Cardiovascular Physiology Lab Report
Introduction
Cardiovascular Dynamics and the Cardiovascular Physiology experiments both have multiple goals. The first experiment aims to understand how blood flow, pressure gradient, and resistance relate to one another. To understand this, resistance and contributing factors, such as vessel radius, viscosity, and vessel length must be studied. The effects of vessel radius and stroke volume on the ventricular pump should also examined. The experiment also calls for an understanding of cardiovascular compensation. Pump mechanics are further understood through a design of further experiments. The Cardiovascular Physiology experiment attempts to understand the effects of parasympathetic and sympathetic nervous systems on the heart, through vagus nerve stimulation. Refractory periods and relative refractory periods will be studied in direct stimulations of the heart, as well as the five phases of the cardiac cycle. Lastly, the effects of temperature, hormones, and ions will be understood. Epinephrine, pilocarpine, atropine and digitalis are the hormones used to modify the heart. Sodium, potassium and calcium are the ions used in this experiment.
Methods In the Vessel Resistance section for the Cardiovascular Dynamics experiment, two glass beakers, a tube connecting them and a pressure meter were used. The left beaker represented the heart, the right breaker represented the body and the tube was the artery. For the Pump Mechanics …show more content…
section, three glass beakers and two tubes were used, along with three pressure meters. There were also two valves, one representing the bicuspid valve and one representing the aortic semi-lunar valve. The left beaker simulated blood being pumped from the lungs, the middle beaker was the left side of the heart, and the right beaker represented the body. The left flow tube represented a vein and the right flow tube represented an artery. A suspended three chambered heart, an oscilloscope monitor, a heart tray and 23o Ringers solution were required for the Electrical Stimulation and Modifiers of the Heart section in the Cardiovascular Physiology experiment. The Electrical Stimulation section additionally needed Epinephrine, atropine, pilocarpine, digitalis, calcium ions, sodium ions and potassium ions The first section of the Cardiovascular Dynamics experiment measured Vessel Resistance. In the first activity, pressure was manipulated to measure its effects on blood flow. A starting pressure of 25 mm Hg was set in place and increments of 25 mm Hg was made, until a value of 225 mm Hg was reached. The second activity studied the effects of the tube radius (artery) on blood flow. The starting radius was 1.5 mm and it was increased by 1.0 mm, until a radius of 6.0 was reached. The third activity tested the effect of viscosity on blood flow. Blood viscosity started at 1.0 and increments of 1.0 were made to reach a blood viscosity of 6.0. The next activity observed the effect of vessel length on blood flow. Length started at 10 mm and increased by 10 mm, to reach a vessel length of 50 mm. The second section studied Pump Mechanics. In the fifth activity, the radius of the right flow tube was manipulated to measure the effects of vessel radius on the heart pump. The radius of the right flow tube started at 3.0 mm and was increased by 0.5 mm to arrive at 6.0 mm. Activity six manipulated stroke volume and determined its effect on the heart pump. Stroke volume was initially set in place for 10 ml and was increased by 10 ml to test a final stroke volume of 120 ml. Results from each test were recorded and plotted. Activity seven was carried out to examine the ways in which the cardiovascular system compensates for deficiencies. A baseline test was first done and the data was recorded. Then, the radius of the right low tube was decreased and the results of the test were recorded. Three tests were designed to compensate for the effects of the decreased radius of the right flow tube. In the first compensation, the ventricular pressure was increased to 225 mm Hg. In the second test, lung the radius of the left flow tube was increased. For the last compensation the starting pump volume was reduced to 60 ml and the end pump volume was reduced to 25 ml. In the final activity, decreases in the right flow tube radius versus the left flow tube radius were examined. Pressure decreases in the left and right beaker were also studied separately. Lastly, an increase in the pressure of the right beaker was inspected. The first section of the Cardiovascular Physiology experiment measured direct stimulation and vagus nerve stimulation of a three chambered frog heart.
In the first activity, direct single stimulation was delivered to the heart at the beginning, peak, and end of ventricular contraction and its effect were observed and recorded. Then, multiple stimuli were delivered and the effects were observed and recorded. In the second activity, multiple stimuli were delivered to the vagus nerve of the heart and the effects were
recorded. The second section examined the effects of various drugs, hormones and ions, as they modified heart rate. Epinephrine, pilocarpine, atropine, and digitalis were tested and the heart was flushed out with 23o Ringers solution between each test. Temperature effects were observed using 5o, 23o, and 32o Ringers solution. Once the heart rate was stable, following each test, the data was recorded. Lastly, the effects of sodium, potassium, and calcium ions were tested.
Results
Experiment 5
Figure 1- The Effect of Pressure on Blood Flow. As ventricular pressure increases, blood flow linearly increases.
Figure 2- The Effect of Vessel Radius on Blood Flow. There is a positive curved relationship between vessel radius and blood flow. As arterial radius increases, blood flow increases.
Figure 3- The Effect of Viscosity on Blood Flow. There is a negative curved relationship between viscosity and blood flow. As blood viscosity increases, blood flow decreases.
Figure 4- The Effect of Vessel Length on Blood Flow. Regions of the body that are more proximal to the heart have a higher rate of blood flow.
Figure 5- The Effect of Vessel Radius on Pump. As arterial radius increases, more blood can flow from the heart to the rest of the body.
Figure 6- The Effect of Stroke Volume on Pump. Increases in stroke volume do not cause increase in blood flow.
| |Flow (ml/min) |Rad. L (mm) |Rad. R (mm) |Str. V |Rate |Pressure L |Pressure Diff. R |
| | | | |(ml) |(stroke/min) |(mm Hg) |(mm Hg) |
|Baseline |5086.8 |3.0 |3.0 |70 |72.7 |40 |40 |
|Right flow tube radius |1678.1 |3.0 |2.0 |70 |24.0 |40 |40 |
|decreased to 2.0 mm | | | | | | | |
|Increase pump pressure |4245.1 |30 |2.0 |70 |60.6 |40 |140 |
|to 225 mm Hg | | | | | | | |
|Increase left tube |1985.1 |6.0 |2.0 |70 |28.4 |40 |40 |
|radius | | | | | | | |
|Decrease start pump |1678.1 |3.0 |2.0 |35 |47.9 |40 |40 |
|volume to 60 ml and end | | | | | | | |
|pump volume to 25 ml | | | | | | | |
Table 1- Cardiovascular compensation in response to decreased arterial radius. An increase in pump pressure proves to be the most effective solution, followed by increased left tube radius. Change in stroke volume did not counteract the effect of decreased arterial radius.
| |Flow (ml/min) |Rad. L (mm |Rad. R (mm) |Str. V |Rate |Pressure L |Pressure Diff. R |
| | | | |(ml) |(stroke/min) |(mmHg) |(mm Hg) |
|Decreasing right |1678.1 |3.0 |2.0 |70 |24.0 |40 |40 |
|flow tube radius | | | | | | | |
| |124.1 |3.0 |1.0 |70 |1.8 |40 |40 |
|Decreasing left |1678.1 |2.0 |3.0 |70 |24.0 |40 |40 |
|flow tube radius | | | | | | | |
| |124.1 |1.0 |3.0 |70 |1.8 |40 |40 |
|Decrease pressure |2034.7 |3.0 |3.0 |70 |29.1 |10 |40 |
|in left beaker | | | | | | | |
|Decrease pressure |6474.1 |3.0 |3.0 |70 |92.5 |40 |70 |
|in right beaker | | | | | | | |
|Increase pressure |2034.7 |3.0 |3.0 |70 |29.1 |40 |10 |
|in right beaker | | | | | | | |
Table 2- Radius and pressure manipulations in the left and right beaker to alter blood flow. The left (vein) and right (artery) tube showed equal effects in response to decreases in the tube radius. Decreasing the pressure in the right beaker (body) increased flow rate. Increasing the pressure in the right beaker (body) and decreasing the pressure in the left beaker (lungs) had the same effect of lowering blood flow rate.
Experiment 6
Figure 7- Trace of heart rate, of a three chambered heart, with no electrical stimulation.
Figure 8- Trace of heart rate with single electrical stimulation delivered at the beginning of the ventricular contraction shows no change in heart rate.
Figure 9- Trace of heart rate with a single electrical stimulation delivered near the peak of the ventricular contraction shows an extra ventricular contraction, followed by a 1.5 second compensatory pause
Figure 10- Trace of heart rate with a single electrical stimulation delivered during the “fall” of ventricular contraction shows an extra ventricular contraction, stronger than the one seen in the previous figure. The compensatory pause is also longer.
Figure 11- Trace of heart rate with multiple stimuli delivered at a rate of 20 stimuli per second. Extra systoles are evident, followed by a compensatory pause.
Table 3- Vagus nerve stimulation. Heart rate and heart rate status for 10 seconds before stimulus, 10 second intervals after stimulus, and two 10 second periods after stopping stimulus. Heart rate drops immediately following the stimulus and ceases to contract. It then climbs back up to normal rhythm.
Table 4- Effects of altered stimulation frequency of the vagus nerve. A higher stimulus rate slows heart rate down faster and causes it to stop contracting. A reduced stimulus rate takes longer to slow the heart down.
Table 5- Effects of Epinephrine, Pilocarpine, Atropine, Digitalis and Temperature. Epinephrine and Atropine increase heart rate, while pilocarpine and digitalis decrease heart rate. Heart also increases with increased temperature.
Effects of Ca++, Na+ and K+ Ions
Sodium ions depolarize the cell membrane, causing and increase in action potential and an increase in heart rate. Calcium ions sustain the action potential, so they would function to produce stronger heart or faster contractility. Potassium ions decrease heart rate because they cause calcium channels to close.
Discussion
Lab 5
An increase in pump pressure can increase blood flow because the pressure was higher relative the pressure in the body. More force can be exerted by the pump to expel the volume of blood faster. Increased pressure in the pump means that there are a greater number of gas molecules. Blood pumped into the ventricles will be expelled faster because there is less room for liquid molecules to occupy the space. An increase in the left tube radius corresponds to an increase in the radius of the vein, delivering blood from the lungs. Since the radius of the right tube (artery was decreased), blood flowed out of the ventricular pump at a slower rate. To compensate for this, the radius of the vein was made larger to allow blood to flow into the ventricular pump faster. It was hypothesized that decreasing start volume and end volume would cause blood to be pumped to the body faster. However, stroke volume had no effect on the flow of the blood. Reducing stroke volume reduced the volume of blood expelled from the pump.
Decreasing the right flow tube radius simulated a decrease in the radius of the artery, carrying the blood from the left ventricle to the rest of the body. Decreasing the radius of the left flow tube imitated a decrease in the radius of the vein, carrying blood from the lungs to the left ventricle. Decreasing the pressure in the left beaker replicates a decrease in lung pressure. Decreases and increases in pressure in the right beaker are analogous to a decrease in blood pressure of the body.
Lab 6
Heart rate eventually returned back to normal despite continued stimulation of the vagus nerve because inhibitory transmitters, such as acetylcholine would have been depleted. Isolated heart are not attached to the human body, therefore they cannot replenish their source of neurotransmitters, delivered from preganglionic nerves.
Vagus nerve stimulation would cause a decrease in heart rate, by causing a decrease in the excitability of the tissue around the AV node. Transmission of signals is reduced, thus the heart rate slows down. In healthy humans, sympathetic fibres would function to return heart rate back to normal by increasing transmission at the SA node. Parasympathetic innervation slows down heart rate and sympathetic innervation speeds up heart rate. They oppose the effects of one another
It is not possible to predict whether heart rate would increase or decrease with respect to muscarine and sotalol. Muscarine mimics acetylcholine which is an excitatory neurotransmitter. Sotalol is a beta-blocker and potassium channel blocker, so it slows down the heart rate. Both drugs bind on different receptors, so they are not directly antagonistic. Therefore, the concentrations or amount of each drug would need to be known to determine the effects. The same concept applies to nicotine and pilocarpine. Nicotine is a stimulant that binds to nicotinic acetylcholine receptors. Pilocarpine slows heart rate and binds to muscarinic acetylcholine receptors. Once again, the two drugs are not directly antagonistic and it is not possible to predict the effects, without knowing the amount used. Conversely, epinephrine and atropine both separately increase heart rate, therefore their combined effect would also increase heart rate. In the lab experiment, epinephrine increased heart rate to 80, while digitalis decreased heart rate to 41. By summate the effects of the two, heart rate will decrease because digitalis has a stronger effect.
Cardiovascular Dynamics and Cardiovascular Physiology (Lab 5 and 6)
Michelle Fowler 996870097 BGYC34 (Lec 60) Prof. Stephen Reid February 18, 2011
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|Time Period |HR |HR Status |Observation |
| | |(normal, stable or | |
| | |changing) | |
|Pre Stimulus |62 |normal | |
| |29 |changing | |
|10 s post stimulus | | | |
| |- - |- - - - - - - - | |
|20 s post stimulus | | | |
| |19 |changing | |
|30 s post stimulus | | | |
| |44 |changing | |
|40 s post stimulus | | | |
| |48 |changing | |
|50 s post stimulus | | | |
| |50 |stable | |
|60 s post stimulus | | | |
| |51 |stable | |
|70 s post stimulus | | | |
|10 s after stopping |62 |normal | |
|stimulus | | | |
|20 s after stopping |62 |normal | |
|stimulus | | | |
|Stimulus |HR upon |Observation |
|Rate |stabilisation | |
|(stimuli/sec) | | |
| |49 |Heart rate slows down and stops contracting after 14 seconds and begins |
|50 | |contracting again after 30 seconds. Heart rate stabilizes after 56 seconds |
| |48 |Heart rate slows down and stops contracting after 37 seconds and begins |
|40 | |contracting again after 53 seconds. Heart rate stabilizes after 80 seconds |
| |28 |Heart rate slows down and stabilizes after 25 seconds |
|30 | | |
| |38 |Heart rate slows down and stabilizing after 30 seconds |
|20 | | |
| |52 |Heart rate slows down and stabilizes after 40 seconds |
|10 | | |
|Solution |Heart Rate |
|23 °C Ringers |60 |
|Epinephrine |80 |
|23 °C Ringers |60 |
|Pilocarpine |45 |
|23 °C Ringers |60 |
|Atropine |70 |
|23 °C Ringers |60 |
|Digitalis |41 |
|23 °C Ringers |60 |
|5 °C Ringers |50 |
|23 °C Ringers |60 |
|32 °C Ringers |70 |
|23 °C Ringers |60 |
Cardiovascular Dynamics and the Cardiovascular Physiology experiments both have multiple goals. The first experiment aims to understand how blood flow, pressure gradient, and resistance relate to one another. To understand this, resistance and contributing factors, such as vessel radius, viscosity, and vessel length must be studied. The effects of vessel radius and stroke volume on the ventricular pump should also examined. The experiment also calls for an understanding of cardiovascular compensation. Pump mechanics are further understood through a design of further experiments. The Cardiovascular Physiology experiment attempts to understand the effects of parasympathetic and sympathetic nervous systems on the heart, through vagus nerve stimulation. Refractory periods and relative refractory periods will be studied in direct stimulations of the heart, as well as the five phases of the cardiac cycle. Lastly, the effects of temperature, hormones, and ions will be understood. Epinephrine, pilocarpine, atropine and digitalis are the hormones used to modify the heart. Sodium, potassium and calcium are the ions used in this experiment.
Methods In the Vessel Resistance section for the Cardiovascular Dynamics experiment, two glass beakers, a tube connecting them and a pressure meter were used. The left beaker represented the heart, the right breaker represented the body and the tube was the artery. For the Pump Mechanics …show more content…
section, three glass beakers and two tubes were used, along with three pressure meters. There were also two valves, one representing the bicuspid valve and one representing the aortic semi-lunar valve. The left beaker simulated blood being pumped from the lungs, the middle beaker was the left side of the heart, and the right beaker represented the body. The left flow tube represented a vein and the right flow tube represented an artery. A suspended three chambered heart, an oscilloscope monitor, a heart tray and 23o Ringers solution were required for the Electrical Stimulation and Modifiers of the Heart section in the Cardiovascular Physiology experiment. The Electrical Stimulation section additionally needed Epinephrine, atropine, pilocarpine, digitalis, calcium ions, sodium ions and potassium ions The first section of the Cardiovascular Dynamics experiment measured Vessel Resistance. In the first activity, pressure was manipulated to measure its effects on blood flow. A starting pressure of 25 mm Hg was set in place and increments of 25 mm Hg was made, until a value of 225 mm Hg was reached. The second activity studied the effects of the tube radius (artery) on blood flow. The starting radius was 1.5 mm and it was increased by 1.0 mm, until a radius of 6.0 was reached. The third activity tested the effect of viscosity on blood flow. Blood viscosity started at 1.0 and increments of 1.0 were made to reach a blood viscosity of 6.0. The next activity observed the effect of vessel length on blood flow. Length started at 10 mm and increased by 10 mm, to reach a vessel length of 50 mm. The second section studied Pump Mechanics. In the fifth activity, the radius of the right flow tube was manipulated to measure the effects of vessel radius on the heart pump. The radius of the right flow tube started at 3.0 mm and was increased by 0.5 mm to arrive at 6.0 mm. Activity six manipulated stroke volume and determined its effect on the heart pump. Stroke volume was initially set in place for 10 ml and was increased by 10 ml to test a final stroke volume of 120 ml. Results from each test were recorded and plotted. Activity seven was carried out to examine the ways in which the cardiovascular system compensates for deficiencies. A baseline test was first done and the data was recorded. Then, the radius of the right low tube was decreased and the results of the test were recorded. Three tests were designed to compensate for the effects of the decreased radius of the right flow tube. In the first compensation, the ventricular pressure was increased to 225 mm Hg. In the second test, lung the radius of the left flow tube was increased. For the last compensation the starting pump volume was reduced to 60 ml and the end pump volume was reduced to 25 ml. In the final activity, decreases in the right flow tube radius versus the left flow tube radius were examined. Pressure decreases in the left and right beaker were also studied separately. Lastly, an increase in the pressure of the right beaker was inspected. The first section of the Cardiovascular Physiology experiment measured direct stimulation and vagus nerve stimulation of a three chambered frog heart.
In the first activity, direct single stimulation was delivered to the heart at the beginning, peak, and end of ventricular contraction and its effect were observed and recorded. Then, multiple stimuli were delivered and the effects were observed and recorded. In the second activity, multiple stimuli were delivered to the vagus nerve of the heart and the effects were
recorded. The second section examined the effects of various drugs, hormones and ions, as they modified heart rate. Epinephrine, pilocarpine, atropine, and digitalis were tested and the heart was flushed out with 23o Ringers solution between each test. Temperature effects were observed using 5o, 23o, and 32o Ringers solution. Once the heart rate was stable, following each test, the data was recorded. Lastly, the effects of sodium, potassium, and calcium ions were tested.
Results
Experiment 5
Figure 1- The Effect of Pressure on Blood Flow. As ventricular pressure increases, blood flow linearly increases.
Figure 2- The Effect of Vessel Radius on Blood Flow. There is a positive curved relationship between vessel radius and blood flow. As arterial radius increases, blood flow increases.
Figure 3- The Effect of Viscosity on Blood Flow. There is a negative curved relationship between viscosity and blood flow. As blood viscosity increases, blood flow decreases.
Figure 4- The Effect of Vessel Length on Blood Flow. Regions of the body that are more proximal to the heart have a higher rate of blood flow.
Figure 5- The Effect of Vessel Radius on Pump. As arterial radius increases, more blood can flow from the heart to the rest of the body.
Figure 6- The Effect of Stroke Volume on Pump. Increases in stroke volume do not cause increase in blood flow.
| |Flow (ml/min) |Rad. L (mm) |Rad. R (mm) |Str. V |Rate |Pressure L |Pressure Diff. R |
| | | | |(ml) |(stroke/min) |(mm Hg) |(mm Hg) |
|Baseline |5086.8 |3.0 |3.0 |70 |72.7 |40 |40 |
|Right flow tube radius |1678.1 |3.0 |2.0 |70 |24.0 |40 |40 |
|decreased to 2.0 mm | | | | | | | |
|Increase pump pressure |4245.1 |30 |2.0 |70 |60.6 |40 |140 |
|to 225 mm Hg | | | | | | | |
|Increase left tube |1985.1 |6.0 |2.0 |70 |28.4 |40 |40 |
|radius | | | | | | | |
|Decrease start pump |1678.1 |3.0 |2.0 |35 |47.9 |40 |40 |
|volume to 60 ml and end | | | | | | | |
|pump volume to 25 ml | | | | | | | |
Table 1- Cardiovascular compensation in response to decreased arterial radius. An increase in pump pressure proves to be the most effective solution, followed by increased left tube radius. Change in stroke volume did not counteract the effect of decreased arterial radius.
| |Flow (ml/min) |Rad. L (mm |Rad. R (mm) |Str. V |Rate |Pressure L |Pressure Diff. R |
| | | | |(ml) |(stroke/min) |(mmHg) |(mm Hg) |
|Decreasing right |1678.1 |3.0 |2.0 |70 |24.0 |40 |40 |
|flow tube radius | | | | | | | |
| |124.1 |3.0 |1.0 |70 |1.8 |40 |40 |
|Decreasing left |1678.1 |2.0 |3.0 |70 |24.0 |40 |40 |
|flow tube radius | | | | | | | |
| |124.1 |1.0 |3.0 |70 |1.8 |40 |40 |
|Decrease pressure |2034.7 |3.0 |3.0 |70 |29.1 |10 |40 |
|in left beaker | | | | | | | |
|Decrease pressure |6474.1 |3.0 |3.0 |70 |92.5 |40 |70 |
|in right beaker | | | | | | | |
|Increase pressure |2034.7 |3.0 |3.0 |70 |29.1 |40 |10 |
|in right beaker | | | | | | | |
Table 2- Radius and pressure manipulations in the left and right beaker to alter blood flow. The left (vein) and right (artery) tube showed equal effects in response to decreases in the tube radius. Decreasing the pressure in the right beaker (body) increased flow rate. Increasing the pressure in the right beaker (body) and decreasing the pressure in the left beaker (lungs) had the same effect of lowering blood flow rate.
Experiment 6
Figure 7- Trace of heart rate, of a three chambered heart, with no electrical stimulation.
Figure 8- Trace of heart rate with single electrical stimulation delivered at the beginning of the ventricular contraction shows no change in heart rate.
Figure 9- Trace of heart rate with a single electrical stimulation delivered near the peak of the ventricular contraction shows an extra ventricular contraction, followed by a 1.5 second compensatory pause
Figure 10- Trace of heart rate with a single electrical stimulation delivered during the “fall” of ventricular contraction shows an extra ventricular contraction, stronger than the one seen in the previous figure. The compensatory pause is also longer.
Figure 11- Trace of heart rate with multiple stimuli delivered at a rate of 20 stimuli per second. Extra systoles are evident, followed by a compensatory pause.
Table 3- Vagus nerve stimulation. Heart rate and heart rate status for 10 seconds before stimulus, 10 second intervals after stimulus, and two 10 second periods after stopping stimulus. Heart rate drops immediately following the stimulus and ceases to contract. It then climbs back up to normal rhythm.
Table 4- Effects of altered stimulation frequency of the vagus nerve. A higher stimulus rate slows heart rate down faster and causes it to stop contracting. A reduced stimulus rate takes longer to slow the heart down.
Table 5- Effects of Epinephrine, Pilocarpine, Atropine, Digitalis and Temperature. Epinephrine and Atropine increase heart rate, while pilocarpine and digitalis decrease heart rate. Heart also increases with increased temperature.
Effects of Ca++, Na+ and K+ Ions
Sodium ions depolarize the cell membrane, causing and increase in action potential and an increase in heart rate. Calcium ions sustain the action potential, so they would function to produce stronger heart or faster contractility. Potassium ions decrease heart rate because they cause calcium channels to close.
Discussion
Lab 5
An increase in pump pressure can increase blood flow because the pressure was higher relative the pressure in the body. More force can be exerted by the pump to expel the volume of blood faster. Increased pressure in the pump means that there are a greater number of gas molecules. Blood pumped into the ventricles will be expelled faster because there is less room for liquid molecules to occupy the space. An increase in the left tube radius corresponds to an increase in the radius of the vein, delivering blood from the lungs. Since the radius of the right tube (artery was decreased), blood flowed out of the ventricular pump at a slower rate. To compensate for this, the radius of the vein was made larger to allow blood to flow into the ventricular pump faster. It was hypothesized that decreasing start volume and end volume would cause blood to be pumped to the body faster. However, stroke volume had no effect on the flow of the blood. Reducing stroke volume reduced the volume of blood expelled from the pump.
Decreasing the right flow tube radius simulated a decrease in the radius of the artery, carrying the blood from the left ventricle to the rest of the body. Decreasing the radius of the left flow tube imitated a decrease in the radius of the vein, carrying blood from the lungs to the left ventricle. Decreasing the pressure in the left beaker replicates a decrease in lung pressure. Decreases and increases in pressure in the right beaker are analogous to a decrease in blood pressure of the body.
Lab 6
Heart rate eventually returned back to normal despite continued stimulation of the vagus nerve because inhibitory transmitters, such as acetylcholine would have been depleted. Isolated heart are not attached to the human body, therefore they cannot replenish their source of neurotransmitters, delivered from preganglionic nerves.
Vagus nerve stimulation would cause a decrease in heart rate, by causing a decrease in the excitability of the tissue around the AV node. Transmission of signals is reduced, thus the heart rate slows down. In healthy humans, sympathetic fibres would function to return heart rate back to normal by increasing transmission at the SA node. Parasympathetic innervation slows down heart rate and sympathetic innervation speeds up heart rate. They oppose the effects of one another
It is not possible to predict whether heart rate would increase or decrease with respect to muscarine and sotalol. Muscarine mimics acetylcholine which is an excitatory neurotransmitter. Sotalol is a beta-blocker and potassium channel blocker, so it slows down the heart rate. Both drugs bind on different receptors, so they are not directly antagonistic. Therefore, the concentrations or amount of each drug would need to be known to determine the effects. The same concept applies to nicotine and pilocarpine. Nicotine is a stimulant that binds to nicotinic acetylcholine receptors. Pilocarpine slows heart rate and binds to muscarinic acetylcholine receptors. Once again, the two drugs are not directly antagonistic and it is not possible to predict the effects, without knowing the amount used. Conversely, epinephrine and atropine both separately increase heart rate, therefore their combined effect would also increase heart rate. In the lab experiment, epinephrine increased heart rate to 80, while digitalis decreased heart rate to 41. By summate the effects of the two, heart rate will decrease because digitalis has a stronger effect.
Cardiovascular Dynamics and Cardiovascular Physiology (Lab 5 and 6)
Michelle Fowler 996870097 BGYC34 (Lec 60) Prof. Stephen Reid February 18, 2011
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|Time Period |HR |HR Status |Observation |
| | |(normal, stable or | |
| | |changing) | |
|Pre Stimulus |62 |normal | |
| |29 |changing | |
|10 s post stimulus | | | |
| |- - |- - - - - - - - | |
|20 s post stimulus | | | |
| |19 |changing | |
|30 s post stimulus | | | |
| |44 |changing | |
|40 s post stimulus | | | |
| |48 |changing | |
|50 s post stimulus | | | |
| |50 |stable | |
|60 s post stimulus | | | |
| |51 |stable | |
|70 s post stimulus | | | |
|10 s after stopping |62 |normal | |
|stimulus | | | |
|20 s after stopping |62 |normal | |
|stimulus | | | |
|Stimulus |HR upon |Observation |
|Rate |stabilisation | |
|(stimuli/sec) | | |
| |49 |Heart rate slows down and stops contracting after 14 seconds and begins |
|50 | |contracting again after 30 seconds. Heart rate stabilizes after 56 seconds |
| |48 |Heart rate slows down and stops contracting after 37 seconds and begins |
|40 | |contracting again after 53 seconds. Heart rate stabilizes after 80 seconds |
| |28 |Heart rate slows down and stabilizes after 25 seconds |
|30 | | |
| |38 |Heart rate slows down and stabilizing after 30 seconds |
|20 | | |
| |52 |Heart rate slows down and stabilizes after 40 seconds |
|10 | | |
|Solution |Heart Rate |
|23 °C Ringers |60 |
|Epinephrine |80 |
|23 °C Ringers |60 |
|Pilocarpine |45 |
|23 °C Ringers |60 |
|Atropine |70 |
|23 °C Ringers |60 |
|Digitalis |41 |
|23 °C Ringers |60 |
|5 °C Ringers |50 |
|23 °C Ringers |60 |
|32 °C Ringers |70 |
|23 °C Ringers |60 |