How Does Acetylcholine Increase The Heart Rate

The purpose of this lab was to determine the normal heart rate of a Daphnia Magna and decipher the different effects that various substances had on it. A Daphnia Magna is a species of water fleas and can be located in the Northern United Sates against the coastline of the Atlantic in rocky pools. The water flea’s habitat consists of rivers and streams, temporary pools, lakes and ponds, and brackish water. The Daphnia Magna range from two to five millimeters in length and are shaped like a kidney bean (Elenbaas, Molly). Relating to this lab experiment we learned in class that the normal heart rate is measured anywhere between 60 and 100 beats per minute (BPM). If your resting BPM is measured at a level above the number 100 it is known as Tachycardia. This term indicates that your heart level has exceeded the normal range. Also if your heart rate is indicated below 60 then it is called Bradycardia, which means the heart is beating slower than normal. When your heart rate is affected by a substance in the body it is called a Chronotropic agent. When the heart rate decreases because of a substance or chemical it is called a negative Chronotropic and when it is affected oppositely by increasing it is known as a positive Chronotropic agent. In this experiment we added many different substances to the slide on which the water flea was placed to calculate the increase or decrease in its heart rate due to the ingredients in the substances. The first substance used was

The chart does not confirm what our hypothesis was: that the higher the concentration of the caffeine solution the more the beats per minute of the daphnia. This, though, might be a mistake since the caffeine solution may not have been exactly as we wanted it in each occasion, hence making the results inaccurate. Also, when trying to press the “=” button of the calculator faster, many of those additions were not calculated since the calculator can’t add as fast as we press the button.

From figure 5 it can be seen that before the addition of epinephrine, Daphnia had an average heart rate of 277.663+/-18 heart beats per minutes. However, when epinephrine was added, the average heart rate was decreased to 291.467+/-57 heart beats per minute. However, after performing Mann-Whitney U test, it was found that after the addition of epinephrine, no significant difference was observed in Daphnia's heart beats.

Exercise increases heart rate by a process of sympathetic autonomic stimulation. Sympathetic (adrenergic) nerves increase the excitability of the sino-atrial node and reduce the P-R interval .As exercise continues, the physiological changes in the body are continuously monitored by a number of physiological systems and the balance of activity of the sympathetic system (speeding up) and the parasympathetic system (slowing down) is constantly adjusted. When exercise is over, the heart rate does not drop immediately as the body has to undergo a period of re adaption to return to the resting state.

B. Part B. PowerPhys Experiment 4 – Effect of Exercise on Cardiac Output (13 points total)

Each student got a white tub and filled it up with tap water from the sink. Students were paired with two or three other people and formed their groups. Each group got 1 stopwatch, 1 thermometer, and also learned how to each other’s pulse. The temperature of the water used from the sink were adjusted beforehand to about 23°C; room temperature. Water temperature was not re-adjusted to be hotter or colder.

Atropine showed the only a minor increase in amplitude and period. The BPM was the detected as increase up to 30 seconds then a drop back down to 44, then the heart rate shot back up to 48 before recovering.

Then using a disposable pipette we placed two drops of room temperature water (21 degrees) on top of the Daphnia. Then placing it careful under the microscope with a for 15 seconds using a tally counter and clicked away how many heart beats we observed and did this three times for three trials, in between the times would give the daphnia a two minute recovery period. We then would process the trials information and calculate an average. After the information calculated we then  multiplied our results by four to see the average heart beats per minute with room temperature water. We gave the daphnia five minute to recover then went on to proceed with two drops of hot water (40 degrees celsius) placed on top of the Daphnia using the pipette. Again three trials for 15 second using the tally clicker following after a two minute break. The same followed for the cold water (0 degree celsius) placing two drops on top of the Daphnia administered by pipette. In between the transitional water temperature trials we then cleaned up the excess water before placing new drops of water by gently soaking up the water with kimwipes. After five minutes we tallied the heartbeats of the Daphnia before administering the epinephrine. Then again gently gave two doses of epinephrine using a new pipette. Then after we observed and tallying the heart beats before administering the epinephrine, three times again recording our results then averaging it. Then we placed two drops of the epinephrine on top of the daphnia, tallying the heartbeats and recording and calculating our trial results. Then after two minutes we observed and tallied the effects after the epinephrine had been used.  Each trial again consisted of observation under the microscope, tallying and observing the behavior internally and externally of the

Though data from vagal stimulation was disregarded, it is still important to mention the responses that should have been elicited had the vagus nerve been stimulated properly. The vagus nerve (cranial nerve X) is a part of the parasympathetic nervous system and reduce heart rate when given enough electrical stimulation. Vagal escape occurs when the vagus nerve has been stimulated to the point of the nerve ceasing to repolarize, and then resuming sending action potential for heartbeat. The result is a cease or slowing of heart rate temporarily, and then heart rate starting up again. When atropine is applied to the heart along with vagal stimulation, the atropine blocks any response the vagus nerve should send (Sarnoff et al,

9. When the heart is externally stimulated just after the start of the contraction cycle, why does this have no affect on heart rate?

In 1921, an Austrian researcher named Otto Loewi found the primary neurotransmitter. frogIn his analysis (which came to him in a fantasy), he utilized two frog hearts. One (heart #1) was still associated with the vagus nerve. Heart #1 was put in a chamber that was loaded with saline. This chamber was associated with a second chamber that contained heart #2. Along these lines, liquid from chamber #1 was permitted to stream into chamber #2. Electrical incitement of the vagus nerve (which was connected to heart #1) brought on heart #1 to back off. Loewi likewise watched that after a postponement, heart #2 additionally backed off. From this trial, Loewi speculated that electrical incitement of the vagus nerve discharged a synthetic into the liquid

I enjoy that for your discussion post you did a table. As many of our fellow students have mention the chart is a great reference point. It is easy to understand and comprehend. Along with the information in the chart is accurate. In my discussion post I also discussed how tachycardia and increased contractility is a direct result of the sympathetic nervous system stimulation. That the benefits of increased contractility are increased cardiac output that helps maintain blood pressure.

The purpose of the experiment is to see how different variables affect pulse rate and blood pressure.

Now that the experiment has been tested, the results are in there comes the analysis part of the process. After I had determined my calculation I saw where my beats per minute were over a hundred; this consider me to be Tachycardia. Tachycardia refers to an abnormally fast resting heart rate. When examining what Tachycardia was and how it can be affected made me see that different scenarios will affect the beats per minute. Anxiety, caffeine, stress can all cause someone to have such a rapid heartbeat. I remember from when taking the echocardiogram that I was stressed

2) Both drugs do not influence the rate of rhythmic contractions yet they alter force and peak. The rate should remain fairly constant as it signifies the transmission of impulses being sent from the nervous system, any slowing in rate would suggest deprivation of nerve supply yet this is not the case as the same gut is used for both drugs and all concentrations.