MEDSCI 311

8/18/2019 MEDSCI 311

http://slidepdf.com/reader/full/medsci-311 1/15

!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Cardiovascular Control lab

Conducted by: Group B3

Members: William Lin, Olivia Mackay, Geena Loke, Chloe Li, Samuel Yu

Introduction

Postural reflexes are events which are in close concurrence with our everyday activity; from the slightest changes

from supine to standing up, to the suspension above ground, the body is able to mediate the fundamental

cardiovascular functions of heart rate, blood pressure, as well as vascular resistance to ensure that the vital functions

of the body such as cerebroperfusion, and mean arterial pressure as well as cardiac output is maintained at a near

constant level (Boron & Boulpaep, 2009). As younger individuals, physiological events following that of an abrupt

postural change is often so minute and transient, such that there is no sensation of discomfort whatsoever. When we

readily stand up from a supine position, the gravitational pull on the venous circulation causes a rapid but brief

decrease in mean arterial blood pressure which is sensed by the aortic and carotid baroreceptors, eliciting a response

by which sympathetic drive is increased to restore normative cardiovascular functions (Boron & Boulpaep, 2009)

(Olufsen, 2005). The sympathetic nervous system, being a branch off the autonomic nervous system, innervates and

affects target organs via the alpha-adrenergic and beta adrenergic (Rang & Dale, 2012). The stimulation of these

receptor sites activate a G-protein mediate transduction pathway, which ultimately cause positive chronotropic and

inotropic changes upon agonist binding; these mechanisms allows for the restoration in homeostasis as well as period

by which the body is able to adjust to this postural change; under normal circumstances, this reflex occurs within

the periods of seconds, however, in patients with orthostatic intolerance (specifically elderlies) (James, 1999), this

mechanism does not occur readily to maintain a constant rate of cerebral perfusion, resulting in syncope (fainting)

(Fuca, 2006). Studies have been conducted in suggesting a positive correlation between age and the prevalence of

venous insufficiency, furthermore, venous insufficiency is also attributed to individuals whom are standing for a

long period of time (Seligman, 1956) ("The role of body position and gravity in the symptoms and treatment of

various medical diseases", 2004).

Apart from the homeostatic mechanisms mediating cardiovascular control, the body is also able to aid venous return

voluntarily via the actions of skeletal muscle pumps (Casey & Hart, 2008). The skeletal muscle pumps consist of a

system whereby the rhythmic contractions of skeletal muscles help to induce cyclic compressions and

decompression of venous valves, thereby promoting a unidirectional flow of venous blood back to the heart via a

“pumping” action (Korthuis, 2011). Studies conducted on the action of skeletal muscle pumps and venous return

have suggested that exercising of the muscles i.e. rhythmic contractions help to increase the rate of intramuscular

blood flow and thereby venous flow by 40% (Casey & Hart, 2008).

Under normal circumstances, these physiological adaptations are all occurring in the background to our

consciousness, the removal of any one of these factors would therefore result in a greater-than-controlled changes

in cardiovascular function. With this being said, we conducted 3 sets of experiments consisting of the subject being

tilted across angles of 45o and 82o under a “standing”, “floating” and “floating with compression” protocol. The aim

of the experiment is to deduce a relationship between cardiovascular and degree of venous pooling due to gravity

when there is: 1) only minimal activation of skeletal muscles (standing) 2) skeletal muscle pumps are completely

removed (floating, suspended) 3) when the actions of tonus muscle activity is substituted with intramuscular

compression via compression leggings. Furthermore, our secondary aim is to be able to examine the effectiveness

of compression leggings in aiding venous return and if this compression is equivalent in its effect to that of a resting,

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

tonal activation of muscles in the lower extremity. Our experimental protocol differs from previous studies relating

to compressional therapy in the sense that we have inserted an additional variable by suspending the subject whilst

wearing compression leggings (Williamson, Mitchell, Olesen, Raven & Secher, 1994).

In regards to our experimental protocol, the following have been hypothesized:

1) An increase in angular tilt will pronounce the effect of gravitational pull against the column of returning venous

blood, this will induce a response by which there is an increase in both systolic/diastolic pressures as well as heart

rate to compensate for a decrease in cardiac output.

2) The degree by which the measured parameters (pressures and heart rate) deviate from baseline becomes a function

of the degree of tilt and therefore the vertical component of gravity acting on the venous circulation

3) Abolishing the activity of skeletal muscle pumps will further heighten the increase in measured parameters (in a

suspended position)

4) Compression leggings will in effect act to reduce the degree of venous pooling; it should be expected that under

compression, the data acquired should be similar to that obtained during the “standing” tilt.

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Methods

Preparation

Refer to Image 1-3, (in additional section) for set-up guidelines

General

With the tilt table at its zero position (i.e. parallel to the ground), allow the subject to lie down in a supine position.

The angle of the table is then adjusted within minimal ranges of +/- 5o to ensure there is no strain on the subject’s

neck. After this adjustment has been made, zero the protractor readings via settings displayed on the measurement

apparatus (The app “Protractor 360o” was used in our experiment; this app this downloadable from the Apple store,

as well as Android app market)

Measurement of Arterial Blood pressure

The Human Non-invasive blood pressure monitor (NIBP 100D) is used for this experimental protocol. Ensure that

the air tubing connected to the front panel of the NIBP controller is secure and tight, adjust with screw driver is

necessary. After ensuring that the NIBP controller has been switched on, proceed to opening up the “Human NIBP

settings” on LabChart; a command prompt of “Scanning for Devices” will appear, a green tick should appear beside

“HumanNIBP” suggesting that the controller has been switched on. Click the “Device scan” option to begin scanning

procedures.

With the subject in a supine position, apply finger cuffs to the middle finger of the subject; the right hand was chosen

for this experiment. When applying the finger cuff, ensure that it is wrapped around with appropriate tightness i.e.

will not cut off blood supply but will also ensure a certain degree of pressure against the finger. The photocell and

LED components in the interior of the finger cuff should be aligned symmetrically to the middle of the finger.

Once the finger cuff has been applied on to the subject, attach the wrist unit with the bulk of the component on the

dorsal side of the wrist. Ensure that the force transducer and the air hose has been plugged into the same unit i.e.

both C1 ports or C2 ports, and make sure that the red dot on either component is aligned with each other.

Attach the upper arm strap approximately aligned to the level of the heart. Once these procedures have been

completed, calibrate the HCU transducer and the reference point (on the arm strap) by placing them at the same

level. Once the two components are at level with each other, go into LabChart (Click Setup -> Human NIBP settings

-> Zero) to zero and thus calibrate the two components. Once this has zeroing procedure has been completed, place

the HCU transducer to the finger cuff (For this particular experiment, the HCU transducer was attached to the black

Velcro strap of the arm unit). Attach the reference end to the arm strap, at level with the heart.

Ensure that the LabChart recording for pressure measurement is functional through testing it with the non-recording

function of LabChart

ECG Setup

For this experimental protocol, Lead II was used

Begin by wiping the respect areas on the subject (Ventral surface of the left and right wrists, and Lateral surface of

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

the left and right leg, in close proximity to the ankle region). Place electrodes as stated on the ECG controller to the

respective regions indicated by peeling off the non-adhesive layer of the electrodes. Four electrodes were used in

this experiment: LA, RA, LL, which were the measuring electrodes and RL which was the ground electrode. Select

Lead II via twisting the knob on the lead selection box.

Open Chart v8 program in conjunction with PowerLab, ensure the following options are set-up correctly:

Channel 1: ON

Bio Amp Settings

Range: 1 mV

Notch Filter: ON

High Pass: 0.1 Hz

Low Pass: 100 Hz

Invert: ON

Sampling Speed: 200/s

(MEDSCI 311: Cardiovascular biology Laboratory guide, 2016)

Finalizing preparation process:

The straps on the tilt table were clipped on and tightened such as the subject would not slip down as he/she is elevated

at an angle. With this being said, ensure that the subject is still able to breath effortlessly with no excessive

compression against their chest and respective regions. Using masking tape or duct tape, position the phone with the

protractor app displaying beside the subject such that the screen is visible during elevation or tilting of the table.

Experiment

NOTE: Ensure that during the data collection process, comments/markers should be used to suggest the change

from one condition to another e.g. Resting to Active tilting etc.

Baseline

With preparation procedures all completed, begin to record ECG and Pressure recordings on their respective

programs for a period of 10 minutes. During this period, ensure that there is minimal movements or factors that may

render the data as being inaccurate (such as excitement, laughter etc.)

Standard tilt – Standing (A)

Ensure that the subject’s feet is rested on the feet stand of the tilt table. With the subject in their supine position at

an angular tilt of 0o, measure the normalized “resting” cardiovascular functions. After this 10-minute period, proceed

to raise the tilt table to 45o under a constant speed (the angle should be confirmed with the protractor, which is zeroed

before each tilt). Record cardiovascular functions both during the active tilting phase and when the angle has been

reached for a period of 10 minutes. Once this 10-minute recording period if completed, lower the table back to its

zero position; rest the subject for another 10 minutes before continuing to tilt him/her to 82 degrees.

When elevating subject to 82 degrees, repeat that described above for the 45-degree tilt. (Note: 82 degrees was

chosen because it is the maximum which the tilt table was able to elevate to)

Tilt – Floating (B)

Ensure that the subject has is feet suspended i.e. not touching the feet stand, furthermore, ensure the straps are tight

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Image 2. Position of the arm unit with strap

lacement and HCU transducer (reference end)

osition

enough such that the subject will not slip. Repeat the experimental procedure described for the “Standard tilt –

Standing” (A of the methods)

Tilt – Compression with floating

Have the subject wear compression tights and ensure that the subject is in the same position as that for the “Floating”

protocol. For this experiment Skins © A200 men's thermal compression long tights were used for the subject (can

be purchased in sports retail stores). Repeat the experimental procedure for that described in A/B of the methods

Data Collection

Mean values were obtained throughout the 10 minute period for Systolic pressure (mmHg), Diastolic pressure

(mmHg) and heart rate (BPM). The “averaging” function can be accessed via LabChart and using the marker tool to

select applicable regions for data collection

Mean values for the first 30 seconds can also be obtained via the same method described above

Systolic/Diastolic ratio was calculated from the equation:

!"#$%&'()*'+#$%&'( -+$'% .!"#$%&'( /-0##1-0

*'+#$%&'( /-0##1-0

Additional information

Image 1. Position of the wrist unit with air tubing

and pressure transducer and HCU transducer placement

8,.16 35.6

A., 637.5B +5-C,D113,D6,+51-32D,

E%F 6,+51-32D,

E%F 6,+51-32D,;GDHD,D52D D5-@

A,9 16,+IJ A,935.6

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Image 3. General guideline in terms of the position and posture of subject as

well as strap position.

8/18/2019 MEDSCI 311


8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Table 2. Mean Systolic (mmHg), Diastolic (mmHg) and Heart rate (BPM) measurements for subjects under “Floating”

conditions across angles 0o (Baseline), 45

o and 82

o , as well as measurements acquired during the tilting process

Baseline measurements were used concurrently to that which was used in table 1. Again, it is evident that, that the 3

measured parameters followed a general trend of increase as the subject was moved from a baseline (supine) position

to its respective angles at 45 o and 82

o. The peak pressures both systolic and diastolic are generated at 82

o, however,

it is noticeable that systolic pressure increased by a further 12.8 mmHg in comparison to the peak systolic pressure

generated for the “Standing” protocol at 82 o

; in contrast, the peak diastolic pressure for the “floating” protocol

remained reasonably similar, deviating by only 4.56 mmHg to that recorded for the peak diastolic pressure during

“standing” protocol. For the “Floating” protocol, it can be noted that the relative increases in systolic pressure during

active tilting and that when the angle was reached were proportionately similar. Between baseline and the active

tilting phase, the systolic pressure increased by 25.75 mmHg; a further increase of 22.38 mmHg is evident when this

45o was reached. This contrasts to that observed in the “standing” protocol whereby the most pronounced increase

is during active tilting. Similarly, when the subject was raised to 82 o, increases in pressure were also proportionately

similar, with increases of 42.35 and 41.96 mmHg observed respectively during active tilting and when angles were

reached. Although the peak diastolic pressures generated were relatively similar between the “standing” and

“floating” protocols, the increase in diastolic pressure during active tilting to 45 o

and when this angle was reached

is much more pronounced than that observed in the previous “standing” protocol (Between baseline and active tilting,

increase in pressure is 27.45 mmHg, a further increase of 32.96 mmHg is observed when the angle is reached). The

measured heart rates were all relatively higher than that in the “standing protocol”; however, the peak heart rate is

somewhat lower than that measured for the “standing protocol”, (90.43 BPM compared to 93.76 BPM respectively).

Floating

Baseline (0o) Tilting to 45

o At 45

o Tilting to 82

o At 82

o

Systolic (mmHg) 123.06 148.81 171.19 165.41 207.34

Diastolic (mmHg) 69.6 97.05 129.54 102.88 149.91

Heart rate (BPM) 81.18 88.34 83.01 89.32 90.43

!"##

!">&

!"&'

!

!"'!"$

!"(

!")

'

*+,-./0- 1/.2/03 25 $>

=-37--,

82 $> =-37--, 9 : , 2 5 . / ; < =

/ + , 2 5 . / ;

!"#$%&'()*'+#$%&'( 6+$'% . /'&$ $% 78

451655#

!"##!"(!

!"&)

!

!"'!"$

!"(

!")

'

*+,-./0- 1/.2/03 25 )'

6-37--,

82 )' 6-37--, 9 : , 2 5 . / ; < =

/ + , 2 5 . / ;

!"#$%&'()*'+#$%&'( 6+$'% . /'&$'01 $%

23 451655#

Figure 3a. Systolic Diastolic Ratio changes measured across baseline, active

tilting and when angular tilt is reached (45 degrees), under “floating

conditions”

Under floating conditions, tilting to 45 degrees, there is also a linear

depression in systolic/diastolic ratio, against suggested that as the

subject is elevated against gravity, the diastolic pressures increase to a

larger extend than that of systolic (i.e. 1.32 at 45 degrees)

Figure 2b. Systolic Diastolic Ratio changes measured across baseline, active

tilting and when angular tilt is reached (82 degrees), under “floating

conditions”

The degree of systolic/diastolic ratio depression is less pronounced than

that observed in figure 2a. The calculated values for systolic/diastolic

ratio were larger than that in figure 2a, suggesting that at 82 degrees

(floating), the relative increases in systolic and diastolic pressures are

relatively more in proportion

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Table 3. Mean Systolic (mmHg), Diastolic (mmHg) and Heart rate (BPM) measurements for subjects under “Floating with

compression” conditions across angles 0o (Baseline), 45

o and 82

o , as well as measurements acquired during the tilting process

Similar to the two previous experimental protocols, the results obtained from “Floating with compression” also

comes to suggest a trend of increase values (for all three parameters) in correspondence to angle elevation (from 0

to 82 degrees). In respect to systolic and diastolic blood pressures recorded, baseline values were noticeably lower

than that recorded for the non-compression protocols; baseline systolic pressure was 108.15 mmHg and diastolic

was 51.95 mmHg compared to baseline measurements (ref. tables 1 and 2). Despite the fact that systolic pressures

were lower at baseline, the increase in angular tilt induced increases in blood pressure that resulted in similar values

to those observed for non-compression, standing protocol (ref. table 1). When the subject was titled to 82o, the peak

systolic pressure was measured at 194.73, which differs by that measured when the subject was tilted to 82o whilst

standing, by +0.19 mmHg. In comparison to systolic pressures, diastolic pressures continued to remain at values

much lower than that observed in non-compressional protocols by approximately +/- 10 mmHg; the final diastolic

pressure measured at an 82o tilt (compressional float) was 132.61 mmHg compared to 145.35 and 149.91 mmHg

which were measured for standing and floating (non-compression) respectively. The measured heart rates for

subjects under different angular tilts were similar to that measured for subject under standing, non-compression

states, with values deviating within a range of approximately +/- 3 BPM. However, with this being said, the heart

rate at 82

o

tilt for “Floating with compression” was lower than heart rate at 82

o

tilt for “standing, withoutcompression” (86.49 and 93.76 BPM respectively).

Floating with compression

Baseline Tilting to 45

o

At 45

o

Tilting to 82

o

At 82

o

Systolic (mmHg) 108.15 141.89 168.19 135.3 194.73

Diastolic (mmHg) 51.95 85.44 110.67 80.42 132.61

Heart rate (BPM) 79.63 83.04 82.96 83.27 86.49

'"?)

!"((!">'

!

!"'

!"$

!"(

!")

'

'"'

*+,-./0- 1/.2/03 25 $> 82 $>

9 : , 2 5

. / ; < = / + , 2 5 . / ;

!"$%&'()*'+#$%&'( -+$'% . /'&$'01 $%

78 451655#'"?)

!"()

!"$#

!

!"'

!"$

!"(

!")

'

'"'

*+,-./0- 1/ .2 /03 25 %? 82 %?

9 : , 2 5

. / ; < = / + , 2 5 . / ;

!"$%&'()*'+#$%&'( -+$'% . /'&$'01 $% 23

451655#

Figure 3a. Systolic Diastolic Ratio changes measured across baseline, active

tilting and when angular tilt is reached (45 degrees), under “floating with

compression” protocol

It is evident that the baseline systolic/diastolic ratio (2.08) is higher than

that calculated for figures 1 and 2 (1.77); this suggests that under

compression, the systolic pressure is, in proportion, higher than the

measured for the “non-compressional protocols”. Furthermore, although

the general relationships is that of a descending one in response to

elevation, the systolic/diastolic ratios once the elevation angle is reached

is higher than that in figures 1 and 2, suggesting that diastolic pressure

does not increase as disproportionately as that observed previously.

Figure 3b. Systolic Diastolic Ratio changes measured across baseline, active tilting

and when angular tilt is reached (82 degrees), under “floating with compression”

rotocol

The systolic/diastolic ratio values under this protocol is very similar both in

it descending relationship as well as the value itself; values deviate from

figure 3a values by less than +/- 0.5 points.

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Discussion

Part A of the experiment: “Standing tilt: consisted of the subject being tilted across the respective angles (45 and 82o)

with feet resting against the foot stand. As the action of tilting the subject was operated through the external

machinery conducted via the tilt table, there is minimal contraction from the skeletal-muscle pumps itself and it is

therefore assumed that only a resting muscular tone exists in the regions of the lower extremity. Skeletal-muscle

pumps have been shown to demonstrate an elevated rate of venous emptying and peripheral blood flow of 40%

(Casey & Hart, 2008); in order to examine the relationship between basal venous tone and the effects of gravity on

the circulatory system, it would only be appropriate to eliminate or minimize the effects of this mechanical pump.

Indeed, with the skeletal-muscle pumps removed as a component in this experiment, elevation in diastolic, systolic

pressures as well as heart rate was evident as the subject was moved across respective angular tilts. The physiology

attributing to the changes observed in these three parameters can be first retraced back to the relationship between

posture and the circulatory system. When the subject is under a supine position, his circulatory system and the heart

itself is effectively in one plane, this removes the effect of the vertical component of gravity working against venous

return from the periphery; likewise, the action of squatting also minimizes the effect of gravity, as it reduces the

vertical distance between the heart and the periphery (Rossberg & Pe!az, 1988). The relationship described above

is consistent with the baseline recordings made for subject (ref. table 1 and 2); under a supine position, the subject

exhibited systolic/diastolic pressures of 123.06/69.6 mmHg and a heart rate of 81.18 which falls under the normative

physiological ranges ("Understanding Blood Pressure Readings", 2016). In theory, when the subject is elevated

across varying angles, the effect of gravitational pull against the column of returning venous blood becomes a

function of the angular tilt (0-90o); likewise, this is also consistent with what is exhibited in the results shown in

table 1. The values of systolic/diastolic pressures at angles 45 o and 82o were 168.42/114.61 and 194.54/145.35

mmHg, respectively; if we were to model the fluctuation in blood pressure with vectors representing the x and y

components of gravity (Olufsen, 2005), at 45o, the vertical component would be substantially less than the vertical

component at 82o, providing that a constant distance from ground is maintained throughout the experiment. Although

this model lies consistent with the values obtained in our experiment, it is still preliminary as we are solely

accounting for the effective components of gravity.

It should be acknowledged that the previous studies relating postural changes to cardiovascular functions occurred

under conditions whereby the subject is actively changing between supine and standing postures (Olufsen, 2005),

furthermore, the rhythmic contractions of the skeletal muscle pumps following standing-up is also assumed in these

experiments (Rossberg & Pe!az, 1988). Relating to our experiment conducted, the minimal contributions from the

skeletal muscle pumps would mean even after homeostatic measures e.g. baroreflex and sympathetic drive have

come in to play, the effect of gravity would still predominate against the circulatory system, thereby inducing a

considerable degree of stress upon the cardiovascular system and sympathetic nervous system (Sparrow, Tifft,

Rosner & Weiss, 1984). The constant high systolic pressures and diastolic pressure could be attributed to a long

period of elevation with minimal activity from the skeletal-muscle pumps. Under a normal postural reflex (i.e. supine

to standing), the blood pressure of a subject is expected to show that of an initial rise from baseline, which is

progressively dampened down as bodily adjustments occur. In our experiment (Olufsen, 2005), an increased pooling

due to elevation of the subject is believed to result in baroreceptor relaxation, thereby un-inhibiting sympathetic

drive, causing arteriole and venous vasoconstriction. Furthermore, the increase in sympathetic stimulation to the

ventricular walls will increase contractility and inotropic state of the heart, resulting in a greater active pressure

generated at ventricular systole. (Boron & Boulpaep, 2009) The systolic/diastolic ratios that were calculated (ref.

figure 1a, 1b) suggests that of a decline (in ratio) in response to increased tilt; this suggests that with increased

8/18/2019 MEDSCI 311


8/18/2019 MEDSCI 311


8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Conclusion

Our experimental data highlighted the relationship between gravity induced venous pooling with changes in

cardiovascular function. It is evident that the skeletal muscle pumps are a vital bodily mechanism aiding venous

return and increasing the linear flow of blood even at resting tonus activity i.e. as highlighted in the “standing”

protocol. Abolishing the activities of the skeletal muscle pumps produced greater-than-controlled changes in

cardiovascular parameters (blood pressure and heart rate) which were indicative of increased cardiovascular stress.

However, as hypothesized, it is evident that the employment of compression leggings reduced the effects of

gravitation induced venous congestion, as highlighted by the restoration of cardiovascular parameters to that

measured during the “standing” protocol. With comparison between the “standing” and “floating with compression”

protocols alone, it is evident that compression has its effect across all positions i.e. supine as well as standing; this

finding is consistent with the pre-established findings from studies conducted to examine the effect of compression

leggings in treating venous insufficiency.

However, there were some draw backs regarding the experimental protocol. Firstly, due to equipment limitations,

the tilt table was only able to extend to an angle of 82o, this deviated from our desired maximum angular tilt (90

o)

by 8 degrees; despite this, it has been suggested in previous studies that an angular tilt above 70o is sufficient to

provide effects relating to vertical position, as a result it may be assumed that this equipment limitation does not

affect our findings as much as predicted ("Provocation of hypotension during head-up tilt testing in subjects with no

history of syncope or presyncope", 1996). The experimental data acquired were in some sense, crudely reflective of

an explicit physiological relationship; the absence of other crucial measurements such as ejection fractions,

intramuscular pressure and venous pressure renders our findings only partially congruent to our hypothesis. Factors

such as stress and anxiety from the subject has been suggested to attribute to an increase in blood pressure and heart

rate

Reference

Boron, W., & Boulpaep, E. (2009). Medical physiology. Philadelphia, PA: Saunders/Elsevier.

Casey, D., & Hart, E. (2008). Cardiovascular function in humans during exercise: role of the muscle pump. The

Journal Of Physiology, 586(21), 5045-5046. http://dx.doi.org/10.1113/jphysiol.2008.162123

Fuca, G. (2006). The venous system is the main determinant of hypotension in patients with vasovagal syncope.

Europace, 8(10), 839-845. http://dx.doi.org/10.1093/europace/eul095

Grewal, T., James, C., & Macefield, V. (2009). Frequency-dependent modulation of muscle sympathetic nerve

activity by sinusoidal galvanic vestibular stimulation in human subjects. Exp Brain Res, 197(4), 379-386.

http://dx.doi.org/10.1007/s00221-009-1926-y

James, M. (1999). Orthostatic blood pressure changes and arterial baroreflex sensitivity in elderly subjects. Age And

Ageing, 28(6), 522-530. http://dx.doi.org/10.1093/ageing/28.6.522

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Knellwolf, T., Hammam, E., & Macefield, V. (2016). THE VESTIBULAR SYSTEM DOES NOT MODULATE

FUSIMOTOR DRIVE TO MUSCLE SPINDLES IN RELAXED LEG MUSCLES OF SUBJECTS IN A NEAR-

VERTICAL POSITION. Journal Of Neurophysiology, jn.01125.2015. http://dx.doi.org/10.1152/jn.01125.2015

Korthuis, R. (2011). Skeletal muscle circulation. San Rafael, Calif.: Morgan & Claypool Life Sciences.

Lee, C., & Porter, K. (2007). Suspension trauma. Emergency Medicine Journal, 24(4), 237-238.

http://dx.doi.org/10.1136/emj.2007.046391

MEDSCI 311: Cardiovascular biology Laboratory guide. (2016). Auckland.

Miller, J., Pegelow, D., Jacques, A., & Dempsey, J. (2005). Skeletal muscle pump versus respiratory muscle pump:

modulation of venous return from the locomotor limb in humans. The Journal Of Physiology, 563(3), 925-943.

http://dx.doi.org/10.1113/jphysiol.2004.076422

Molinoff, P. (1984). alpha- and beta-Adrenergic Receptor Subtypes Properties, Distribution and Regulation. Drugs,

28(Supplement 2), 1-15. http://dx.doi.org/10.2165/00003495-198400282-00002

Olufsen, M. (2005). Blood pressure and blood flow variation during postural change from sitting to standing: model

development and validation. Journal Of Applied Physiology, 99(4), 1523-1537.

http://dx.doi.org/10.1152/japplphysiol.00177.2005

Provocation of hypotension during head-up tilt testing in subjects with no history of syncope or presyncope. (1996).

ACC Current Journal Review, 5(5), 57. http://dx.doi.org/10.1016/1062-1458(96)85238-x

Rang, H., & Dale, M. (2012). Rang and Dale's pharmacology. Edinburgh: Elsevier/Churchill Livingstone.

Rossberg, F., & Pe!az, J. (1988). Initial cardiovascular response on change of posture from squatting to standing.

European Journal Of Applied Physiology And Occupational Physiology, 57(1), 93-97.

http://dx.doi.org/10.1007/bf00691245

Seligman, B. (1956). Chronic Venous Insufficiency. Angiology, 7(5), 427-431.

http://dx.doi.org/10.1177/000331975600700503

Sparrow, D., Tifft, C., Rosner, B., & Weiss, S. (1984). Postural changes in diastolic blood pressure and the risk of

myocardial infarction: the Normative Aging Study. Circulation, 70(4), 533-537.

http://dx.doi.org/10.1161/01.cir.70.4.533

The role of body position and gravity in the symptoms and treatment of various medical diseases. (2004). SWISS

MED WKLY, 134, 543–551.

Understanding Blood Pressure Readings. (2016). Heart.org. Retrieved 29 March 2016, from

http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/AboutHighBloodPressure/Understanding-

Blood-Pressure-Readings_UCM_301764_Article.jsp#.VvsVmxJ946g

8/18/2019 MEDSCI 311


!"#$%& ()) * %+,-./0+1234+, 2/56,/4 4+7 8.44.+9 :.5 ;<=(=><?@

Williamson, J., Mitchell, J., Olesen, H., Raven, P., & Secher, N. (1994). Reflex increase in blood pressure induced

by leg compression in man. The Journal Of Physiology, 475(2), 351-357.

http://dx.doi.org/10.1113/jphysiol.1994.sp020076

Documents

MEDSCI 311