The influence of footward acceleration upon the fluid systems of the intracranial cavity

Citation preview

THE INFLUENCE OF FOOTW ARD ACCELERATION UPON THE FLUID SYSTEMS OF THE INTRACRANIAL CAVITY

A Thesis Presented to The Faculty of the Graduate School The University of Southern California

In P a rtia l Fulfillment of the Requirements for the Degree Master of Science in Physiology

by Edward Louis Beckman December 1950

UMI Number: EP63579

All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion.

UMI' DissBrtstiem. Publishing

UMI EP63579 Published by ProQuest LLC (2014). Copyright in the Dissertation held by the Author. Microform Edition © ProQuest LLC. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code

ProGuest ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48 10 6 - 1346

PJ^

SI

of Phase I I ,

or in goats Nos.

the peak surge is not as marked in

these tracings. The cardiac output was determined by indirect methods from the pulse pressure at the heart and the number of heart beats per minute.

The heart rate was determined by the

' a r t e r i a l pulse frequency.

There was a general bradycardia

!

34 of varying severity demonstrated by a ll

animals above -2 g.

The stroke volume was determined by the method of Hamilton (23) from the a r t e r i a l pressure at heart level.

On the

basis of the x-ray studies, the pressure at gauge level was ifound to be equal to the pressure at heart level minus the hydrostatic column factor, which was found to be equal to the venous pressure.

Hence, the a r t e r i a l pressure at heart (

1

level could be determined by the arterio-venous pressures at base of brain level. - Prom the l e f t heart pressure de­ termined in this manner, or the aortic pressures measured directly in goats Nos. lif, 15 and 20,

the stroke volume was ‘

determined for pre-run and f if te e n second g stress periods. ■These values times the respective control and f if te e n second i

g heart rates gave an indication of the re la tiv e change of |cardiac output before and during exposure to acceleration. The mean cardiac output for a ll experiments in Phase II de­ creased to 9^ Per cent of the pre-run mean of J4.866 cc. per minute a fte r exposure to a mean stress of -3*5 g for f i f ­ teen seconds (Table V).

The average pre-run cardiac output !

: in Phase I I I was [{,711 cc. per minute with a decrease to ,73 per cent during exposure to a mean stress of 4 .9 g (Table VI). Next in evaluating the effects of negative g upon jthe in tra c ra n ia l vascular system, the determination of the 1

3$ A-V pressure across the internal and external c irc u its of the head was necessary.

These pressures at carotid and jug­

ular gauge level were equal to those pressures measured at the heart plus the hydrostatic column times the g factor. The change in mean a r t e r i a l pressure in mm. Hg. (Figure 1,B) minus the venous pressure (Figure 1, C) is summarized in Tables I I I and IV.

The change in the A-V pressure d if ­

ference produced by the negative g stress was found to vary considerably with individual animals.

The animals which

;withstood the experimental stress well, likewise maintained th e ir A-V pressure at adequate levels during the period of acceleration.

In general,

the animals in Phase I I I main­

tained t h e ir A-V difference more adequately during s tre s s than did the animals used in Phase I I .

The animals used

, in Phase I I were found to withstand the stress of the experiment poorly.

This suggests that the obstruction of

the r ig h t common carotid artery in making end pressure measurements exerted a deleterious effect upon the cephai ic circulatio n.

The A-V pressure difference was found to be

decreased from the control levels in some experiments but ’the mean change in A-V pressure during exposure to a mean footward acceleration of if. 5 g was an increase to 121 per one o f the factors had to change.

The pres-

i

sure (E) was measured and found to have changed in s ig n if i­ c a n tly .

Therefore, there must have been a r e la tiv e decrease

in the resistance of the external cephalic c i r c u it as com­ pared with the resistance of the in tracran ial c i r c u i t ,

thus

shunting a proportionately greater volume of blood through the external c ir c u it with distention and rupture of the vascular channels. DISCUSSION The above described investigations were designed to evaluate the changes in the in tracran ial pressure r e la tio n ­ ships produced by exposure of goats to the stresses of foo t-t ward acceleration and to re la te them to the reported occur­ rence of cerebral dysfunction.

The subjective observation

of cerebral dysfunction occurring during exposure to negative g was f i r s t reported by Armstrong and Heim (2) from centrifuge experiments upon themselves.

Simmons and

Henry (19) demonstrated the occurrence of one to two cycles i

per second waves in the electroencephalogram of rabbits

38 a f te r exposure to -7 g for sixty seconds*

Several others,

including th is author, have experienced and reported the occurrence of cerebral confusion following exposure to nega­ tive g ( 2 6 ). :

Despite the agreement upon subjective findings, the

explanations as to the physiological mechanism involved present a wide d iversity of opinion.

Cerebral dysfunction

i ! from negative g has been attributed to the following factors: i

(1 ) rupture of the in tra c ra n ia l a r t e r i a l tree and, in pari tic u la r ,

the posterior communicating branch of the Circle

of Willis

(2, l6 );

(2) rupture of the dural sinuses or con- ,

necting vessels with production of subdural hematoma (2l|, 27);

(3) cerebral anoxia based upon a decreased A-V pres­

sure difference (1 9 ) and blood flow (l£) or upon decreased ,blood oxygen content resu lta n t from decreased resp iratio n i

'

( 2 6 ); and (I|.) upon the production of carotid sinus syncope ■(19) of the cerebral type as described by Soma Weiss ( 2 8 ). Therefore,

an evaluation of these concepts in the lig h t

1

of the, present investigation seems warranted. Prior to making inferences to the data obtained, 3t is necessary to review the changes introduced into the animal system as a part of the experimental procedure.

In

!

' a l l experiments,

the exposures to g stre ss were repeated

at approximately five to ten minute in terv als u n til a series o f-twenty-or~more~runs-had been -accomplished- or u n til" th e -----

39 animal succumbed to the procedure.

Thus, in a ll experiments

a progressive deterioration of the vasomotor system occurred which in some cases in Phase I was irre v e rs ib le .

All ex­

periments in Phases II and I I I were terminal and in a l l these cases,

a shock like state developed p rio r to termina­

tion of the experiment.

Examination of the mucous membranes f

of the head .between experimental exposures and examination

;

of the brain and other tissu es of the head at postmortem revealed that some degree of vasodilatation occurred early

1In the experimental sequence and progressed.

This finding

i

was likewise borne out by the pulse pressure curves (Figure ' ■5 ) which indicated that the cephalic portion of the vascular, system was in a s ta te of vasodilatation permitting rapid run off through the a r t e r i o l a r bed.

These observations would

further indicate th a t the animal did not reestab lish com­ plete cardiovascular compensation a fte r the i n i t i a l expo­ t

sures to negative g. An additional deviation from normal was produced by a reduction in the circulating blood volume, concomitant

,with the production of edema of the tissues d is ta l to the heart, as described by Stauffer and Hyman (20). Despite r the loss of blood volume, the a r t e r i a l pressure as measured in Phases II and I I I meaintained a satisfacto ry level u n til jthe terminal exposures in each series.

I t is therefore

, I

14-0 I

believed that although these abnormalities introduced a somewhat decreased level of pressure, the pressure r e ­ lationships between the various systems of the in tracran ial cavity were nonetheless maintained at a physiologically satisfacto ry level. In the f i r s t phase of the experiment in which ten .animals were exposed to negative g stress of varying levels without any experimental a lte ra tio n of the vascular system, no consistent demonstrable irrev ersib le changes within the in tracran ial vascular system were evidenced.

Cerebral vaso­

d ila ta tio n was observed in those animals sacrificed immedia­ tely a fte r the experimental procedures.

Microscopic studies

revealed no ring hemorrhages or evidence of cerebral edema to suggest that severe cerebral anoxia or disproportionate intravascular pressure had existed.

I t was not possible

from the findings of these experiments to determine whether the cerebral vasodilatation occurred during the exposure to negative g or whether i t was a resultant vasomotor pheno­ menon occurring after the exposure to the t e s t situ a tio n .

t

. No change in the size of the cerebral vessels of one monkey was observed by d irect photography through a lu c ite calvariun during exposure to negative g (27)#

Thus, i t maybe in fer-

i red that eith er no change or vasodilatation occurred during 1

: the exposure to high negative g accelerations both within i

1

hi the In tracran ial cavity as well as In the extraeranial tissues* Prom the study of the pressure relationships between the venous and a r t e r i a l blood systems and the cerebrospinal flu id within the in tracran ial cavity,

the absence of de­

monstrable in tra c ra n ia l pathology may be predicted*

Since

the increase in pressure within the venous channels was

j

paralleled by a simultaneous and approximately equal increase in the cerebrospinal flu id pressure, the venous flu id sys­ tem was thereby adequately protected*

Furthermore, a com­

parison of the a r t e r i a l and venous pressures discloses that the maximum recorded pressure difference was 25>0 mm. of mercury^ which pressure developed during a negative 2 g exposure,

As the magnitude of the force of footward acceler­

ation was increased, the A-V pressure difference decreased somewhat so that the pressure applied to the a r te r i o la r and capillary walls within the cranium which would produce rupture was decreased with increased magnitudes of accelera­ tion.

Even the maximum A-V pressure difference recorded was i not of a magnitude su fficien t to produce rupture of normal a r t e r io la r vessels on the basis th a t Hamilton (23) r e ­ i1

corded sy stolic pressures of greater than 300 mm. of merI

‘ cury on humans during routine therapeutic administration of ■ i

1subcutaneous adrenalin.

1*2 The isolated finding of a subdural hemorrhage in one ‘animal of the eighteen examined after exposure to footward acceleration is not explained on the basis of the pressure measurements.

This type of injury is common in in ju rie s in

which a re la tiv e motion of the brain mass within the bony casement is introduced.

This method of subdural hemorrhage

production has been demonstrated by Pudenz and Sheldon (29) ; by high speed photography of the brain of a monkey viewed I through a lu c ite calvarium during the application of concussive blows.

The observations made of the goat thrash­

ing about during the exposure to acceleration in this par­ tic u la r experiment would therefore suggest this mechanism as an etiolo gical factor in th is case.

Prom the above

.findings, i t would not be anticipated that a disruption of the in tracran ial vascular system would be a common mechanism for the production of the cerebral dysfunction observed f o l­ lowing exposure to negative acceleration. The cerebrospinal f lu id pressures were measured in these experiments as a means of evaluating the intracran ial pressure relationships and as m indication of the r e la tiv e change in the cerebrovascular resistan ce.

Kety and others

, ( 1 2 ) studied the relationship of increased in tra c ra n ia l pressure to the cerebral blood flow on patients having various types of space occupying in tracran ial lesions.

!

These investigators found that the in tracran ial pressure as measured by the cerebrospinal flu id pressure was signi­ fic a n tly correlated with the cerebrovascular resistan ce. They also found that an increase in cerebrospinal flu id pressure and, therefore, in cerebrovascular resistance of up to

50 mm. of cerebrospinal flu id (33 ®m. Hg|) was com­

pensated f o r by the human body without any sig n ifican t de;crease in cerebral blood flow.

■

1

They sta te that compensation

is re fle x ly accomplished by an increase in systemic blood 'pressure.

Interestingly enough, from th e ir figures,

i t ap­

pears that the mean blood pressure compensatory r i s e was negligib le since the mean blood pressure of th e ir cases which maintained a normal cerebral blood flow was 95 mm.o f mercury. *

1

In the measurements of cerebrospinal flu id pressure on goats subjected to footward acceleration, the cerebro­ spinal flu id pressure was found to be increased during ex­

posure to the s tre s s and to vary concomitantly with and to be equal to the jugular venous pressure measured a t the same lev e l.

The cerebrospinal flu id pressure and jugular

ivenous pressure are acknowledged to be approximately equal in the normal recumbent position.

The cerebrospinal fluid

;pressure as determined by Kety and others (12) is an ex­ pression of the amount of deviation from the normal

1

cerebrospinal fluid or jugular venous pressure produced in the cerebrospinal flu id by an increase in volume of the cranial contents.

The cerebrovascular resistance was simi­

la rly an expression of the pressure d if f e r e n tia l between the in tra c ra n ia l cerebrospinal f lu id and venous systems. Therefore, in evaluating the cerebral vascular r e ­ sistance during exposure to the s tr e s s of negative g,

the

■

pressure relationship s between the cerebrospinal flu id and venous systems were compared.

Since the cerebrospinal flu id

pressure as measured from the ciste rn a magna and the venous pressure as measured at the same level in the jugular vein were found to remain approximately equal over a wide range of pressure changes, little

i t maybe inferred that there was

change in the cerebrovascular resistance between the

:normal control and the accelerative stress condition.

Thus,

i t would seem th a t the arterio-venous pressure d iff e re n tia l between the common carotid artery and the jugular vein and the volume of blood pumped to the head are the lim iting factors in maintaining the cerebral blood flow at an ade­ quate level in goats subjected to footward acceleration iOf the magnitude used in these experiments. Prom the theo retical consideration of the hemodynamic system, i t was assumed and demonstrated th a t the a r te r ia l and venous pressures in the head of the

animal were ap-

;

k5 proximately equal to the output pressure at the heart plus the pressure of the hydrostatic column between the heart and the point of measurement, times the g fa c to r.

Similar

inferences as to hydrostatic column effects maybe made regarding the proximal portion of the animal’s hemodynamic system.

I f the vessels of the abdominal cavity and other

parts of the proximal portion of the body were well enough supported so as to function as r ig id tubes during accelera­ tion,

then the pressures in the a r t e r i a l and venous systems

proximal to the heart could be calculated by measuring the height of the column of f lu id from the heart to the point of measurement and this value corrected by multiplying by the magnitude of the g force applied.

Since the main

vessels to the proximal p art of the body traverse the ab­ dominal cavity, which is poorly supported and which acts as a flu id under g, pressures le ss than ambient cannot be sup­ ported.

Therefore, i t is to be expected th a t during expo­

sure to negative acceleration the footward or proximal portion of the body w ill be poorly supplied with blood, at a l l .

if

This was demonstrated by Romberg (22), who studied

blood d istrib u tio n under g by quick freezing the animals in CO2 while the force was being applied.

He found that

the vessels of the proximal part of the body were collapsed and emptied of blood.

I t may therefore be inferred th a t

46 with the onset of exposure to footward acceleration,

.

a por­

tion of the blood volume normally circu latin g through the proximal portion of the body would be shunted to the d is ta l portion of the body.

The volume of the shunted blood would .

be proportional to the magnitude of the g force applied. In addition, th is shunting of the blood would not necessarily be apparent from studies of the cardiac output.

In e ffe c t, ,

the g force applied takes over part of the work of the heart and forces blood d ire c tly from the a r t e r i a l and venous channels of the proximal portion of the body to the d is ta l portion of the body without the necessity of having that .blood volume pass through the h eart.

This was evidenced by

the pressure measurements of the carotid artery made with the cannula directed toward the heart in which case a high surge pressure was observed at the onset of the application ; of the g force.

Similarly, measurements of pressure a t the '

arch of the aorta (Figure 3) and in the in fe rio r vena cava at heart level (Figure I4.) show an increase in mean pressure at the onset of the acceleration lastin g three to five seconds, a f te r which the pressures returned to the pre-run \

le v e l.

Therefore, although the cardiac output as determined^

by the method of Hamilton was found to decrease during the application of the g force, the volume of blood supplied to the d is ta l portion of the animal was considerably greater

than would be assumed from the cardiac output determination i

alone and was possibly even greater than the volume of blood supplied to the cephalic p art of the animal under normal conditions.

This was further indicated by the tremendous

vasodilatation and extensive hemorrhages produced in the :d is ta l portion of the experimental animal during exposure to the g s tre s s .

The volume of the vascular system of the

j

d is ta l portion of the animal, therefore, must be tremendous­ ly increased during exposures to negative g.

The e ffe c t

of the introduction of a volume of blood equal to the stroke volume of the heart into th at increased capacity would be expected to produce a lower pulse pressure than would have been produced -under normal conditions.

Therefore, the es­

timation of stroke volume by the method of Hamilton and from th a t, the determination of the cardiac output would not be accurate under these conditions e ith e r .

Thus, i t

seems probable from these findings th a t the d istrib u tio n of blood between the cephalic and caudal portions of the body

1

of the animal which occurs under normal positioning in the e a rth ’s g rav itatio n al fie ld is considerably altered when the animal i s subjected to high magnitudes of accelerative ‘force.

Under normal conditions,

an adequate cardiac output

may be taken as an indication of an adequate volume of blood| (being supplied to the head and other v i t a l organs.

However,

^8 'when the animal system is

acted upon by high magnitudes of

accelerative force acting in the head to t a i l axis* the heart becomes re la tiv e ly decompensated and is unable to maintain enough pressure in the system to supply blood to the proximal (caudal) portion of the body* measurement then, i f

The cardiac

accurate, would not be an indication

of the amount of blood supplied to the cephalic and caudal portions of the body since the d is trib u tio n ra tio is changed During the stress of high footward acceleration, the g reater part or even the en tire cardiac output would be supplied to the head.

Prom the amount of vasodilatation and hemorrhage

observed at autopsy, i t i s apparent that a great portion of the cardiac output during application of negative g stre ss must be d istrib u te d to the cephalic portion of the animal i f the A-V pressure is to be maintained. Additional evidence of vasod ilatatio n in the vascular system of the cephalic portion of the animal exposed to footward acceleration is obtained by inspection of the ven- j i

ous pressure tracings (Figure ij.), where venous pulsations

f

i during application of g stre ss are seen which are synchroi

!

nous with the a rte ria l pulsations and are evidence of vaso- : d ila ta tio n , ficance.

i.

e .,

the cap illary pulse of c lin ic a l sig n i­

k9 From the above evidence i t

can only be stated that a

vasodilatation of the vessels of the d is ta l portion o f the experimental animal occurred*

The pathological finding of

cerebral vasodilatation cannot be d ire c tly related to the condition of the cerebral vessels during the d ir s t exposure of the animal to the g stress nor to the response of the cerebral vasculature immediately post-run.

I t has been sug-|

gested th a t the carotid sinus re fle x would cause cerebraL vasconstriction as a r e s u lt of the increased carotid presi i sure in the inverted position . I t seems improbable th at th is re fle x would supervene over the normal in tr in s ic cere- , b ra l vasomotor control to the detriment of the brain. Furthermore, since the neurocyto-architectural studies done at the Montreal Neurological I n s titu te

( l 6 ) showed no

.demonstrable pathological changes in cats subjected to th i r t y second exposures to If.5 negative g twenty times a I day fo r four days (ten minutes per day for four days), vaso­ constriction , i f i t occurred, was not su ffic ie n t to produce anoxic neuronal damage.

Similar studies in Phase I of th is

■experiment likewise demonstrated normal neuronal stru ctu re. Thus, i t seems most probable th a t so long as the A-V pressure across the cerebral resistance is adequate,

the in trin s ic

and ex trin sic vasomotor mechanisms of the brain w ill main­ ta in adequate cerebral blood flow.

Since the A-V

50

f

differences as measured showed only a moderate decrease with increasing magnitudes of footward acceleration so long as extreme bradycardia or asystole did not intervene, i t may be inferred that the cerebral blood flow was most probably maintained under the conditions of negative g stre ss as used in th is experiment. Several specific reflexes have also been suggested as the mechanism producing cerebral dysfunction:

(1 )

!

the

mechanism of carotid sinus syncope of the cerebral type ( 2 7 ), and ( 2 ) localized cerebral vasoconstriction on the b a s i s vof labyrinthine stimulation by increased labyrinthine pressure (30).

The measurements made in these experiments offer no

evidence which bears upon the influence of these reflexes iupon the cerebrovascular system during negative g. A more exact evaluation of cerebral blood flow and cerebral dysfunction during exposure to the s tre ss of foot­ ward acceleration must await the development of more quan­ t i t a t i v e methods for the evaluation of cerebral physiology and techniques which may b e applied to the problems of ;cerebral physiology during application of high forces of Iacceleration. »

:

CONCLUSIONS 1.

Gross and pathological examinations of the brain

51 goats subjected to rapid,

short exposures to graded magni­

tudes of footward acceleration disclosed no consistent patho­ logical finding to indicate disruption of the in te g rity cf the in tra c ra n ia l flu id systems under the experimental pro­ cedure . 2.

Under the conditions of footward acceleration

applied in these experiments, cerebrospinal flu id pressure

, i

as measured from the c istern a magna and the venous pres, sure as measured in the common jugular vein were approxi­ mately equal a t a ll times♦ 3.

The pressure in the common jugular vein of goats \

subjected to graded magnitudes of footward acceleration was found to vary proportionately with the magnitude of ac­ celeration and to be equal in magnitude to th a t pressure which would be exerted by a column of blood extending from the point of measurement in the jugular vein to the midpoint of the cardiac silhouette as measured on a roentgenogram. 1|.

The arterial-venous pressure d iffe re n tia l mea­

sured between the common carotid artery and jugular vein was found to decrease an in sig n ifican t amount with an in ­ crease of the magnitude of the applied footward accelera­ tion. 5.

The rig h t in tra -a u ric u la r pressure as measured

by cannulation was found to maintain approximately the

1

same pressure levels under control condition and during application of footward acceleration within the lim its of accuracy of the experimental methods used. *

6.

Bradycardia was consistently produced in the ex­

perimental animals during the application of negative g s tre s s . 7.

The measurement of cardiac output as calculated

from the stroke volume a fte r the method of Hamilton was found to be unsatisfactory for application to the condi­ tions of th is study.

8.

I t is suggested that the re la tiv e

change in the

Jcardiac output as calculated does not represent the true volume of blood circu latin g through the cephalic vascular ( system during exposure to footward acceleration because of (the concomitant shunting of the blood from the d is ta l por­ t i o n of the vascular system. 9.

I t i s furth er suggested that the blood flow

through the In tracra n ial cavity i s likewise maintained during exposure to the stre ss of negative g under the con­ ditions of th is experiment.

I i

BI BL I OGRAP HY

I

BIBLIOGRAPHY

(1)

Roxburgh, H . , Personal Communication. RAP I n s titu te of Aviation Medicine, Royal A ircraft E stablish­ ment, Farnsborough, England.

(2 )

Armstrong, H. G. and J. W. ^eim, "The Effects of Ac­ c e l e r a t i o n on L iv in g O rganism s , 11 A ir Corps T e ch n i­

c a l R ep ort No. 4 3 6 2 , War D epartm ent, A ir C orps, M a te r ie l D i v i s i o n , D ayton, O hio, December 1 , 1937* E. 0. No. 6 6 4 - 1 - 2 5 0 . C3)

H ow ell *s T extb ook on P h y s io lo g y . E d ite d by John P . FultonI Phi1 adelphia• W. B• Saunders Company, F ifteenth Edition, 1 9 4 6 .

(4)

Bingham, E. C. and R. R. Roepke, "Rheology of the Blood, Part 4* F luidity of the Whole Blood at 37° Centigrade, 11 J. Gen. Physiol. , 2 8 :1 3 1 -1 4 9 , 194^*

(5 )

N u ttin g , P. G., "A Study o f th e E l a s t i c V is c o u s De­ form ation,** P r o c . Am. S o c . o f T e s t in g M a t e r ia ls , 2 1 : 116 2 - 1 1 6 8 , 1 9 2 1 .

(6 )

B a y l i s s , W. M. and L. H i l l , M0n I n t r a c r a n ia l P r e ssu r e and th e C er eb ra l C ir c u la t io n , P a rt I,** .J. P h y s io l. , l8 : 3 3 5 - 3 6 o , 1 8 9 5 , c i t i n g A lex a n d er Monro, "O bserva­ t i o n s on th e S tr u c tu r e and F u n c tio n s o f th e N ervous S ystem * 11 1783* . "On In trac ran ial Pressure and the Cerebral Circulation, Part I , " J . Physiol. , 1 8 :3 5 3 , 1 8 9 5 .

.( 8 )'

, "On In tra c ra n ia l Pressure and the Cerebral Circulation, Part I ," J . Physiol. , 1 8 :3 5 9 , 1895*

(9 )

Weed, L. H., "Experimental Studies of In tra cran ial Pressure," Chapter 3 , In the In tracran ial Pressure in Health, and Disease, An Investigation of the Most Recent Advances. Proceedings of the Associa­ tio n for Research in Nervous and Mental Diseases, New York, Vol. 8 , December 2 8 , 2 9 , 1 9 2 7 .

CIO)

Wolff, H. G. and H. S. Forbes, "The Cerebral CireiiL ac­ t i o n ," Chapter 6 , In the In tracran ial Pressure in Health and Disease. An Investigation of the Most Recent Advances. Proceedings, Vol. 8 , New York, December 2 8 , 2 9 , 1 9 2 ? .

■ 5(+ (1 1 )

K ety , S . S . and C. F . S ch m id t, "The N itr o u s Oxide Method f o r th e Q u a n t it a tiv e .D e t e r m in a t io n o f C ereb ra l B lo o d Plow i n Man: T h eory, P ro ced u re, and Normal V a lu e s ,” J . C lin . I n v e s 1 1g a t i o n . 27:1+76-511*, 191+8.

( 12)

Kety, S .

(1 3 )

S . , H. A. Shenkin and C« F . S ch m id t, "The E f f e c t o f I n c r e a s e d I n t r a c r a n ia l P r e ssu r e upon C ereb ra l C ir c u la to r y F u n c tio n s i n Man,” J . C lin . I n v e s t i g a t i o n . 27:497* 194^* . ”The E f f e c t o f I n c r e a s e d I n t r a c r a n ia l P r e s ­ su r e upon C er eb ra l C ir c u la t o r y F u n c tio n s i n Man,” J . C lin . I n v e s t i g a t i o n . 2 7 : lj.98. 1948*

ui+)

F e r r i s , E. B . , J r . , ”0 b j e c t i v e Measurement o f R e la ­ t i v e I n t r a c r a n ia l B lood Flow i n Man,” A rch . N e u r o l. & P aych i a t . . 4 6 :3 7 7 * 1941*

(1 5 )

J o n g b lo e d , J . and A. K. N oyons,. ”Der E i n f l u s s von L B e sc h le u n ig u n g e n a u f den K r s is la u f a p p a r a t ,” PlC-gers A rch iv f u r d ie Gesamte P h y s i o l o g i e . 23 3* 9571933^35^

( 16 )

J a s p e r , H. H ., P e r s o n a l Com m unication. M ontreal N e u r o lo g ic a l I n s t i t u t e , January 2 0 , 1947*

(17)

Rushmer, R. F . , E. L. Beckman and D. L ee, ”The t e c t i o n o f th e C ereb ra l C ir c u la t io n by th e s p in a l F lu id under th e I n f lu e n c e o f R a d ia l c e l e r a t i o n , ” Am. J. P h y s i o l . . 1 5 1 :3 5 5 -3 6 5 *

( 18)

Shaw, R. S . , J . L. Gamble, J . P. Henry and 0 . G auer, ”Venous P r e ssu r e i n th e Head under N e g a tiv e Ac­ c e l e r a t i o n , ” Aero M ed ica l L a b o ra to ry Memorandum R ep ort S e r i a l N o. MCREXDli-6q5-74g, A ir M a te r ie l Command, D ayton , O hio, January l5 » 1948*

(19)

Simmons, D. G. and J* P. H enry, ”The E le c t r o e n c e p h a lo g r a p h ic Changes O ccu rrin g d u r in g N e g a tiv e Ac­ c e l e r a t i o n , ” A ir F orce T e c h n ic a l R eport £ 0 . 5 9 6 6 . War D epartm ent, M a te r ie l D i v i s i o n , D ayton, Ohio, May, 1 9 5 0 .

( 20)

S t a u f f e r , F. R. and C. Hyman, ”F lu id S h i f t s d u rirg E xposure to A c c e le r a t io n : «S tu d y o f th e R apid Changes under N e g a tiv e G ,” Am. J. P h y s i o l . . 153* 6 ^ :1 9 4 8 .

Pro­ C erebro­ Ac­ 1947*

55 (21)

R o s e n f e ld , S . and C. F. Lombard, " C a r d io v a sc u la r Pressor Reflex Mechanism and Cerebral Circulation under Negative G Head-to-Tail Acceleration,"

J . A v ia t io n Med. ,

2 1 :2 9 8 -3 0 3 , 1 9 5 0 .

(22)

Romberg, H. W., "Das anatomische Bild der Blutverteilung bei beschleunigungs Wirking," L uftfahrtmedizin. ij.: 192-202, I 9 IJ.O.

(23)

Hamilton, W. F. and J. W. Remington, "The Measurement of the Stroke Volume from the Pressure P ulse,” Am. J . P h y s i o l . . li|.8 :ll*., 1 9 l|7 .

(214.)

Lombard, C. F. and o t h e r s , "The E f f e c t s o f N e g a tiv e ' R a d ia l A c c e le r a t io n on Large E x p er im en ta l A nim als ■ ( G o a ts )," P r o j e c t R ep ort on C o n tra c t N 6 o r i7 7 . Task 1, Department of Aviation Medicine, Univer­ s ity "of Southern California, November 30, 19^8.

(25)

Spielmeyer, W., Technik der %kroskopi schen Untersuchung des Nervensystems» Third Edition, page 2 9 . Julius Springer, Verlag, 192lf.

(2 6 )

Lombard, C. F ., H. P. Roth and D. R. Drury, "The Influence of Radial Acceleration (Centrifugal Force) on Respiration on Human Beings," J. Aviation Med. . 1 9 : 3 6 0 , 19U8*

(2 7 )

Gamble, J . L. and o t h e r s , " P h y s io lo g ic a l Changes dur­ in g N e g a tiv e A c c e l e r a t i o n , " Aero M ed ica l Laboratory Memorandum R ep ort MCREXD-o95-7IiL. A ir M a te r ie l t Command, D ayton , O h io, J u ly 2 5 , 19k&*

( 28 )

Weiss, S. and J. P. Baker, "The Carotid Sinus Reflex In Health and Disease, I t s Role in the Causation of Fainting and Convulsions," Medicine. Analytical Reviews of General Medicine. Neurology and Pedia­ t r i c s , XI, Baltimore: Williams and Wilkins Com­ pany, 1932, page 331.

(2 9 )

Pudenz, R. H. and C. H* Shelden, "The Lucite Calvarium, A Method for Direct Observation of the Brain, , Part I I , Cranial Trauma and Brain Movement," £• Neurosurg. , 3*^87-505* 19i|6.

(30)

Spiegel, E. A., G, C. Hermy and H. T. Wycis, "Changes of Cerebral C irculation Induced by Labyrinthine Stimulation," Am. J. Physiol. . lq.2:589-593> 19Mf*

56 TABLE I SU M M A RY TABLE OF EXPERIM ENTAL M EASUREM ENTS OBTAINED

bo

Phase

3 4 5

6 7

III

17

20 2 1 1

oj 01 3 H 3 51

pi,

g«s q

5 5 .a s Mfc mfi

as s £ >£

», o

5 5 5 5 5

8 8

14 15

4 2-5 6 2-5

15 15

16

12 2-7 15 2-8

15 15

19

9 5

10 20

9 7 7

21

8

23 24

8 2-8 2-8 2-8 2-6 2-8 2-8 2-8 2-8 2-8

60 15

60

15 30

60 15 30

60 15

Pathology

© «H © -P

15 15 15 15 15 15 15 15 15 15 15

5 2-8 15 10 1.2-5 15

2

fj nH

*H P O 9 £ j© c 3 W

10* 12

18** 20

Ih

tHO -p o

10 11

17

8

•H ® ■p >

©

a

3

. * T 3 i H®h®

4 2-5 5 3 10 5 2 5

8

9

II

14

20

00

© u

*h

p m f i rd Goat aa no. Runs t§

1 2

O < 5

c

©

& a 5 *1

X X X X X X X X X X X X X X X X

s si ° X X X X X X X X X X X

X X X X X X X X X X

X X

X X X X

X X X X

X X X X

X X X X

X X X X

X X X X X X X X X X X X

X X X X X X X X X X X X

X X X

X X X

X X X

X X X X X X X

X X X X X X X

X X X X X X X X X X X X

(Control) (Control)

* Goat used again after six months1 survival ** Experiment conducted on goat immediately after accidental death from medullary puncture

©© O *H

X X X X X X X X X X X

X X X X X X X

s X

X X

57

TABLE I I PROTOCOL A N DRESULTS OF EXPERIM ENTS IN PHASE I

tion of Goat G Runs N q Runs Level (Sec)

1

U

-5

15

, 2

20

-5

15

3

17

-5

15

4

20

-5

15

5

2

-5

15

6

1

-8

15

-8

15

1

-2

15

3

-5

3

-5

15

: 7

8 9

i

1

10

10

-5

15

11

2

-5

15

23

Control

24-

Control

Cause of Death

Survival Time After Exposure

Respiratory Failure Experimental Exsanguinetion Respiratory Failure Experimental Exsanguination Respiratory Failure Experimental Exsanguination Experimental Exsanguination Respiratory Paralysis (Curare) Respiratory Paralysis (Curare) Experimental Exsanguination Experimental Exsanguination Esqjerimental Exsanguination Experimental Exsanguination

Pathological Evidence of Vascular Damage Gross

Microscopic

0

None

None

24 hrs.

None

None :

0

6 days

L. Cerebellar None Subdural Hematoma None None ; None

1 day

Cerebral Vaso­ dilatation None

96 hr s •

None

None :

0

Cerebral vaso­ dilatation

None

0

Cerebral Vaso­ dilatation

None

5 mos.

None

None

13 days

None

None

None

None I

None

None 1

0

None

58

TABLE III ARTERIO-VENOUS PRESSURE

Mean Pre-run Pressure Phase Goat G in ramHg 10 1 .1 128 140 3.0 5.0 134 121 4.0 2 .0 113

12

Mean Pressure After 151 *G

138 201 259 215 183

Mean Mean A-V A-V Diff. Diff. Pre-run with G in m mHg in m mHg 108 70 118 71 118 55 65 109 95 103

A-V Diff. 15" G A-V Diff. Pre (Per Cent) 65

60 47

60 92

123

171

118

262 198

122

4.6

127 145 133 129 123

1.2 2.0

130 132

229 204 247 172 203

5.1

128

232

14 2 .2 4.0 3.1 5.8

113 107 107

147 163

132

128

273

126

87

93 58 17 69

15 2 .1

100

225

88

107

121

X - 3.2

124

203

115

101

87

1.5 3.6 4.6 3.0

2 .6

, H = 19

141 125 115 115

129 176 76 137 142 125

122

152

124

145

120

106

108

101 61 16

104 103

1205 144 54

110

107

108 125 119 90

59

TABLE IV ARTERIO-VENOUS PRESSURE

Mean Pre-run Pressure Phase Goat G in m mHg

in

16 1.9

126

5.1 8.9 8.9

98

102

17 2.3 5.0 4.0

Mean Pressure After 151 *G

Mean A-V Diff. Pre-run in ismHg

180

110

118

254

65

260 248

92 96 59

132 54 48

140 171 137

211 261 220

138

151

100

175 143

161 100 105 89 99 151

92 70 84 69 73 124

2 .8

140

213

126

8.5

211

2.2

146 147

129 135

5.1

136

19 4.2 3.1

99 87 89 103 93

6.0

7.0 8.4 4.9

20

112

187 217 239 177 227 296 293 250

122 87 75

81

202

2 .1

263 292 367 183

113

21 2 .0

116

192

106

112

260

104

118

346 293 223

no no

Mean X r 4.9 N = 30

122

115 115

125 125 125 127

111

130 116

109

168

245

308

82

75 248

112 118

132

130

107 144 57

126 120

5.0 3.0 4.0 8.5

120

113 87 65

95 89 107

2 .1

5.0 8.4 5.8 4.0 3.0 7.3

Mean A-V A M TDiff. 15« G Diff. A-V Diff. Pre With G in m mHg (Per Gent)

113

175

156

173

143 150 176

187 133

168

132 130 136 145 123 118

125 125 124 132 147 171

118

94 79 89

202 282

84 69 79

112

142

116

247

107

125

119

60 TABLE V CARDIAC OUTPUT CALCULATED O NCORRECTED BLOOD PRESSURE AT HEART LEVEL (3) (2) (3)

(4)

(5)

15" G Pre-run Hrt. Hrt. Rate % Rate in In beat beat Col 4 Gaat G/min /min Col 3

10 1 .1 3 .0 5.0 4 .0 2 .0

160

100

180 180 180 180

160

140 150 140

160

78 83 78 89

100 120 120 120 120 120 120 140 5.1 120

100

100

80 80 80

67 67 67 83 50

12 1 .5 3 .6 4 .6 3 .0 2 .6 4 .6 1 .2 2 .0 '14 2 .2 4 .0 3 .1 5 .8

160 160 160 160

15 2.1 160 Mean 2=3.5 145 N = 19

100 60 120 80 60 120 40

(6 )

100

62

90

69

15" G Hrt. output % in cc/ Col 1< min. Col 9

105 6080 88 5940

6400 4100

111 6480 83 6300 65 8900

4100 5800

105 69 105 65 65

34 27

70

203 3400 250 3250

7000 5440

205 167

21

50 51 34

238 2500 127 4800

4000 4080

160

3400

60

90 4500 187 3850

29 43 70

132 2650 160 3750 270 3110

42

86 7850 88 4000

40 38 32 27

17

(11)

40 29 40 29 36

57 50

62

(HO)

38 33 36 35 55

22

100 20

(9)

Pre­ Pre­ run run Hrt. 15" G Stroke Stroke % output Vol. Vol. Col 7 in cc/ in ce in cc Col 5 min.

100

75 25

(8 )

26 49 25 34 32 29 33

68

22 25

60 26 43

74 5450 187 5100 90 4565 149 4866

6900

3600 3480 3440

85 76 93

136

4200

92 134

5100 880 2800

22

1200 2600 4132

65 52 23*5 57 94

61 TABLE VI CARDIAC OUTPUT CALCULATED O NCORRECTED BLOOD PRESSURE AT HEART LEVEL

( 1 ) (2 )

(3)

(4 ) (5) 15« G Pre-run Hrt* Hrt. Rate Rate in * in beat beat Col 4 Goat G /min. /min. Col 3

120

120 160 140 100

120

120

100

135

75 90 75

56 75 56 45

16 1 .9

140

5.1 8.9 8.9

140

17 2.3 5.0 4.0

2 .8

140

120

8.5

135 135

2.2

160

5.1

150

140 135

19 4.2 3.1

120 120

60 105

6 .0

135 135

60

7.0 8.4 4.9

20 2 .1

120 150 150 135 135 135

60

75 90 75

100

PreRun ^ Hrt. % Output Col 7 in cc/ Col 5min.

(10)

86

28

25

89

114

24

26

108 60

9100

3000 4160 5600

93

3250

2500

2660 1650 2600 2850 1980

47 145 105

2800 2700

103 75

2160 2100 1200 2860

56 92 36

66

3840 2280 3370 3560 3560 4650

3150 1870

89 40

157 127

2100

2200 1260 900

104

1470

990 750 2080

61

100

83;

88

90 50

88 44 55 75 50 67 67 ' 56 67

3910 3780

66 2 7

40 25

20 26

22 22

no 85

2400

15

29 38 33

196 190

1800

20

23 17 24 32 19 25 27 38 31 14

20 20

140 118 83

36

112

20 20

105

38 35 25

92

22

80 140

3500 2700^

3100 2710

3600

89

13

18

138

105 90 95 90 105 105 105 98

78 67 70

6750 5700 7550

11000

110 100

63 48 49

4300 3960 3250 3870

67 67

14900 13500

5150

88

90 35

a 44 34 43 53 49 55 29'

100 110 61

60

41 42 56 69

10800

5800

21 2 .0

165 135 135 150 135 135

(11)

15* G Hrt. Output ^ in cc/ Col 10 min. Col 9

120

135

135

(9)

1440 1760

2 .1

120

Pre- 15* G run Stroke Stroke Vol. Vol. in cc.3n cc.

(8 )

62

120

5.0 8.4 5.8 4.0 3.0 7.3 X- 4.9

(7)

11 12 12 12

90 75 90 75

5.0 3.0 4.0 8.5

(6 )

72'

14

12

100

13

10

108 83

61

107

1620 1620

4711'

5600 2865'

77 123 63 77

110

64

80

86 56 52 123

64 70 43 35 37 38 53 73

6L TO EVALUATE THE INTRACRANIAL FLUID RELATIONSHIPS DURING THE S T R E S S OF FOOTWARD ACCELERATION LET

V

LET

hmBLOOD

LET

TOTAL BLOOD FLOW • CARDIAC OUTPUT PRESSU R E ■ O U T PU T

P R E S S U R E OF

LET

rr

RESISTANCE IN CAUDAL PORTION

LET

rz-

RESISTANCE IN CEREBROVASCULAR SYSTEM

LET

OF VASCULAR

SYSTEM

(A aiu m * h a o rt a i m idpoint)

r3 - RESISTANCE IN CEPHALIC PORTION OF VASCULAR S Y S T E M - rz RESISTANCE IN CEPHALIC PORTION OF VASCULAR SYSTEM

LET

*■

LET

V BLOOD *2* BLOOD V BLOOD

LET LET

FLOW

to

CAUDAL

p o r t io n

FLOW T O CEPHALIC

sy stem

PORTION OF VASCULAR

SYSTEM

CONDITION

II

(DURING G STR ES S)

TO EVALUATE THESE ASSUMPTIONS BY MEASUREMENT:

Ef V EC

It*I.♦ »» f |

v a scu la r

(UNDER 5 6 S T R E S S , BLOOD WEIGHS 5 TIMES AS MUCH AS UNDER NORMAL GRAVITATIONAL FORCE)

TH A T■

1 - ■-L + -L

of

FLOW TO BRAIN

CONDITION I (NORMAL) ASSUM E

Rt

THE HEART

TOTAL RESISTANCE TO BLOOD FLOW

\-

Ef *

- E d.

(PARALLEL CIRCUITS)

r4

X *X *_ L r,

r2

rs

Ecsf

I - • E -E _ A- — -

- ADEQUATE CEREBRAL BLOOD FLOW

5 G FORCE

M C2 5 0 /

CONDITION

I

CONDITION DIAGRAM O F C IR C U L A T O R Y

D IA G RA M

OF

C IR C U L A T O R Y

H E M O D Y N A M IC

SY STEM

R E L A T IO N S H IP S

AT

TO I

SHOW

OF

G

FO OTW ARD

A C C E L E R A T IO N OF

FIGURE

I

5

G

II

SY STEM

DURING

EQUAL TO

STR ESS FOR CE