Running head: PHYSIOLOGY PRACTICAL 2: TOAD HEART 1

Name:

La Trobe University

Animal Physiology

ZOO2AP

Physiology Practical 2: Toad Heart

Abstract

The cardiac muscle activity in a frog heart was examined when the heart was subjected to
changes in temperature, various degrees of stretch, and different drug treatments. The heart
rate and contractile forces were investigated by applying varying temperatures to the frog
heart in Ringer’s solutions. In other separate procedures, we investigated the effect of
increasing the degree of stretch, and the effect of introducing various drug treatments of
Acetylcholine, Atropine, Epinephrine, and Pilocarpine. Increase in temperature resulted in
reduction in heart rate, while increasing the degree of stretch lead to increased contractile
force. Conversely, addition of Epinephrine increased the heart rate, while the other treatments
reduced the heart rate.

Introduction

There are many external influences that can affect the heart’s cardiac output by increasing or
decreasing the heart rate. Some of these influences are mediated by the nervous system while
others are a response to environmental changes, such as temperature, and physiological
changes, such as changes in ionic concentrations.

Frog Heart

There are 3 chambers in a frog heart: two atria (right atria and left atria), and a single
ventricle (see figure 1). The right atrium receives deoxygenated blood that has been drained
from various body organs through blood veins, while the left atrium receives oxygenated
blood from the frog’s skin and lungs.
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Figure 1: Frog heart and blood circulation

Both atria empty blood into the ventricle which has narrow chambers to reduce the mixing of
oxygenated blood and deoxygenated blood from the two atria. Relatively pure oxygenated
blood from the left atrium is emptied into the ventricle when the ventricle contracts, and then
sent into the carotid arteries that supply the head and brain. The deoxygenated blood from the
right atrium travels through the pulmocutaneous arteries and sends it back to the lungs and
skin to pick more oxygen. The blood passing into the aortic arches is thoroughly mixed, but
still contains enough oxygen required by the rest of the body.

Physiology of Frog Heart

The main function of the heart is to pump blood to where it is required. To perform its
cardiac functions, the heart is made of cardiac muscle, a specialized tissue that differs from
skeletal muscle both functionally and morphologically. Cardiac muscle has some special
properties, one of them being rhythmicity. The cardiac muscle can initiate rhythmic
contractions on its own, without requiring an external stimulation. This is due to the presence
of “leaky” cell membranes, where sodium and calcium ions leak into the cells. The leaking of
these ions causes specialized heart muscle cells known as pacemakers to spontaneously
depolarize and repolarize to threshold. This fires an action potential that initiates contractions
in cardiac muscle. The cells with high “leaky” rate and depolarize fastest control the
contraction rate for all cardiac cells. This cells act as pacemakers for the heart. The sinoatrial
(SA) node is the pacemaker in the mammalian heart. In frog heart, the sinus venosus is the
pacemaker. The sinus venosus is an enlarged region between the right atrium and the vena
cava, which receives blood from the posterior and anterior caval veins and delivers it into the
right atrium (Guyton and Hall).

The depolarization and repolarization sequences spread in the entire heart through electrical
connections between the cells of cardiac muscle, otherwise known as gap junctions. The
Physiology Practical 2: Toad Heart 3

whole process takes place in rhythmic fashion, leading to an intrinsic, regular heartbeat. To
maintain a regular heartbeat, the heart continuously receives input from both the sympathetic
and parasympathetic nervous systems.

Aim

The aim of this experiment was to explore and understand the basic principles of cardiac
muscle physiology and the effects of temperature, the degree of stretch, and various drug
treatments.
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Results

Exercise 1: Baseline data for ECG and cardiac cycle.

Below is the recording for baseline data for ECG and cardiac cycle.

Figure 2: Baseline data recording

These results show that that the normal ECG of the frog heart is 0.63mV on average. This
was consistent with what was observed on the relatively slow and steady atrial and
ventricular contractions. It was possible to perceive the movement of blood through the
vessels and observe the expansion of arteries during systole.
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Exercise 2: Temperature Effects

Here, we recorded the results for the heart rate, ECG and the contraction forces under
different temperatures. The results are as presented in figure 3 below.

Figure 3: The effect of temperature on

heart rate and ECG

It is observed that as the temperature increases from 4oC to 45oC, the frog heart rate reduces
from 123.6 BPM to 62 BPM.
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Exercise 3: Starling’s law of the heart

The results presented in figure 4 below show the relationship obtained between the degree of
stretch and the heart contractile force.

Figure 4: The
relationship between
stretch and contractile
force

According to Starling’s law of the heart, as the muscle fibre is stretched, the force of
contraction increases as more blood flows into the ventricle. From these results, as the degree
of stretch increases from 1 to 5, the heart’s contractile force is observed to increase slightly
from 0.034 to 0.035. However, there is a sharp drop when the degree of stretch is at 4.
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Exercise 4: Drug Effects

Figure 5: Effects of
drugs on the heart

This results indicate that drugs affect the heart rate at different degrees, with acetylcholine
and pilocarpine producing the largest effect (-48.3% and -47.3%), followed by atropine +
acetylcholine (34.3%). However, epinephrine has a positive effect (+21.6%), which means
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that it increased the heart rate by 21.6% as opposed to the other drugs that reduced the heart
rate.

Discussion

The frog heart has a single ventricle which receives blood from the two atria and pumps it
through the truncus arteriosus. This means that if atria and ventricle contract simultaneously,
it would not be possible for the atria to fill the ventricle, hence the delay between atrial and
ventricular contractions. The ECG QRS complex shown in figure 2 represents the beginning
of ventricular contraction. This complex depicts the polarization and repolarization of
ventricles and atria. Depolarization of the ventricles leads to contraction, pumping blood to
the pulmonary and systemic arteries.

The heart rate decreases the temperature increases from cold (4 oC) to warm (45oC). This
observation is attributed to the fact that at lower temperatures, there is increased
physiological activity to maintain body heat. Conversely, at warm temperatures, the
temperature of the body of the frog matches that of the environment and requires little heat to
maintain its body temperature. Using the Q10 concept is useful in determining active and
passive body processes. The contractile force increases with the degree of stretch, which is in
agreement with Starling’s law. During an exercise, more blood is pumped into the heart,
causing a greater contractile force. The introduction of Epinephrine increases the heart rate,
while Acetylcholine, Pilocarpine, and Atropine + Acetylcholine reduces the heartbeat.
Epinephrine acts as adrenergic agonist and binds to adrenergic receptors, increasing the heart
rate. Acetylcholine is a neurotransmitter which works on muscarinic and ganglion receptors.
The nicotinic receptors binds to these receptors and the effect of Acetylcholine causes
increase in the parasympathetic tone, thus decreasing the heart rate. Pilocarpine acts as a
cholinergic agonist and decreases heart rate by binding to nicotinic receptors. Atropine works
by blocking acetylcholine receptors, increasing sympathetic tone which leads to a lower heart
rate.

In conclusion, this experiment provides a clear understanding of sequences of atrial and

ventricular contractions in frog heart. The results demonstrate that the contractile force and
the heart rate can be manipulated by factors such as temperature changes, varying the degree
of ventricular stretch, and drug treatments.
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Reference

Guyton, Arthur C. and John Edward Hall. Textbook of Medical Physiology. Madrid, Spain:
Elsevier España, 2006.