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EFFECTS OF ALTITUDE ON PRESSURE-FLOW RELATIONSHIPS

IN THE VASCULAR BED OF THE HIND LIMB

OF THE DOG

APPROVED:

(X^JLA cil v 1-—("_d< Major Professor

Minor :'Profess or i V

H. 7U/vU Director of the Department of Biology

Dean of the Graduate School

EFFECTS OF ALTITUDE ON PRESSURE-FLOW RELATIONSHIPS

IN THE VASCULAR BED OF THE HIND LIMB

OF THE DOG

THESIS

Presented to the Graduate Council of the

North Texas State University in Partial

Fulfillment of the Requirements

For the Degree of

MASTER OF ARTS

By

Donald E. Roberts, B. A,

Denton, Texas

August, 1966

TABLE OP CONTENTS

Page

LIST OF TABLES iv

LIST OP ILLUSTRATIONS V

Chapter

I. INTRODUCTION 1

Literature Statement of the Problem

II. MATERIALS AND METHODS 14

Animal Preparation Perfusion Device Decompression Chamber Procedure

III. RESULTS 2k

IV. CONCLUSION 59

Discussion of Results Summary

APPENDIX 74

BIBLIOGRAPHY 82

ill

LIST OF TABLES

Table Page

I. Standard Deviations of Selected Points on Mean Pressure-Plow Curves 36

II. Standard Deviation of Mean Regression Slopes of

Peripheral Resistance Versus Time 58

III. Perfusion Pressure at Ground Level . . . . . . . 75

IV. Perfusion Pressure at 5,000 Feet 76

V. Perfusion Pressure at 10,000 Feet 77

VI. Perfusion Pressure at 15,000 Feet 78

VII. Perfusion Pressure at 20,000 Feet 79

VIII. Perfusion Pressure at 25*000 Feet 80

IX. Perfusion Pressure at Return to Ground Plus Zero 81

iv

LIST OF ILLUSTRATIONS

Figure Page

1. Schematic Diagram of Perfusion System 16

2. Perfusion Apparatus 17

3. Linearly Increasing Flow Rates. 19

4. Pressure Recordings of Femoral Perfusions . . . 25

5. Mean Pressure-Flow Curve at 1.0 for 14 Animals Using Saline at Ground Level 27

6. Mean Pressure-Flow Curve at 1.0 for 11 Aminals at Ground Level • 28

7. Mean Pressure-Flow Curve at 1.0 for 15 Animals at 5,000 Feet 29





12. Mean Pressure-Flow Curves at 1.5 for 15 Animals at Ground Level 37





v

Figure Page


18. Mean Pressure-Flow Curve at Return Plus Zero for 15 Animals Following Rapid Recompression 4\<

19. Mean Pressure-Flow Curve at Return Plus Ten for Two Animals Following Rapid Recompression . 48

20. Mean Pressure-Flow Curve at Return Plus 18 for Two Animals Following Rapid Recompression . 49

21. Mean Pressure-Flow Curve at 1.5 for 4 Animals at Return Plus 4 Following Rapid Recompression 50

22. Mean Pressure-Flow Curve at 1.5 for 2 Animals at Return Plus 10 Following Rapid Recompression 52

23• Mean Pressure-Flow Curve at Return Plus Zero for 9 Animals 53

24. Mean Pressure-Flow Curve at 1.5 for 10 Animals at Return Plus 4 55

25. Mean Pressure-Flow Curve at 1.5 for 4 Animals at Return Plus 10 56

26. Mean Pressure-Flow Curve at 1.5 for 4 Animals

at Return Plus 20 57

27. Composite Pressure-Flow Curves at 1.0 6l

28. Composite Pressure-Flow Curves at 1.5 63

29. Composite Pressure-Flow Curves at 1.0 with the Pressure at Each Altitude Compared to Ground 64

30. Composite Pressure-Flow Curves at 1.5 with the Pressure at Each Altitude Compared to Ground 66

31. Composite Pressure-Flow Curves at 1.0 at Return to Ground with Rapid and Normal Recompression 68

32. Composite Pressure-Flow Curves at 1.5 at Normal Return to Ground 69

vi

Figure Page

33• Composite Pressure-Flow Curves at 1.5 at Rapid Return to Ground 70

vii

CHAPTER I

INTRODUCTION

Vascular resistance is the force exerted by the vascular

bed to Impede blood flow. The degree of resistance is primarily

determined by the vascular bed itself in regulation of its

blood supply.

Literature

Bayliss (1) in 1902 showed that the arterial smooth muscle

will respond to a stretch stimulus. The stimulus used was

distension of the vessel to elicit a contraction of the smooth

muscle resulting in a vasoconstriction. A decrease of the

normal intraluminal pressure resulted in relaxation of the

vessel or a decrease in vascular tone. Bayliss showed that,

a sudden increase in arterial pressure resulted in a decreased

volume in the hind leg of a dog while a circulatory arrest

for five seconds resulted in an increased volume in the hind

leg. He concluded that this was the result of an active vaso-

constriction or vasodilation. Bayliss explained this as being

a property of the vascular smooth muscle and not subject to

neural control.

Folkow (5, 7) supported Bayliss's theory of myogenic action

of vascular smooth muscle. Folkow showed that muscular vessels

reacted to decreased intravascular tension by dilation. Following

denervation blood vessels were exposed to an increased blood

pressure, which resulted in an increased blood flow at first,

followed by a decrease; with pressure remaining constant.

This decrease in flow was interpreted as a vasoconstriction,

Phillips et al. (24) found that the immediate effect

of an increased intraluminal pressure was to reduce resistance

to blood flow. They attributed this to a passive dilation

of the vascular channels. They found that an increased intra-

luminal pressure never produced an augmented resistance.

Gaskell and Burton (9) used changes in blood flow into

an appendage during postural changes to show that a distension

of the venous bed elicits a constriction of local arterioles

by a veni-vasomotor reflex. This reflex was shown to be elicited

by a rise in venous pressure and distension of the veins.

Yamada and Burton (28) used venous occlusion plethysmography

to study the veni-vasomotor reflex in the fingers of five normal

human subjects. They showed that a decreased tissue pressure

produced a decreased blood flow. The decrease in blood flow

was 60 per cent of control when the finger was exposed to

a pressure of 40 millimeters of mercury below atmospheric.

With exposure to 100 millimeters of mercury below atmospheric,

the blood flow dropped to 10 per cent of control. This was

interpreted as evidence that distension of the venous bed

elicits a oonstriction of local arterioles.

Jones (17, 18) worked with the vascular bed in the Gracilis

muscle of the dog. He showed that when a vascular bed exhibited

a high degree of vascular tone it was associated with a low

VOg. Jones supported the veni-vasomotor reflex theory by

showing that an increase in venous pressure produced an initial

decrease in blood flow and an increase in resistance. He also

demonstrated that autoregulatory responses were present in

the absence of neural connections.

Greenfield and Patterson (13) disputed the theory of a

veni-vasomotor reflex. They showed that a degree of venous

back pressure sufficient to cause a steady increase in the

volume of the forearm was not associated with any significant

alteration in the blood flow.

Hansom and Johnson (15) found that when arterial pressure

in the hind leg of the dog was reduced the arterial resistance

decreased while the venous resistance remained constant.

As the blood flow decreased due to a reduced arterial pressure

head, the venous oxygen decreased and carbon dioxide concen-

tration increased while the oxygen consumption fell. They

concluded that autoregulation in the hind limb of the dog was

due to tissue hypoxia.

Texter et al. (27) showed that total bed resistance in

the intestinal vascular bed decreases as a function of flow

in the range of 20 to 60 milliliters per minute and Increases

as a function of flow in the range of 90 to 270 milliliters

per minute. The onset and cessation of resistance increase

to flow change were found to be 64 millimeters of mercury and

205 millimeters of mercury respectively. The changes observed

resulted from changes of flow resistance In vessels less than

0.5 millimeters in diameter. This was interpreted by the

investigators to mean that the intestinal vascular bed has

a local mechanism which antagonized changes of flow rate pro-

duced by variation of arterial pressure.

Sagawa and Guyton (25) have shown that the cranial cir-

culation in dogs exhibits no sign of autoregulatory mechanism,

but instead has a linear proportional relationship.

Hinshaw (16), using isolated dog hind leg and intestine,

found that a pressor substance was released when the arterial

pressure was Increased, which resulted in an increase in re-

sistance. Hinshaw interpreted this as evidence of no auto-

regulation in the leg and intestine.

Frohlich and Gillenwater (8) found in the canine spleen

that over a range of 6? to 313 millimeters of mercury an in-

creased pressure produced a decreased resistance and an in-

creased blood flow; indicating no autoregulation.

Stainsby (26) used dog leg muscle to show that many of

the autoregulatory responses were metabollcally linked. Among

the responses studied were isoemic autoregulation, active

hyperemia, reactive hyperemia, postcontraction hyperemia, and

hypoxic hyperemia,

Haddy and Scott (14) have found in the dog forelimb that

in the steady state, resistance to flow falls as a function

of flow rate.

Levy and Share (21) have shown that blood flow In dog

hind limb Is an exponential function of pressure. They have

shown that the apparent viscosity of the blood decreases as

the radius of the tube decreases while the apparent viscosity

increases when mean velocity falls below certain critical

levels.

Levy (22) has shown that small variations of the blood

in small tubes would result in great changes in apparent vis-

cosity. He has also shown that the anomalous rheologic pro-

perties of blood exert a negligible net influence under set

conditions.

Subatmospherlc Pressure

Numerous experiments have been conducted on humans re-

lating changes in blood flow patterns to changes in atmospheric

pressure. These studies were based on the premise that a

decreased atmospheric pressure acts to increase the transmural

force exerted across the vessel wall. According to Greenfield

(12), when a distending force is applied to a blood vessel,

the vessel will initially dilate due to the increase in trans-

mural pressure. In response to this distension, the vascular

tone increases, thus resisting the force, and the calibre of the

vessel returns to its control level.

The studies by Greenfield and his co-workers, as well as

other investigators, involved exposure of an appendage to a

decreased atmospheric pressure for short periods of time.

Other workers have exposed the entire animal to a decreased

atmospheric pressure.

Whole Body Exposure

Lipin and Whitehorn (23), using dogs with whole body ex-

posure to a pressure of 179 millimeters of mercury, found no

change in central blood pressure, heart rate or cardiac output.

They did find a reduction in skin temperature.

Girling (10, 11) found that during decompression of rabbits,

resistance in the femoral artery did not change up to an alti-

tude of 20,000 feet. At 30,000 feet he observed an increase

of 100 per cent over control levels. He found that breathing

100 per cent oxygen had no effect on this response.

Kaiser et al. (19) concluded that an increased sympathetic

tone of blood vessels of an extremity was responsible for .

diminished blood flow to extremities during decompression.

Knisely (20) observed a constriction of arterioles of

the sclera upon decompression.

Lipin and Whitehorn (23) suggested that vasomotor reflexes

originating in the distended gastrointestinal traot and acces-

sory air sinus or as the result of accumulations of extravas-

cular gas in the body tissues may be responsible for the effects

noted.

Appendage Exposure

Greenfield and Patterson (12), using venous occlusion

plethysmography, measured blood flow into the human forearm

following exposure of the forearm to a pressure 100 millimeters

of mercury lower than atmospheric pressure for five seconds.

They found that a moderate distension was followed by a period

of reduced blood flow, but a severe distension was followed

by a period of increased blood flow. They concluded that the

vasoconstriction following exposure to a reduced atmospheric

pressure was a response of the blood vessels to increased

transmural pressure in the vessels and did not depend on dis-

tension of capacity vessels.

Blair and Greenfield (2) analyzed blood flowing from the

forearm following exposure of the forearm to a pressure reduced

50 millimeters of mercury from atmospheric pressure. They

found an increase in the oxygen saturation in conjunction with

the increase in vascular tone resulting from the pressure

response.

Blair et al. (2) used the human forearm and found that

upon exposure to a decreased atmospheric pressure the blood

flow into the forearm vessels Increased due to dilation of

the resistance vessels. The fact that an accumulation of

fluid in the tissues surrounding the vessels only slightly

decreased the effect led the investigators to conclude that

the effect noted is an active constriction of the vascular

smooth muscle.

Coles and Greenfield (3) measured heat elimination as

an index of blood flow in the human hand exposed to various

subatmospheric pressures. They observed that a pressure reduced

8

by 30 millimeters of mercury produced no change. When the

pressure was reduced by 60 millimeters of mercury to 100 milli-

meters of mercury, the rate of heat elimination decreased.

They concluded that this indicated a reduction in blood flow.

Exposing the hand to a pressure reduced by 200 millimeters of

mercury from atmospheric pressure produced an increase in heat

elimination due to dilation of resistance vessels.

Coles et al. (^) observed a decrease in blood flow to

the calf of the human leg following local exposure to a pressure

100 millimeters of mercury to 200 millimeters of mercury below

atmospheric pressure. The method used was heat elimination.

The decrease was seen only when the blood vessels were allowed

to become distended during suction and, according to these

investigators, was not due to the effect of decreased pressure

on other structures. They suggested that if the viscosity

of the blood and perfusion pressure remained constant, the

decrease in blood flow Indicated an increased peripheral resis-

tance from vasoconstriction. They also postulated that the

decrease in local atmospheric pressure increased pressure

between the lumen and the surrounding tissue by an equal amount.

Since the pressure in the tissues closely followed atmospheric

pressure, they showed that the differential pressure.across

the walls of the blood vessel increased by the same amount as

atmospheric pressure decreased. Goles* results indicated

that the calibre of the blood vessel reflected a balance between

transmural pressure and vessel wall tension.

Folkow (6) has shown that vascular tone Is confined to

precapillary resistance vessels and precapillary sphincters.

He demonstrated that tone was not exhibited by A-V shunts

or vessels on the venous side, Folkow concluded that trans-

mural pressure per se will affect vascular smooth muscle acti-

vity in precapillary resistance and sphincter sections In the

manner proposed by Bayllss.

The vasoconstriction or vasodilatation following exposure

to subatmospherlc pressure could result from a change in the

vascular smooth muscle tone. This change in vascular smooth

muscle tone could produce a shift of blood volume from the

central system to the peripheral system or from the peripheral

system to the central system. Such a shift of blood volume

could result in certain areas of the body becoming anoxic.

Such a condition might result in orthostatic intolerance, which

refers to a shift of blood Into the legs and away from the

brain, producing cerebral anoxia and syncope. This condition

has been noted In aviators and subjects returning from the

high speed centrifuge and In astronauts returning from a weight-

less state.

The fact that exposure of a blood vessel to an increased

transmural force or an Increased intraluminal force results

in a peripheral vasoconstriction appears to be well established.

The mechanism of this action is not known; however, it has

been thought to be either myogenic, neural or metabolically

controlled, with data supporting each theory.

10

Statement of the Problem

The purpose of this investigation was to study the effects

of decreasing barometric pressure upon the pressure-flow rela-

tionships In a peripheral vascular bed in an attempt at better

delineation of the autojregulatory mechanisms. A decrease In

barometric pressure does influence the transmural pressure

and could theoretically affect smooth muscle tone. An evalu-

ation of the extent of the transmural effect is essential to

understanding vascular dynamics at altitudes.

CHAPTER BIBLIOGRAPHY

1. Bayllss, W. M., "On the Local Reactions of Arterial Wall to Changes In Internal Pressure," Journal of Physiology* 28(1902}, 220-238.

2. :r? T>, A., W. E, Glover, A. D. H. Greenfield, and o. Roddie, "The Increased Tone In Forearm Resistance

Blood Vessels Exposed to Increased Transmural Pressure," Journal of Physiology, 149(1959)» 614-624.

3. Coles, D. R. and A. D. M. Greenfield, "The Reactions of Blood Vessels of the Hand During Increases in Trans-mural Pressure," J ournal of Physiology. 131(1956)* 277-289.

4. Coles, D. R., B. S. L. Kidd and G. C. Patterson, "The Reaction of Blood Vessels of Human Calf to Increases in Transmural Pressure," Journal of Physiology. 134 (1956), 665-674.

5. Folkow, B., "A Study of Factors Influencing the Tone of Denervated Blood Vessels Perfused at Various Pressures," Acta Physiologlca Scandlnavica. 27(1952), 99-112.

6. Folkow, B., "Autoregulation in Muscle and Skin," Circu-lation Research. 15(1964), 19-24.

7. Folkow, B., "Intravascular Pressure as a Factor Regulating the Tone of the Small Blood Vessels," Acta Physiologlca Scandlnavica. 17(1949)* 289~309«

8. Frohlich, E. D. and J. Y. Gillenwater, "Pressure-Flow Relationships in Perfused Dog Spleen," American Journal of Physiology. 204(1963), 645-648.

9. Gaskell, P. and A. C. Burton, "Local Postural Vasomotor Reflexes Arising from Limb Veins," Circulation Research. 1(1953), 27-39.

10. Girling, F. and C. Maheux, "Peripheral Circulation and Simulated Altitude," Journal of Aviation Medicine. 23(1952), 216-217.

11. Girling, F. and C. Maheux, "Peripheral Circulation and Simulated Altitude," Journal of Aviation Medicine. 24(1953), 446-448.

11

12

12. Greenfield, A. D. M. and G. C. Patterson, "Reactions of Blood Vessels of Human Forearm to Increases in Trans-mural Pressure," Journal of Physiology, 125(195*0» 508-524.

13. Greenfield, A. D. M. and G. C. Patterson, "The Effect of Small Degrees of Venous Distension on the Apparent Rate of Blood Inflow to the Forearm," Journal of Physiology. 125(195*0. 525-532.

14. Haddy, F. J. and J. B. Scott, "The Effect of Flow Rate, Venous Pressure, Metabolites, and Oxygen Upon Resistance to Blood Flow Through Dog Forelimb," Circulation Research* 15(1964), 49-59.

15. Hansom, K. M. and P. C, Johnson, "Vascular Resistance and Arterial Pressure in Autoperfused Dog Hind Limb," American Journal of Physiology. 203(1962), 615-620.

16. Hinshaw, L. E., "Arterial and Venous Pressure-Resistance Relationships in Perfused Leg and Intestine," American Journal of Physiology. 203(1962), 271-274.

17. Jones, R. D. and R. M. Berne, "Vasodilation in Skeletal Muscle," American Journal of Physiology. 204(1963)» 46l-46o.

18. Jones, R. D., "Intrinsic Regulation of Skeletal Muscle Blood Flow," Circulation Research. 14(1964), 126-138.

19. Kaiser, M. H„ T. M. Lin, G. Roback, L. Beusnor, H. K. Ivy, P. K. Moon and A. C. Ivy, "Report Number 6," School of Aviation Medicine Project Number 21-23-019» August, 1954.

20. Knlsely, M. H., "Wright Field Report Number Eng. 14-45-696-lC," Bulletin of Decompression Sickness. (1943)* 147.

21. Levy, M. N. and L. Share, "The Influence of Erythrocyte Concentration Upon the Pressure-Flow Relationships in the Dog Hind Limb," Circulation Research, 1(1953)» 247-254.

22. Levy, M. N,, "Influence of Anomalous Blood Viscosity on Resistance to Flow in the Dog's Hind Leg," Circulation Research. 4(1956), 533-539.

23. Lipin, J. L. and W. V. Whitehom, "Circulatory Adjustments to Reduced Barometric Pressure," Journal of Aviation Medicine. 22(1951)» 278-285.

13

2*+. Phillips, F. A., H. B. Shirley and. M. N. Levy, "The Imme-diate Influence of Increased Venous Pressure Upon Re-sistance to Flow in Dog*s Hind Leg," Circulation Research, 3(1955), 357-362.

25. Sagawa, K. and A. C. Guyton, "Pressure-Flow Relationships In Isolated Canine Cerebral Circulation," American Journal of Physiology, 200(1961), 711-71^.

26. Stalnsby, W. N., "Autoregulat1on in Skeletal Muscle," Circulation Research. 15(196^), 39-^.

27. Texter, E. C., S. Merrill, M. Schwartz, G. VanDerstappen and F. J. Haddy, "Relationship of Blood Flow to Pressure in the Intestinal Vascular Bed of the Dog," American Journal of Physiology. 202(1962), 253-256.

28. Yamada, S. and A. C. Burton, "Effect of Reduced Tissue Pressure on Blood. Flow of the Fingers t Veni-Vasomotor Reflex," Journal of Applied Physiology. 6(195^)» 501-508.

CHAPTER II

MATERIALS AND METHODS

Animal Preparation

Fifteen mongrel dogs ranging in weight from 7•2 kilograms

to 13.4 kilograms were anesthetized by an injection of sodium

pentobarbital, 33 milligrams per kilogram body weight. In-

jections were given in the cephalic or saphenous rein.

A glass cannula was inserted through the oral cavity into

the trachea. A plastic "I" tube fitted to the glass cannula

was attached to a 100 per cent oxygen source. The other arm

of the tube was fitted with a rubber balloon with a slit

in the end. The animal was allowed a minimum of thirty minutes

for respiration to equilibrate.

The skin over the left femoral triangle was cleaned and

an incision of about two inches was made directly over the

femoral artery. The femoral artery and vein were exposed by

blunt dissection and 5 milligrams per kilogram body weight

of heparin was Injected in the femoral vein to prevent clotting.

Ligatures were placed loosely around the proximal and

distal ends of the exposed artery in preparation for by-pass

cannulation. An Increased tension on these ligatures served

to close the arterial lumen. The artery was milked distally

and a transverse Incision was made into the arterial lumen

with iris sissors.„

14-

15

Polyethylene tubes (Clay-Adams Intramedic P.E. 240 or

P.E. 190) filled with heparinized saline and clamped with

hemostats were inserted Into the artery proximally and distally

and llgated. The free ends were joined and the hemostats were

removed, restoring blood flow to the leg.

The animal was placed in the decompression chamber.

Hemostats were placed on the polyethylene cannulas and the

free ends separated. The proximal end was joined to a larger

polyethylene tube (P.E, 280). The tubing made a short loop

outside the chamber, where a three-way valve was inserted.

Upon reentry the tubing progressed through a Statham PH 23-

4D-300 differential strain gauge and into a MTH tube with one

side connected to the perfusion apparatus and the other side

Joining the distal tube in the femoral artery. An externally

controlled solenoid switch capable of closing the MTW tube

was positioned between the tube and the transducer. A schematic

diagram of this system is shown in Figure 1.

The system was completely filled with heparinized saline.

Release of the hemostats allowed blood to flow from the proximal

end of the femoral artery through the by-pass system and then

back into the leg through the distal cannula.

Perfusion Device

The perfusion apparatus (Figure 2) consisted of a 110

volt A.C. motor adapted to a Graham variable transmission

capable of producing constant speeds ranging from zero to

16

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Decompression chamber

valve

distal connection

solenoid switch

transducer

cam

proximal connection

Pig. 1—Schematic diagram of perfusion system

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1100 revolutions per minute. The drive shaft from the trans-

mission, operating through a reduction gear mechanism, was

capable of rotating an excentric cam whose pitch was mathemat-

ically calculated so as to apply a linearly accelerated drive

on the plunger of a 35 cubic centimeter syringe. The pitch

of the cam was derived from the formula y = tj(x+1), where y

equals the flow rate in cubic centimeters per minute and x

equals the time of travel in seconds. The flow rates at any

second may be determined graphically (Figure 3)» ^he calibration

curves shown in Figure 3 were calculated from the equation

0.339 =:£7\» where y equals the total acceleration time divided y

by 18 and x equals the flow rate in cubic centimeters per

minute. The system provided an infinite number of calibrated,

linearly accelerated perfusion rates; however, only those elic-

iting a maximum flow of 268 cubic centimeters per minute were

used.

Decompression Chamber

The decompression chamber was a steel cylinder 58 inches

long having a diameter of 30 inches. A door having an internal

diameter of 30 inches and a round sight port was located in

one end. Rectangular sight ports were located on each side (

of the chamber.

A vacuum pump with motor served to decompress the chamber

to a maximum altitude of 100,000 feet at a rate up to 5*000

feet per minute. A control was available to maintain any

specific altitude for an indeterminate period.

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A control panel mounted on the outside contained a Wallace

and Tiernan absolute pressure gauge reading in millimeters

of mercury and altitude in feet. The panel also contained

a rate of climb indicator and on-off controls for the perfusion

apparatus.

The chamber was equipped with a 2 inch drain connection

and i inch oxygen connection. The drain connection was fitted

with a hand operated double valve and served to bleed air into

the chamber. The oxygen connection was a quick disconnect

stainless steel connector.

An electrical panel mounted on the inside wall had connec-

tions for monitoring up to 25 variables. The panel consisted

of socket connectors wired through the chamber wall and cor-

responding socket connectors on the outside wall.

Information from the Statham transducer was routed through

the panel and into a Brush amplifier with an ink-writing oscil-

lograph.

Procedure

Prior to placing the animal in the decompression chamber, A

the amplifier was balanced with the Statham filled with hepa-

rinized saline at ambient pressure and adjusted to chart zero.

The animal was placed in the chamber and all connections were

made as discussed in the section on animal preparation.

The first perfusion consisted of heparlnized saline and

was performed at a rate of 1.0, which had a maximum flow rate

21

of 131 cubic centimeters per minute. The arterial pressure

was monitored and a hemostat applied to the external loop,

which stopped normal arterial inflow and inhibited back flow

of blood from perfusor. When the back pressure stabilized,

the perfusion pump was turned on. Upon completion of perfusion

the back pressure was again allowed to stabilize and the hemostat

was released. The arterial pressure was again recorded and

the oscillograph turned off.

Befill of the perfusion syringe was accomplished by starting

the perfusion mot01; which rotated the cam to the refill position.

Steel springs attaching the syringe plunger to the gear housing

plus the arterial pressure filled the syringe with whole blood

from the animal.

The ground level run consisted of a saline perfusion to

clear the system of saline plus perfusion of whole blood at

1.0, 1*3 and 2.0.

As a check on the balancing of the amplifier the zero

was checked by closing the solenoid valve (Figure l) following

perfusion and before removing the hemostat from the external

loop. The three-way valve (Figure 1) was opened to the outside,

allowing the pressure In the system to escape^ and, if necessary,

the zero was adjusted with the pen bias control on the Brush

amplifier.

Following completion of the ground level perfusions, the

vacuum pump on the decompression chamber was started and the

chamber was decompressed at a rate of 2,000 feet per minute.

22

The pump was stopped when the altitude reached 5*000 feet,

and another series of perfusions was performed. There were

no zero checks performed except at ground level. The procedure

was repeated at 10,000 feet, 15*000 feet, 20,000 feet, 25*000

feet and following return to ground level.

A blood sample of five cubic centimeters was withdrawn

from the external valve (Figure l) at ground level, 15*000

feet» and at 25*000 feet. The volume was replaced by heparinized

saline. The blood sample was analyzed for the COg combining

power by the Van Slyke method (1).


1. Selverd, Charles E., Chemistry for Medical Technologists« St. Louis, The C. V. Mosby Company, 1958*

23

CHAPTER III

RESULTS

Pressure-flow relationships in the isolated vascular

bed of the hind limb were determined in each of fifteen ex-

perimental animals using the perfusion technique at different

altitudes.

The linearly increasing perfusion rates were 1.0 with

a peak flow of 131 cubic centimeters per minute and 1.5 with

a peak flow of 215 cubic centimeters per minute. The altitudes

were ground, 5,000, 10,000, 15*000, 20,000, 25,000 feet, and

return to ground. These data are recorded in Tables III through

IX in the Appendix.

Figure 4 is a typical record obtained during these inves-

tigations. Pressure is recorded on the ordinate, with each

small division representing five millimeters of mercury.

Time is recorded on the abscissa, with each division representing

one second. Similar records were obtained on each dog at each

altitude. The records for the perfusion rate of 1.0 were analyzed

at every other second, starting at one second and ending with

fifty-nine seconds. The records for perfusion at 1.5 were

analyzed at each second from one to thirty-six seconds. Figure

5 illustrates the mean pressure-flow relationship of heparinized

saline perfusion at ground level at a rate of 1,0. Figures

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26

6 through 28 are mean pressure-flow curves Illustrating whole

blood perfusion at flow rates of 1.0 and 1.5 at different al-

titudes. Mean pressure-flow relationships for perfusions at

a rate of 1.0 at ground level, 5»000 feet, 10,000 feet, 15»000

feet, 20,000 feet and 25,000 feet; having a maximum volume

displacement of 26.5 cubic centimeters and a delivery time

of 59 seconds, are presented in Figures 6 through 11.

Examination of Figure 6 reveals a "flat" area of the curve

or an area with an increase In volume without an increase In

pressure. This indicates a distension of the vascular bed.

In the ground level run this occurs at a pressure of 58 milli-

meters of mercury and a flow rate of 64- cubic centimeters per

minute. This distension persists until the flow rate reaches

96 cubic centimeters per minute^ at which time there is an

increase in resistance for the remainder of the curve.

Comparison of Figure 6 with Figure 7 shows that^at 5*000

feet the pressure-flow curve has shifted so that it is entirely

concave to the flow axis. At peak flow the value for the

pressure-flow curve Is 87 + 20 millimeters of mercury, as opposed

to 69 + 17 millimeters of mercury at ground level. At 5»000

feet there is an increase in tone or pressure at a flow rate

of 72 cubic centimeters per minute. This is followed by ,a

dilation until the flow reaches 92 cubic centimeters per minute.

There is a second dilation at a flow rate of 111 cubic centi-

meters per minutei, persisting until the flow rate reaches 120

2?

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cubic centimeters per minute. This second dilatation is more

pronounced than that appearing at ground level.

The pressure-flow curve at 10,000 feet (Figure 8) has

the same basic shape as the one at 5»000 feet, but with a slightly

lower resistance, occurring at a flow of 118 cubic centimeters

per minute and persisting to 131 cubic centimeters per minute.

Pressure at peak flow at 10,000 feet is 83 ± 23 millimeters

of mercury, while that at 5*000 feet is 87 + 20 millimeters

of mercury.

The pressure-flow curve at 15,000 feet (Figure 9) exhibits

an increase in resistance as indicated by Increased pressure

along its entire length. The first dilatation occurs at a

flow rate of 64 cubic centimeters per minute and lasts until

a flow rate of 93 cubic centimeters per minute is reached.

The second dilatation occurs at a flow rate of 109 cubic cen-

timeters per minute, with an increase in resistance occurring

when the flow reaches 122 cubic centimeters per minute. This

curve differs from the ground level curve only in the area

of zero flow to 63 cubic centimeters per minute. The slope

Is less at 15»000 feet; so the entire curve appears higher in

pressure.

The pressure-flow curve at 20,000 feet (Figure 10) re-

veals an increase in pressure or resistance along the entire

curve when compared to ground level. The major difference

in the two curves is the location of the first dilatation.

At 20,000 feet dilatation occurs at a flow of 72 cubic centimeters

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per minute, while at 15»000 feet this occurs at 64- cubic centi-

meters per minute.

The pressure-flow curve at 25»000 feet (Figure 11) is

not significantly different from that at 20,000 feet. The

pressure attained at peak flow is 93 ± 20 millimeters of mercury,

while that at 20,000 feet is 91 + 22 millimeters of mercury.

Four points on the pressure-flow curves at the perfusion

rate of 1.0 corresponding to 9 seconds, 29 seconds, 39 seconds

and 59 seconds were analyzed for standard deviation. The

flow rates at these time points are 20.1 cubic centimeters per

minute, 6^.5 cubic centimeters per minute, 87 cubic centimeters

per minute and 131.^ cubic centimeters per minute respectively.

These data are presented in Table I.

Mean pressure-flow relationships for perfusions at a rate

of 1.5 at ground level, 5»000 feet, 10,000 feet, 15*000 feet,

20,000 feet, and 251000 feet having a maximum volume displacement

of 26.5 cubic centimeters and a delivery time of 36 seconds,

are illustrated in Figures 12 through 17.

The pressure-flow curves at a perfusion rate of.1.5 appear

different from the 1.0 perfusion in that the curve appears to

parallel the volume displacement curve until the flow rate

of 117 cubio centimeters per minute is reached. At this point

there is no further increase in pressure until the flow rate

reaches 165 cubic centimeters per minute. The ground level

pressure-flow curve at 1.5 has a sudden increase in pressure

at a flow rate of 120 cubic centimeters per minute followed

35

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by a sudden decrease at 124 cubic centimeters per minute and

then a longer dilatation until the flow of 165 cubio centimeters

per minute is reached. This sudden increase in pressure is

an increase in vascular tone or a vasoconstriction. The sudden

decrease in resistance indicates a decrease in vasoular tone

or a vasodilation. Resistance again increases at a flow of

165 cubic centimeters per minute and persists until the flow

of 184 cubic centimeters per minute is reached, at which time

an additional dilatation occurs. When the flow reaches 196

cubic centimeters per minute, the resistance again Increases,

reaching a peak of 115 £ 23 millimeters of mercury at peak

flow.

The pressure-flow curve at a rate of 1.5 at 5*000 feet

(Figure 13) has a higher resistance^ starting at a flow of

48 cubic centimeters per minute and persisting for the duration

of the perfusion. At a flow of 120 cubic centimeters per minute

there is a sharp dilatation followed by a similar constriction

period, as in the ground level. Another sudden vasodilation

occurs at a flow rate of 177 cubic centimeters per minute.

At peak flow the pressure is 121 + 19 millimeters of mercury.

The pressure-flow curve at 10,000 feet (Figure 14) de-

viates from that at 5»000 feet at a flow of 81 cubic centi-

meters per minute. The remainder of the curve has an increased

pressure of 10 millimeters of mercury but maintains the same

shape as that at 5»000 feet. The vasodilation occuring at

a flow of 177 cubic centimeters per minute was not as pronounced

39

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as it was at 5,000 feet. The pressure at peak flow is 12? £

26 millimeters of mercury as opposed to 115 £ 23 at ground

level.

Perfusion at 15»000 feet (Figure 15) produced a pressure-

flow curve having the same general sigmoid shape but with a

higher pressure or resistance of 5 millimeters of mercury

along its entire length. In contrast to the other curves,

a decrease in vascular tone appears to occur at a flow of 90

cubic centimeters per minute. The dilatation does not persist

as it did in previous curves. At a flow of 135 cubic centi-

meters per minute a period of no pressure increase exists until

the flow reaches 184 cubic centimeters per minute. At this

flow rate a vasoconstriction was recorded followed by a period

of normal pressure increase. The pressure at peak flow is

134 £ 29 millimeters of mercury.

The pressure-flow curve at 20,000 feet (Figure 16) has

the same slope as that at 15,000 feet until a flow of 126

oubic centimeters per minute was reached. The vasodilation

at a flow of 90 cubic centimeters per minute was not present

in this curve as was demonstrated at the 15»000 foot level.

The curve sector between flows of 126 cubic centimeters per

minute and 203 cubic centimeters per minute has an increased

resistance compared to that at 15»000 feet. The remainder

of the curve has the same slope as the curve at 15*000 feet.

The pressure at peak flow is 137 £ 29 millimeters of mercury

as compared to 115 £ 23 millimeters of mercury at ground level.

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The pressure-flow curve at 25*000 feet (Figure 17) has

the same slope as that at 20,000 feet. The dilatation point

occurring at a flow of 128 cubic centimeters per minute has

a lower pressure than that at 20,000 feet. The peak flow

is IkZ ± 33 millimeters of mercury as compared to 115 £ 23

millimeters of mercury at ground level.

Pour points on the pressure-flow curves at the perfusion

rate of 1.5 corresponding to 15 seconds, 20 seconds, 30 seconds

and 36 seconds were analyzed for standard deviation. The

corresponding flow rates are 90 cubic centimeters per minute,

119 cubic centimeters per minute 179 cubic centimeters per

minute and 21 cubic centimeters per minut^ respectively.

This analysis is presented in Table I.

The records obtained upon returning to ground level were

divided into two groups. One group was recompressed. from

25*000 feet to 5*000 feet at 2,000 feet per minute and then

from 5*000 feet to ground level in ten seconds. The second

group was recompressed at 2,000 feet per minute from 25*000

feet to ground level.

The pressure-flow curve immediately after return to ground

at 1.0 (Figure 18) has a much greater resistance than the

resistance at 25*000 feet. The pressure curve parallels the

volume displacement curve until a flow rate of 33 cubic centi-

meters per minute is attained. A period of no pressure change

during a volume change results until a flow of 56 cubic centi-

meters per minute is reached. At this point there is an inorease

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in tone followed by a dilatation. A sudden dilatation occurs

at a flow of 73 cubic centimeters per minute followed by a

series of constrictions followed by dilatations. As the flow

reaches ^6 cubic centimeters per minute the resistance again

increases at a rate parallel to the volume displacement curve.

A dilatation occurs at a flow of 112 cubic centimeters per

minute and returns to the previous slope.

The pressure or resistance increased greatly along the

entire curve after 10 minutes. The general pattern of the

pressure-flow curve at return plus 10 minutes (Figure -19)

is identical with that taken Immediately upon return to ground.

At peak flow there is a difference of 35 millimeters of mercury.

After 18 minutes the pressure-flow curve (Figure 20) has

shifted to a lower pressure level. The entire curve has a

lower resistance than that recorded immediately upon return

to ground. At the flow of 45 cubic centimeters per minute

a constriction occurs followed by a steady increase in resistance

through the remainder of the curve.

Perfusion at a rate of 1.5 upon return plus 4 minutes

for animals rapidly recompressed from 5*000 feet produced a

pressure-flow curve (Figure 21) with a higher resistance than

that at 25f000 feet. Resistance was increased along the entire

curve, with the curve losing its sigmoid shape. At a flow of

72 cubic centimeters per minute a slight dilatation occurs

with another at the flow of 96 cubic centimeters per minute.

A third dilatation occurred at a flow of 122 cubic centimeters

Time of travel in seconds

48

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51

per minute and a fourth at a flow of 153 cubic centimeters

per minute. A fifth dilatation occurred at a flow of 189

cubic centimeters per minute. Each of these dilatations was

short in duration and was followed by areas of normal pressure

Increase.

In the pressure-flow curve at return plus 10 minutes

(Figure 22) at 1.5 the flow from zero to 90 cubic centimeters

per minute produced an increased resistance while the remainder

had a decreased resistance in comparison with the perfusion

at return plus 4 minutes. A constriction occurs at the flow

of ^3 cubic centimeters per minute, followed by an area of

normal pressure increase. At the flow of 99 cubic centimeters

per minute a series of dilatations occurs until the flow of

156 cubic centimeters per minute is reached. Another dilatation

occurs when the flow is 180 cubic centimeters per minute and

subsides when the flow reaches 203 cubic centimeters per minute.

Perfusion at 1.0 of the normal return animals upon reaching

ground level produced a pressure-flow curve (Figure 23) having

an Increased resistance from zero to 60 cubic centimeters per

minute and a decreased resistance for the remainder of the

perfusion as compared to perfusion at 25*000 feet. A vaso-

dilation occurs at a flow of 15 cubic centimeters per minute.

The area from a flow of k2 cubic centimeters per minute to

91 cubic centimeters per minute has only one millimeter of

mercury change in pressure. Another decrease in resistance

occurs at a flow of 112 cubic centimeters per minute and the

52

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normal pressure increase returns at a flow of 1.2k cubic centi-

meters per minute.

In the animals recorapressed at 2,000 feet per minute the

perfusion at 1.5 four minutes after return produced, a pressure-

flow curve (Figure 2*0 having the same slope as the curve at

25*000 feet. The pressure at peak flow is 152 + 32 millimeters

of mercury as compared to 1^2 + 33 at 25»000 feet. The rest

of the curves approximate each other very closely. A dilatation

occurs at a flow of 113 cubic centimeters per minute, with

the dilatation period lasting until a flow of 172 millimeters

of mercury is reached. At this flow the increase in pressure

again occurs.

The pressure-flow curve at 10 minutes (Figure 25) has

a decreased resistance below a flow of 90 cubic centimeters

per minute and a slight increase in resistance above this point.

The curves parallel each other from this pointy with the return

plus 10 minutes having a lower resistance.

After 20 minutes the pressure-flow curve (Figure 26)

returned to that value obtained upon immediate return to ground

level. The curve reveals much more in the way of vascular

muscle tone changes than the other curves. A dilatation occurs

at a flow of 105 cubic centimeters per minute and another at

126 cubic centimeters per minute. A vasoconstriction occurs

at a flow of 15^ cubic centimeters per minute. Another dila-

tation occurs at a flow of 123 cubic centimeters per minute

and lasts until a flow of 203 cubic centimeters per minute

is reached.

55

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58

Peripheral resistances were calculated for each perfusion

by dividing perfusion pressure in millimeters of mercury by

blood flow in cubic centimeters per minute. Regression lines

were calculated for each perfusion and plotted with peripheral

resistance on the ordinate and time on the abscissa. The

TABLE II

STANDARD DEVIATION OP MEAN REGRESSION SLOPES OF PERIPHERAL RESISTANCE VERSUS TIKE

Altitude 1.0 1.5

Ground - . 0 4 6 0 + .0136 -.0353 1 .0116

5,000 feet -.0460 ± .0136 - . 0 3 6 0 i .0140

10,000 feet -.0477 ± .0149 -.0360 ± .0146

15,000 feet -.0478 ± .0143 -.0372 ± .0157

20,000 feet -.0464 + .0142 -.0385 ± .0152

25,000 feet -.0483 ± .0143 -.0384 ± .0104

Return -.0583 ± .0141 -.0421 ± .0171

mean slopes of these lines are presented in Table II. The

slopes of the regression lines are presented in Table V in

the Appendix.

CHAPTER IV

CONCLUSION

Discussion of Results

The use of linearly accelerated flow rates In perfusion

of the vascular bed allowed the determination of an Infinite

number of points along the pressure-flow curve. This method

produces a true pressure-flow pattern since it begins with

zero flow and accelerates to a maximum flow. In a system

with no back pressure this would eliminate the need for extra-

polation back to zero. If a back pressure does exist, the

pressure will increase from that value with the lower section

of the pressure-flow curve missing. In obtaining the maximum

flow in one perfusion any physiological changes in the vascular

bed resulting from repeated perfusions at many flow rates would

be eliminated.

The first perfusion at ground level, which consisted of

heparlnlzed saline, was performed initially to clear the per-

fusion system of heparlnlzed saline and to allow refilling

with whole blood without changing the animal's total blood

volume. It was not the purpose of this investigation to study

the effects of viscosity on autoregulation; however, the data

were recorded and confirmed the work of Pappenhelmer and Maes

(8) and Haymes and Burton (5)• The comparisons of Figures

59

60

5 and 6 indicate that the higher viscosity of whole blood

does influence autoregulation at increased flow rates.

Figure 27 and Figure 28 graphically illustrate a continued

increase in vascular resistance to perfusion as the barometric

pressure is decreased from 7^0 to 252 millimeters of mercury.

This Increase in resistance confirms the reports of other

investigators using indirect techniques such as skin temperature

(2, 3)» plethysmography (1,4) and visual observation (6).

Marotta and Boon (7) used direct measurements on dogs to in-

vestigate the vascular effects of changes in altitude. The

animals were allowed to breathe 100 per cent oxygen or normal

air. They noted an increase in resistance in all animals

breathing all gas mixture^ except those which were allowed

to equilibrate on 100 per cent oxygen for two hours prior to

decompression. These results are similar to those obtained

in this investigation in that only 30 minutes equilibration

time was utilized.

There exists in the data a relatively large deviation

from the mean. This is the result of using mongrel dogs of

different weights and general body types. More consistent

results could probably be obtained with the use of selected

animals having closely similar weights and shapes or, preferably,

with the use of an inbred strain.

Figure 27 is a composite graph of the mean pressure-flow

curves at 1.0 perfusion rate. These curves possess a uniform

configuration, with each having a higher resistance than the

<M *H £Q O •id

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preceding. Figure 29 is a composite graph of the mean pressure-

flow curves; demonstrating the difference in the pressure pro-

duced at each altitude as compared to ground level. The in-

creasing slope of the curves A, B, C, D and E up to a flow

of approximately 100 cubic centimeters per minute is interpreted

to be due to the inherent vessel elasticity. At that flow

it would appear that vascular smooth muscle no longer exerts

as much resistance, since the curves are essentially parallel

to the flow axis. At 25*000 feet (E, Figure 29) the pattern

changes with an early relaxation but always at a higher resis-

tance .

The curve obtained upon recompression (F, Figure 29) has

an even greater change from ground than that at 25»000 feet.

This could have been the result of changing the pressure of

the pOg from 252 millimeters of mercury to 7 -0 millimeters

of mercury in 12§ minutes, or the effects of edema produced

by imbalance in capillary dynamics produced by an increased

negative tissue pressure at altitudes.

Analysis of the pressure-flow curves at 1.5 (Figure 28)

also indicates an increase in resistance with a decrease in

barometric pressure. The middle sectors of the curves, which

appear more parallel to the flow axis and demonstrate a low

increase in pressure with an increase in volume flow, indicate

that the vascular bed was either undergoing dilatation, opening

additional capillaries, or possibly opening arterlo-venous

shunts.

63

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Figure 30 is a composite graph of the mean pressure-flow

curves demonstrating the difference in the pressure produced

at each altitude as compared to ground level. There is a

similarity in the curves up to 15,000 feet. The middle sectors

of the curves A, B and G illustrate a deorease in resistance,

possibly due to vessel elasticity.

At 25»000 feet (E, Figure 30) the curve again has the

same general shape as the preceding curves. The point at which

the vascular beds and/or arterio-venous shunts responded to

flow and pressure, increased with an increase in altitude.

This could be explained by assuming that an increase in vas-

cular tone or an increase in tissue pressure occurred as baro-

metric pressure decreased. This assumption appears valid since

all data received during these investigations point to an

increase in peripheral resistance as altitude increases.

The curve obtained upon immediate return to ground (F,

Figure 30) follows a resistance pattern comparable to that

at 25»000 feet. This again may be due to the recompression

and the resultant changing of the pressure of the breathing

mixture from a p02 of 252 millimeters of mercury to 7^0 milli-

meters of mercury. An increase in tissue pressure with a

decrease in barometric pressure could result in edema.

Upon return to ground level the resistance would remain

high until the fluid could be reabsorbed. After 10 minutes

(G, Figure 30) the resistance had decreased except at higher

66

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flow rates, indicating a fairly rapid removal of accumulated

extravasculaif fluid.

Figure 31 is a comparison between animals that have been

recompressed at 2,000 feet per minute and those that have been

recompressed rapidly from 5»000 feet. In the dogs recompressed

at 2,000 feet per minute the resistance is higher than at

ground level. This could be the result of the accumulation

of fluids previously explained. At return plus 10 minutes

rapid recompression produces the highest resistance, possibly

caused by constriction of the vascular bed and the edema pro-

duced. This resistance decreased after 18 minutes but still

remained higher than that recorded from animals recompressed

at 2,000 feet per minute. This has a significance at the

•995 level.

Perfusion at 1.5 following recompression (Figure 32)

produced the same results as those produced at 1.0 with some

recovery after a period of time allowing the edema to subside.

The rapid recompression (Figure 33) produced higher resistances,

which again were perhaps due to edema. A comparison of re-

gression lines of peripheral resistance versus time at 1.5

for return to ground and ground level shows significance at

the .95 level. There was significance in the comparison of

the return to ground pressure-flow curve with all altitudes

at 1.5 but not at 1.0. This phenomenon may be an indication

of vascular bed damage due to both rapid recompression and

high flow rates.

68

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71

Metabolites produced in the lower limb could have had

an effect on vascular responses during this investigation.

Deal and Green (8) have shown that pH has a definite effect.

An increase towards the acid side or lower pH results in an

increased blood flow, while an increase in the alkalinity pro-

duces a dilatation in the muscle vascular bed and a constriction

in the skin vascular bed. Periodic analysis of the blood

at different altitudes for the CO2 combining power indicated

no changes that were not within experimental error.

Summary

The conclusions of this investigation may be summarized

as follows t

1. The vascular bed of the hind limb of dogs exhibited

an increase in resistance to perfusion of whole blood

at all altitudes studied. This increase in resistance

is believed to be due to an increase in vasomotor

tone produced by the increase in transmural pressure.

2. The demonstration of an increase in resistance with

a decrease in barometric pressure by the direct method

confirms the work obtained by indirect methods,

3. The resistance produced did not immediately decrease

upon recompression, due to the possible accumulation

of extravascular fluid at decreased barometric pressures•

k. The data obtained could be better expressed in terms

of volume of flow per unit of mass. This would require

the measurement of the weight of the tissue perfused.

72

5. The mean deviations were relatively large and not

readily adaptable to statistical analysis, due to

the heterogenity of the mongrel dogs used.

6. Confirmation of the hypothesis concerning the accumu-

lation of extravascular fluid as a result of decom-

pression will necessitate further investigations.

Some parameters which should be investigated are

tissue pressure, venous pressure and thoracic lymph

flow.

7. Future investigations would also benefit from the

use of inbred strains of experimental animals.


1. Blair, D. A., W. E. Glover, A. D. H. Greenfield and I. C. Roddie, "The Increased Tone in Forearm Resistance Blood Vessels Exposed to Increased Transmural Pressure," Journal of Physiology, 149(1959, 614-624.

2. Coles, D. R. and A. D. M. Greenfield, "The Reactions of Blood Vessels of the Hand During Increases in Transmural Pressure," J ournal of Physiology. 131(1956), 277-289.

3. Coles, D. R., B. S. L. Kldd and G. C. Patterson, "The . Reaction of Blood Vessels of Human Calf to Increases in Transmural Pressure," J ournal of Physiology. 134 (1956), 665-674.

4. Greenfield, A. D. M. and G, C. Patterson, "Reactions of Blood Vessles of Human Forearm to Increases in Trans-mural Pressure," Journal of Physiology, 125(195*0» 508-524.

5. Haynes, R. H. and A. C. Burton, "Role of Non-Newtonian Behavior of Blood in Hemodynamics," American J ournal of Physiology. 197(1959), 943-950.

6. Knlsely, M. H., "Wright Field Report Number Eng. 14-45-696-lC," Bulletin of Decompression Sickness. (1943)»• 147.

7. Marotta, S, F. and D. J. Boon, "Femoral Arterial Circulation in Nonhypoxic Dogs at Reduced Barometric Pressures," American J ournal of Physiology. 210(1966), 953-956.

8. Pappenheimer, J. R. and J. P. Maes, "A Quantitative Measure of Vasomotor Tone in the Hind Limb Muscles of the Dog," American J ournal of Physiology. 87(1942), 187-199.

73

APPENDIX

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BIBLIOGRAPHY

Books

Seiverd, Charles E., Chemistry for Medical Technologists. St. Louis, The C. V. Mosby Company, 1958.

Articles

Bayliss, W. M., "On the Local Reactions of Arterial Wall to Changes in Internal Pressure," Journal of Physiology. 28(1902), 220-238.

Blair, D. A., W. E. Glover, A. D. H. Greenfield and I. C. Roddie, "The Increased Tone in Forearm Resistance Blood Vessels Exposed to Increased Transmural Pressure," J ournal of Physiology. 149(1959), 614-624.

Coles, D. R. and A. D. M. Greenfield, "The Reactions of Blood Vessels of the Hand During Increases in Transmural Pressure," J ournal of Physiology. 131(1956), 277-289.

Coles, D. R., B. S. L. Kldd and G. C. Patterson, "The Reaction of Blood Vessels of Human Calf to Increases in Transmural Pressure," J ournal of Physiology. 134(1956), 665-674.

Folkow, B., "A Study of Factors Influencing the Tone of De-nervated Blood Vessels Perfused at Various Pressures," Acta Physiologlca Scandlnavlca. 27(1952), 99-112.

Folkow, B., "Autoregulatlon in Muscle and Skin," Circulation Research. 15(1964), 19-24.

Folkow, B., "Intravascular Pressure as a Factor Regulating the Tone of the Small Blood Vessels," Acta Physlologlca Scandlnavica. 17(1949), 289-309.

Frohlich, E. D, and J. Y. Glllenwater, "Pressure-Flow Rela-tionships in Perfused Dog Spleen," American J ournal of Physiology. 204(1963), 645-648.

Gaskell, P. and A. C. Burton, "Local Postural Vasomotor Re-flexes Arising from Limb Veins," Circulation Research. 1(1953), 27-39.

82

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Girling, P. and C. Maheux, "Peripheral Circulation and Simu-lated Altitude," Journal of Aviation Medicine. 23(1952), 216-217.

Girling, P, and C. Maheux, "Peripheral Circulation and Simu-lated Altitude," J ournal of Aviation Medicine. 24(1953)» 446-448.

Greenfield, A. D. M. and G. C. Patterson, "Reactions of Blood Vessels of Human Forearm to Increases in Transmural Pres-sure," Journal of Physiology. 125(1954), 508-524.

Greenfield, A. D. M. and G. C. Patterson, "The Effect of Small Degrees of Venous Distension on the Apparent Hate of Blood Inflow to the Forearm," Journal of Physiology. 125(195^), 525-532.

Haddy, F. J. and J. B. Scott, "The Effect of Flow Rate, Venous Pressure, Metabolites, and Oxygen Upon Resistance to Blood Flow Through Dog Forelimb," Circulation Research, 15(1964), 49-59.

Hansom, K. M. and P. C, Johnson, "Vascular Resistance and Arterial Pressure in Autoperfused Dog Hind Limb," American Journal of Physiology. 203(1962), 615-620.

Haynes, R. H. and A. C. Burton, "Role of Non-Newtonian Behavior of Blood in Hemodynamics," American J ournal of Physiology, 197(1959), 943-950.

Hinshaw, L. E., "Arterial and Venous Pressure-Resistance Rela-tionships in Perfused Leg and Intestine," American J ournal of Physiology. 203(1962), 271-274.

Jones, R. D. and R. M. Berne, "Vasodilation in Skeletal Muscle," American J ournal of Physiology. 204(1963), 461-466.

Jones, R. D., "Intrinsic Regulation of Skeletal Muscle Blood Flow," Circulation Research. 14(1964), 126-138.

Kaiser, M. H., T. M. Lin, G. Roback, L. Beusnor, H. K. Ivy, P. K. Moon and A. C. Ivy, "Report Number 6," School of Aviation Medicine Project Number 21-23-019, August, 1954.

Knisely, M. H., "Wright Field Report Number Eng. 14-45-696-lc," Bulletin of Decompression Sickness. (1943), 147.

Levy, M. N. and L. Share, "The Influence of Erythrocyte Concen-tration Upon the Pressure-Flow Relationships in the Dog Hind Limb," Circulation Research. 1(1953), 247-254.

84-

Levy, M. N., "Influence of Anomalous Blood Viscosity on Resis-tance to Flow in the Dog*s Hind Leg," Circulation Research.

' M1956), 533-539.

Lipin, J. L. and W. V. Whitehorn, "Circulatory Adjustments to Reduced Barometric Pressure," Journal of Aviation Medicine. 22(1951), 278-285.

Marotta, S. F. and D. J. Boon, "Femoral Arterial Circulation in Nonhypoxic Dogs at Reduced Barometric Pressures," American Journal of Physiology. 210(1966), 953-956.

Pappenhelmer, J. R. and J. P. Maes, "A Quantitative Measure of Vasomotor Tone in the Hind Limb Muscles of the Dog," American Journal of Physiology. 87(19^2), 187-199.

Phillips, F. A., H. B. Shirley and M. N. Levy, "The Immediate Influence of Increased Venous Pressure Upon Resistance to Flow in Dog's Hind Leg," Circulation Research. 3(1955)» 357-362.

Sagawa, K. and A. C. Guyton, "Pressure-Flow Relationships in Isolated Canine Cerebral Circulation," American Journal of Physiology. 200(1961), 711-71^.

Stainsby, W. N., "Autoregulation in Skeletal Muscle," Circulation Research, 15(196*0 , 39-^.

Texter, E. C., S. Merrill, M. Schwartz, G. VanDerstappen and F. J. Haddy, "Relationship of Blood Flow to Pressure in the Intestinal Vascular Bed of the Dog," American J ournal of Physiology, 202(1962), 253-256.

Yamada, S. and A. C. Burton, "Effect of Reduced Tissue Pressure on Blood Flow of the Fingers: Veni-Vasomotor Reflex," Journal of Applied Physiology. 6(195^)» 501-508.

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