

C Ventricular contraction (0.482sec)

D Ventricular relaxation (0.633sec)

Effect of temperature

10 degree

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2

1
diviya (mV)

0
10 degree

-1

-2
2 3 4 5 6 7 8 9 10
3

35 degree
 Document1

2/27/2018 10:54:44.959 AM
2

1
diviya (mV)

0
35 degree

-1

-2
1:54 1:56 1:58 2:00 2:02 2:04 2:06
5

Chemicals

Adrenaline

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2

1
diviya (mV)

0
aderaline

aderaline
-1

-2
2:48 2:49 2:50 2:51 2:52 2:53 2:54 2:55
8 9

Acy

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2

1
diviya (mV)

-1
Acy

-2
3:28 3:29 3:30 3:31 3:32 3:33 3:34 3:35 3:36 3:37 3:38
12

Atropine
 Document1

2/27/2018 10:57:28.069 AM
2

1
diviya (mV)

-1
Atropine

-2
4:36.5 4:37 4:37.5 4:38 4:38.5 4:39 4:39.5 4:40 4:40.5 4:41 4:41.5 4:42
15

Aderaline

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2

1
diviya (mV)

-1
Aeraline

-2
5:13 5:14 5:15 5:16 5:17 5:18 5:19
16

ACH
 Document1

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2

1
diviya (mV)

-1
ACH

-2
19 19.5 20 20.5 21 21.5 22 22.5 23
18

KCl

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2

1
diviya (mV)

-1
KCl

-2
1:08.5 1:09 1:09.5 1:10 1:10.5 1:11 1:11.5 1:12 1:12.5
20

Discussion
A normally performing heart must be fully expanded before it can efficiently pump again.
Assuming a healthy heart and a typical rate of 70 to 75 beats per minute, each cardiac cycle, or
heartbeat, takes about 0.8 second (Barrett, 2015).Moving on, to test the effect of temperature
on the toads hearts , the ringers solution of different temperatures was used. At 10 0C
temperature the heart beat rate decreased compared to 35 0C temperature. The rate decreased
at 100C because at low temperatures the blood nerves and arties become thin, restricting blood
flow. bradycardia caused by low temperature is mainly because a drop in temperature tends to
increased vagal activity, which leads to a reduction in the steepness of the “resting potential” of
the sinuatrial node myocytes, thus causing a delay in reaching the threshold for depolarisation,
which in turn slows down the heart rate.

To test the effect of chemicals on toad’s heart Acetylcholine, Adrenaline and Atropine were
applied. Atropine and Adrenaline increases the heart beats whereas Acetylcholine slows the
heart beat rate (Cris Lapierre,2010). Acetylcholine Secreted by the parasympathetic division of
the autonomic nervous system, specifically the branch of the vagal nerve that innervates the
heart; acts on muscarinic receptors. Primarily a negative chronotropic agent, although has some
effect on ventricular myocardium as a negative inotropic agent – Increases hyperpolarization in
cells of SA node by enhancing Ik and reduces depolarization by decreasing ICa and Ina; results in
an overall reduction of heart rate – Same mechanisms can result in an AV node block – Reduced
calcium current in ventricular myocytes responsible for slight reduction in contractility

Atropine Reduces parasympathetic (vagal) activity on heart by competing for binding sites of
muscarinic acetylcholine receptors. In a normal individual this acts to increase heart rate (vagal
tone usually dominates). In the denervated frogs (decapitated so no more autonomic control) it
simply acts to reverse the effect of the applied ACh. Excessive increase of extracellular
potassium causes the following: permanent depolarization (resting potential normally
maintained by a high intracellular potassium concentration) ,loss of excitability ,eventual cardiac
arrest during diastole.

Reference

 Cris Lapierre, Physiology of the Heart, Lippincott Williams & Wilkins, New York, 2001.

 Ziser, Cardiovascular Physiology, 7th Edition, Mosby, St. Louis, 2014.