Scott Austin - Frog Heart Lab Report - Section A07 · ! 1!...

1

Introduction:

The heart muscle is unlike other organs in the body, powered electrically and on it’s

own. It is completely capable of function without neuronal input. When removed from the

body, the heart is capable of contraction when supplied with necessary nutrients (Faller,

2004, p. 214).

Contractile and autorhythmic cells are the two main cell types within the heart.

99% of the total cells in the human heart are contractile cells. These cells are responsible

for pumping blood by contracting the heart. Autorhythmic cells comprise the remainder of

cells in the heart, and are responsible for initiating and conducting action potentials within

the heart (Sherwood, 2010, p. 309).

Autorhythmic cells have no resting potential. Instead, they slowly depolarize until

threshold is reached, then fire an action potential. This is known as pacemaker activity

(Sherwood, 2010, p. 309). The spread of an action potential from the autorhythmic cell to

the contractile cell leads to the beating observed in the heart.

Ionic movement of Na+ through hyperpolarization of specific voltage gated channels

is the initial source of the action potential in the autorhythmic cell. K+ channels and Ca2+

channels additionally contribute to the pacemaker potential in the cell. These ionic shifts

result in the pacemaker activity of the heart (Sherwood, 2010, p. 310).

In the bullfrog, autorhythmic cells are found primarily in the sinus venosus. This is

the primary pacemaker in the frog heart. From the primary pacemaker an action potential

is able to spread to contractile cells via gap junctions (Sherwood, 2010, p. 308).

Contractile cells maintain a steadier resting potential than the autorhythmic cells.

This is mainly due to leaky K+ channels, which keep the membrane potential close to the K+

2

equilibrium potential. The action potential looks markedly different in a contractile cell

than in an autorhythmic cell. The contractile cell contains fast Na+ channels providing a

rapid influx of Na+; transient K+ channels leading to a brief repolarization period; L-‐type

Ca2+ channels, which are much slower than it’s T-‐type counterpart, leading to a plateau

period; and a rapid efflux of K+ via voltage gated K+ channels (Sherwood, 2010, p. 314).

Both the parasympathetic and the sympathetic nervous system innervate the heart,

having opposing effects on heart rate and strength of contraction (Sherwood, 2010, p. 325).

The parasympathetic nerve in the heart is the Vagus nerve and releases acetylcholine to

bind with muscarinic receptors leading to a decrease in rate of depolarization and a

decrease in heart rate. Over stimulating the Vagus nerve can lead to bradycardia leading to

cardiac arrest. The sympathetic nervous system releases norepinephrine to bind with β-‐

adrenergic receptors leading to an increased rate of depolarization and an increase in heart

rate (Sherwood, 2010, p. 326).

Cardiac output is determined by heart rate and stroke volume. Stroke volume is

controlled by intrinsic and extrinsic controls. Intrinsic control is based on how much blood

returns to the heart and how much blood is pumped out. This is the Frank-‐Starling law of

the heart. The more filling that takes place, the more force that blood is ejected with.

Larger venous return equals larger stroke volume (Sherwood, 2010, p. 328). Extrinsic

controls in the heart are a result of sympathetic stimulation. Sympathetic stimulation

releases norepinephrine and epinephrine, leading to increased cytosolic Ca2+, which leads

to increased contractile force resulting in increased cardiac output (Sherwood, 2010, p.

329).

3

Methods:

The procedure followed for the lab can be found in the NPB 101L Physiology Lab

Manual (Bautista & Korber, 2009, p. 54). Prior to the experiment the bullfrog was double

pithed by the lab TA’s. The brain and spinal cord were destroyed so the frog could not feel

pain or control its own movement. The frog was kept moist with a paper towel dampened

with deionized water. Once the heart was exposed the tissue was fed nutrients through

application of Ringers saline solution. Ringers solution is rich in electrolyte ions Ca2+, Na+,

and K+.

The abdomen was opened avoiding veins. The pectoral girdle was cut through. The

pericardium was removed and the heart was exposed. The Vagus nerve was isolated and

confirmed through stimulation and observation of bradycardia.

The force transducer was calibrated as per lab manual instruction and the ventricle

was punctured with wire ensuring un-‐insulated areas were in contact with the tissue and

the end of the wire at the force transducer. The left leg of the bullfrog was punctured with

a T-‐pin and ground wires were connected to the T-‐pin.

All experiments were performed as presented in the lab manual. Deviations from

the lab manual occurred in Part 4: Extrasystolic Contractions. For the early diastole

experiment only 1 extrasystole was recorded. Additionally in Part 6: Effects of

Epinephrine, the frog heart was injected three times with epinephrine and data were

collected for 3 minutes post injection.

4

Results:

Part 3: Electrical & Mechanical Activity of the Heart

With a starting baseline tension of 0.0-‐0.1g, average arterial contraction force was

measured. Atrial contractions were analyzed every 15 seconds for 2 minutes utilizing

maximum tension in a P wave (Figure 1).

Figure 1: The tension (g) at 15-‐second intervals over a 2-‐minute duration during atrial contraction in the

bullfrog’s heart represented in the blue line averaged 0.38g. Contraction force initially increased then

decreased, evening out over the data sample. Baseline tension was 0.0-‐0.1g. Time is measured in seconds

along the X-‐axis, and contraction force is measured in grams along the Y-‐axis.

Ventricular contraction force was established by analyzing maximum tension over a

2 minute period every 15 seconds (Figure 2).

0.3

0.35

0.4

0.45

0 15 30 45 60 75 90 105 120

Contraction Force

(grams)

Time (seconds)

Atrial Contraction Force

Measured Tension

5

Figure 2: The tension (g) at 15-‐second intervals over a 2-‐minute duration during atrial contraction in the

bullfrog’s heart represented in the blue line averaged 1.35g. Baseline tension was 0.0-‐0.1g. Force of

contraction declined over the data sample. Time is measured in seconds along the X-‐axis, and contraction

force is measured in grams along the Y-‐axis.

The average heart rate of 38.95 BPM was analyzed measuring the beginning of

contractile phase 1 of the electrical signal of contraction to the same point of the next

electrical signal (Figure 3).

Figure 3: The beats per minute (BPM) at 15-‐second intervals for a 2-‐minute period represented by the blue

line averaged 38.95 BPM. There was an initial increase in BPM, peaking at 40.81, a gradual decrease, finally

increasing. Time is measured in seconds along the X-‐axis, and beats per minute (BPM) are measured along

the Y-‐axis.

The average latency between mechanical and electrical activity was analyzed

measuring from the beginning of phase 0 of the contraction cycle of the electrical activity to

the beginning of ventricular contraction and was calculated to be an average of 0.30

1.2

1.3

1.4

1.5

0 15 30 45 60 75 90 105 120

Contraction Force

(grams)

Time (seconds)

Ventricular Contraction Force

Measured Tension

37

38

39

40

41

0 15 30 45 60 75 90 105 120

Beats Per Minute

(BPM

)

Time (seconds)

Heart Rate (BPM)

Beats Per Minute (BPM)

6

seconds. The measurements taken at 15-‐second intervals over a 2-‐minute time period as

compared to the average baseline latency of 0.30 seconds from phase 0 of the electrical

contraction cycle to the start of mechanical contraction (Figure 4).

Figure 4: The latency between the onset of electrical activity (phase 0) and the initiation of ventricular

contraction was averaged to be 0.30 seconds. Individual measurements were taken every 15-‐seconds over a

2-‐minute time period. Time is measured in seconds along the X-‐axis, and latency is measured in seconds

along the Y-‐axis.

Part 4: Extrasystolic Contractions

Extrasystolic contractions were initiated and measured during late diastole. A

minimum voltage of 4.0V was determined to be the minimum voltage to provide an

extrasystolic contraction and was used as the threshold voltage, with an initial baseline

tension of 0.0-‐0.1g. After the extrasystolic contraction, a rest period of 10 beats was

provided before repeating the process. This was done for 3 trials (Table 1).

0.26

0.28

0.30

0.32

0.34

0 15 30 45 60 75 90 105 120

Latency (seconds)

Time (seconds)

Latency Between Mechanical and Electrical Activity

Latency (seconds)

7

Table 1: Contractile force of ventricular contraction in grams (g) before an extrasystole, for the extrasystole,

and immediately post extrasystole when a 4.0V stimulus was directly applied to the frog heart in late diastole.

Compensatory pause was measured in seconds (sec). Data for 3 trials as well as averages are shown.

Baseline tension was 0.0-‐0.1g.

Threshold voltage of 4.0V was doubled to 8.0V and the experiment was repeated.

Initial baseline tension was 0.0-‐0.1g and the stimulus was applied in late diastole. After the

extrasystolic contraction a rest period of 10 beats was provided to the frog heart before

repeating. Three trials were done and averages were taken and compensatory pause was

measured (Table 2).

Table 2: Contractile force of ventricular contraction measured in grams (g) before an extrasystole, for the

extrasystole, and immediately post extrasystole when an 8.0V stimulus was directly applied to the frog heart

in late diastole. Compensatory pause was measured in seconds (sec). Baseline tension was 0.0-‐0.1g.

An extrasystolic contraction was initiated in early diastole stimulating the frog heart

with a minimum threshold voltage measured at 5.0V. Initial baseline tension was 0.0-‐0.1g.

8

This was done one time. Measurements that were taken for the trial and compensatory

pause of the 5.0V direct stimulation of the frog heart in early diastole (Table 3).

Table 3: Contractile force of ventricular contraction in grams (g) before an extrasystole, for the extrasystole,

immediately post extrasystole when a 5.0V stimulus was directly applied to the frog heart in early diastole.

Compensatory pause was measured in seconds (sec). Baseline tension was 0.0-‐0.1g.

Part 5: Vagal Stimulation

An electrode was hooked onto the Vagus nerve of the frog with a piece of parafilm

isolating the electrode from tissue contact. The minimum threshold voltage to elicit

bradycardia was determined to be 2.75V by observing a decrease in contractile strength.

Contractile strength began at 1.19g and was observed over a 10 second time period with a

frequency of 20 pulses per second (pps) (Figure 5).

Figure 5: Ventricular contraction force measured before and after stimulating the Vagus nerve in the frog.

Stimulation was applied using an electrode directly attached to the nerve. Stimulation measured 2.75V at a

frequency of 20pps (pulse per second). Contractile force before stimulation measured 1.19g and after

stimulation measured 0.75g, declining after stimulation. Ventricular contraction force is measured in grams

along the X-‐axis. Baseline tension was 0.0-‐0.1g.

0 0.2 0.4 0.6 0.8 1 1.2 1.4

Contractile Force Before (g) Contractile Force After (g)

Ventricular Contraction Force (g)

Ventricular Contraction Force Before and After Vagal Stimulation During Bradycardia

9

Heart rate was monitored during the same 10-‐second time period and did not

change (Figure 6).

Figure 6: Heart Rate of 44.11 BPM (beats per minute) before and after stimulating the Vagus nerve in the

frog. Stimulation was applied using an electrode directly attached to the nerve. Stimulation measured 2.75V

at a frequency of 20pps (pulse per second). Beats per minute (BPM) are measured along the X-‐axis, and

remained unchanged.

Stimulus voltage was increased on the Vagus nerve to 4.0V to elicit cardiac arrest.

Initial heart rate was recorded for 30 seconds prior to stimulation and measured using the

5 beats prior to stimulation and averaged. Stimulation of the Vagus nerve was initiated at a

frequency of 20pps (pulse per second). Cardiac arrest lasted for 65 seconds before a

mechanical signal was next detected. A regular rhythm occurred at 81 seconds post

stimulation and Vagal stimulation was terminated. Post stimulation heart rate and

contraction tension were recorded using the 5 beats post termination and averaged (Table

4).

40 41 42 43 44 45

HR Before (BPM) HR After (BPM)


Heart Rate Before and After Vagal Stimulation During Bradycardia

10

Table 4: Measurements for initial activity prior to vagal stimulation and averaged. Baseline tension was 0.0-‐

0.1g. Average contractile tension was 1.01g and average heart rate was 42.98 BPM. Post Vagal stimulation

average contractile tension was 0.42g and average BPM was 31.27, decreasing in both categories, for the 5

beats immediately after Vagal stimulation of 4.0V at 20pps was terminated.

Comparing the initial heart rate with the post cardiac arrest heart rate identifies a

large decrease in BPM post cardiac arrest (Figure 7).

Figure 7: Initial heart rate measured 42.98 BPM. Post cardiac arrest heart rate was averaged at 31.27 BPM

for the 5 beats after stimulation of the Vagus nerve was terminated. Beats per minute (BPM) are measured

along the X-‐axis.

Comparing the initial ventricular contractile force with the post cardiac arrest

ventricular contractile force indicates a large drop in tension after cardiac arrest (Figure 8).

0 5 10 15 20 25 30 35 40 45 50

HR Before (BPM) HR After (BPM)


Heart Rate Before and After Cardiac Arrest

11

Figure 8: Initial ventricular contractile force measured 1.01g. Baseline tension was 0.0-‐0.1g. Post cardiac

arrest contractile force measured 0.42g for the 5 beats after stimulation of the Vagus nerve was terminated.

Tension is measured in grams along the X-‐axis.

Part 6: The Effects of Epinephrine

Epinephrine was injected in the frog’s heart 3 times. An initial tension (g) and heart

rate (BPM) were measured averaging the 5 beats immediately before the injections. BPM

was calculated from the beginning of phase 0 of the electrical signal to the same point of the

next signal. The 5 beats post injection and at 30 second intervals for 3 minutes were

averaged identically to the baseline measurements (Table 5).

Table 5: Initial average tension (g) of 0.48g and beats per minute (BPM) of 43.17 BPM compared with

measurements taken at 30-‐second intervals over a 3 minute time period. Baseline tension was 0.0-‐0.1g.

Averages were measured from the 5 beats immediately after each time point. Tension (g) increased 50% and

heart rate (BPM) increased 35.46% over baseline averages.

Average heart rate continued to increase over the 3 minute time period with the

largest % increase of 10.08% seen from 30 to 60 seconds (Figure 9).

0 0.2 0.4 0.6 0.8 1 1.2

Contractile Force Before (g) Contractile Force After (g)

Tension (g)

Ventricular Contraction Force Before and After Cardiac Arrest

12

Figure 9: Average heart rate (BPM) measured every 30 seconds for a 3-‐minute time period after injecting the

frog heart with epinephrine. Baseline tension was 0.0-‐0.1g. Initial heart rate measured 43.17 BPM and

continued to increase throughout the experiment. Ending average heart rate of 58.48 BPM was an increase of

35.46% over baseline. Averages were calculated with the 5 beats immediately after each time interval. Time

interval is measured in seconds along the X-‐axis and heart rate is measured in BPM along the Y-‐axis.

Average ventricular contraction force (g) peaked at 30 seconds with an 87.50%

increase over baseline tension (Figure 10).

Figure 10: Average ventricular contraction force (g) measured every 30 seconds for a 3-‐minute time period

after injecting the frog heart with epinephrine. Averages were measured from the 5 beats immediately after

each time point. Baseline tension was 0.0-‐0.1g. Tension initially increased and then decreased, ending with

an overall increase in contraction force. Initial tension measured 0.48g increasing 50% over the time period

to 0.72g. Peak tension was measured at 30 seconds of 0.92g, an 87.50% increase over initial tension. Time

interval is measured in seconds along the X-‐axis and ventricular contraction force is measured in grams along

the Y-‐axis.

30.00

40.00

50.00

60.00

Before 0 30 60 90 120 150 180

Heart Rate (BPM

)

Time Interval (seconds)

Average Heart Rate (BPM) at Varying Time Intervals

Heart Rate (BPM)

0.00

0.50

1.00

Before 0 30 60 90 120 150 180

Tension (g)

Time Interval (seconds)

Average Ventricular Contraction Force (g) at Varying Time Intervals

Tension (g)

13

Discussion:

Part 3: Electrical & Mechanical Activity of The Heart

Action potentials generated from autorhythmic cells in the sinus venosus of the frog

heart are spread to contractile cells to initiate contraction. The signals are transmitted

from cell to cell from a specialized structure called an intercalated disc. The intercalated

disc has two types of membrane junctions, desmosomes and gap junctions. Contraction in

the heart creates mechanical stress. Desmosomes provide the mechanical stability needed

to withstand this stress. Gap junctions are responsible for transmitting the electrical signal

from cell to cell (Sherwood, 2010, p. 308).

Atrial cells are separated from ventricular cells and contract separately and with

different amounts of force (Sherwood, 2010, p. 308). This can be observed from measuring

contraction tension and measuring the electrical activity of the cardiac cycle.

The atria generate less electrical activity than the ventricle does due to its smaller

size. When the atria contracts blood rushes to the ventricle, filling the ventricle. When the

ventricle fills and its pressure exceeds aortic pressure the aortic valve opens and blood

leaves the ventricle. This amount of blood leaving the ventricle is the stroke volume

(Sherwood, 2010, p. 323). This variance in mechanical activity was observed in the

measured atrial contraction force of 0.38g and the ventricular contraction force of 1.35g.

The Frank-‐Starling Law of The Heart explains the relationship between stroke

volume and ventricular contraction. The more stretched the ventricle becomes, that is the

larger the end diastolic volume, the larger the force of contraction will be, increasing stroke

volume (Widmaier, Raff, & Strang, 2004, p. 396).

14

Cardiac output is the amount of blood the ventricle pumps out per minute. This is

measured by evaluating the stroke volume and heart rate. Heart rate is regulated from the

electrical activity of the autorhythmic cells and is a result of ionic movement (Sherwood,

2010, p. 325).

Once a contractile cell receives a signal from an autorhythmic cell it begins its action

potential by opening fast Na+ channels and rapidly depolarizes. K+ transient channels

release K+ as the Na+ channels close providing an initial rapid repolarization period. Then

L-‐type Ca2+ channels slowly open creating a plateau phase, and voltage-‐gated K+ channels

rapidly flush out K+ bringing the membrane potential of the contractile cell back to

threshold (Sherwood, 2010, p. 314).

This cycle was used to measure heart rate in beats per minute on the frog heart.

The initial opening of the fast Na+ channels was identified as phase 0 and was measured to

the initiation of the next contraction cycle. The frog had an initial heart rate of 38.95 BPM.

There is a delay between the onset of a contraction from an action potential and the

actual response. This is known as the refractory period, and is to prevent tetanus in the

heart (Sherwood, 2010, p. 316). In the frog, latency between electrical activity and

contractile response was measured at 0.30 seconds. In a study on mammalian hearts of

rabbits, cats, and dogs it was found that this latency period, the absolute refractory period,

remains constant regardless of the heart rate (Dale & Drury, 1932, p. 222).

Sources of error in this experiment were due to an excess of adipose tissue in the

frog heart, inconsistent supply of Ringers solution, and outside movement of the subject’s

table.

Part 4: Extrasystolic Contractions

15

An extrasystolic contraction is also known as a premature ventricular contraction

(PVC) (Sherwood, 2010, p. 319). These occur during the relative refractory period in the

ventricular contractile cell and initiate a contraction before the cell has returned to it’s

resting membrane potential. Due to the extrasystolic contraction, there is an extra delay

before the next contraction occurs. This is known as compensatory pause, and is regulated

by the pacemaker activity in the heart.

A case study on a 68-‐year-‐old patient shows the mechanism of compensatory pause.

After analyzing recorded data from the patient, two beats occurring close together were

followed by a long pause (Carbone, Oreto, & Oreto, 2013, p. 90). This was seen in our

experiments on late diastole stimulation and early diastole stimulation.

It is expected that the extrasystolic contraction would have a greater force of

contraction due to the cell not fully returning to resting potential. In the experiments

conducted this was not seen. Minimum threshold voltage to elicit an extrasystolic

contraction during late diastole was found to be 4.0V. At this voltage the extrasystolic

contraction was found to be 0.03g less forceful than the initial contraction with a

compensatory pause of 0.94 seconds. When the voltage was doubled to 8.0V the

extrasystolic contraction results were the same, with a compensatory pause of 1.01

seconds. During the attempt on early diastole at 5.0V the extrasystolic contraction was

0.22g smaller than the initial contraction with a compensatory pause of 1.26 seconds.

Due to our inability to accurately and precisely initiate the stimulus in the relative

refractory period it was expected to not obtain predicted results. Additionally the frog

heart began to tear, Ringers solution was inconsistently applied, and there was outside

interference of the subject’s table.

16

Part 5: Vagal Stimulation

The Vagus nerve is the parasympathetic input to the heart. Parasympathetic

stimulation in the heart increases membrane permeability to K+ thus making it more

negative, or hyperpolarizing it, leading to a decrease in heart rate (Widmaier, Raff, &

Strang, 2004, p. 395). The Vagus nerve releases acetylcholine, which then binds to a

muscarinic receptor. A G-‐protein cascade occurs with this, inhibiting the cAMP pathway

activity. This ultimately inhibits phosphorylation and reduces activity of voltage-‐gated

channels required for contraction, leading to a decrease in heart rate and contractile force

(Sherwood, 2010, p. 326). This decrease in heart rate and contractile force was observed in

the experiment when cardiac arrest occurred, as expected. The presence of acetylcholine

made the heart unable to return to its pre-‐stimulation heart rate of 42.98 BPM and

contractile force of 1.01g, but would be expected to return to normal heart rate and force of

contraction with time. This was shown in an experiment on mongrel dogs, and gradually

the heart rate did return to normal (Campos & Friedman, 1963, p. 251).

During bradycardia the heart rate slows (Sherwood, 2010, p. 319). The same

experiment on mongrel dogs shows this effect, however was not seen in our experiment on

the frog heart(Campos & Friedman, 1963, p. 251). There was a reduction in contractile

force from 1.19g to 0.75g, however heart rate remained unchanged. This could be due to

not enough stimulus voltage to elicit a delay in rate of beating, or not stimulating the Vagus

nerve for enough time to allow acetylcholine to appropriately inhibit it’s factors.

Additionally in the experiment there was excess Ringers solution, which may have altered

the electrical stimulation on the nerve.

Part 6: The Effects of Epinephrine

17

Opposite of the Vagus nerve, epinephrine is the resultant effect of stimulation of the

sympathetic nervous system. The experiment involved injecting the frog heart with

epinephrine, was administered 3 times, and deviated from the lab manual.

The sympathetic nervous system impacts heart rate and contractile force in times of

need for an increase of such factors, such as in times of exercise or emergency (Sherwood,

2010, p. 327). Antagonistic to acetylcholine, epinephrine increases rate of depolarization

in the cardiac cells leading to an increase in rate of contraction. This increase in rate of

contraction leads to an increase in heart rate and contractile force ultimately increasing

stroke volume and cardiac output (Sherwood, 2010, p. 328).

Epinephrine acts on beta-‐adrenergic receptors in the main pacemaker of the heart.

These receptors stimulate a G-‐protein cascade increasing the cAMP pathway activity in

cardiac cells, increasing phosphorylation. This allows energy requiring processes, such as

the voltage-‐gated channels used in contraction, to remain open longer. This will ultimately

increase contractile strength, and additionally decrease delay between beats of the heart

(Sherwood, 2010, p. 327).

This mechanism was seen in the experiments on the frog heart with an increase in

heart rate of 35.46% over the 3-‐minute data sample. An experiment on bull calves showed

similar results to heart rate increase when injected with epinephrine (Stewart & Webster,

2010, p. 5252).

Contractility has a greater effect with increased presence of epinephrine due to the

greater influx of Ca2+ into the contractile cell. From this increased concentration of

intracellular Ca2+ there is greater cross-‐bridge cycling and the myocardial fibers are able to

generate more force. This process ultimately increases stroke volume leading to an

18

increase in cardiac output, ultimately shifting the Frank-‐Starling curve inward (Sherwood,

2010, p. 329).

This increase in contractility was seen in our experiment with an overall increase of

50% over the 3-‐minute time period. However, due to tearing of the heart muscle and

inconsistent application of Ringers solution the contractile force declined after the 30-‐

second measurement.

19

References: Bautista, E., & Korber, J. (2009). NPB 101L Physiology Lab Manual (2nd Edition). Mason,

Ohio: Cengage Learning, 43-‐54. Campos, H., & Friedman, A. (1963). The Influence of Acute Sympathetic Denervation,

Reserpine and Choline Xylyl Ether on Vagal Escape. Journal of Physiology , 169, 249-‐262.

Carbone, V., Oreto, L., & Oreto, G. (2013). Ventricular Extrasystoles with Interpolation or

Postponed Compensatory Pause during Atrial Fibrillation: Fact or Fiction? Annals of Noninvasive Electrocardiology , 18 (1), 90-‐94.

Dale, A., & Drury, A. (1932). The refractory period of mamalian cardiac muscle, with

especial reference to purkinje tissue. The Journal of Physiology, 76 (2), 201-‐223. Faller, A. (2004). The Human Body: An Introduction to Structure and Function (13th

Edition). Stuttgart, Germany: Thieme, 214. Sherwood, L. (2010). Human Physiology: From Cells to Systems (7th Edition). Belmont:

Brooks/Cole, 308-‐329. Stewart, M., & Webster, J. (2010). Technical note: Effects of an epinephrine infusion on eye

temperature and heart rate variability in bull calves. Journal of Dairy Science, 93 (11), 5252-‐5257.

Widmaier, E., Raff, H., & Strang, K. (2004). Vander, Sherman, & Luciano's Human Physiology:

The Mechanisms of Body Function (9th Edition). New York: McGraw Hill, 394-‐396.

Raw Data:

20

Average Atrial Contraction Force

Average Ventricle Contraction Force

Average Heart Rate

21

Latency between electrical and mechanical activity

Extrasystole obtained from 4.0V stimulation during late diastole

22

Extrasystole obtained from 8.0V stimulation during late diastole

Extrasystole obtained from 5.0V stimulation during early diastole

23

Vagal nerve stimulation at 2.75V for 10 seconds to elicit bradycardia

Cardiac Arrest/Vagal Escape at 4.0V

24

Effects of Epinephrine – Before Injection

Effects of Epinephrine – Immediately Post Injection

25

Effects of Epinephrine – 30 seconds Post Injection

Effects of Epinephrine – 60 Seconds Post Injection

26



27



Scott Austin - Frog Heart Lab Report - Section A07 · ! 1!...

Documents

Transcript of Scott Austin - Frog Heart Lab Report - Section A07 · ! 1!...