BLOODFLOWIN THE HANDANDFOREARMAFTER PARAVERTEBRALBLOCKOF THE SYMPATHETICGANGLIA. EVIDENCEAGAINST

SYMPATHETICVASODILATORNERVESINTHE EXTREMITIES OF MAN

By J. V. WARREN,C. W. WALTER, J. ROMANO,AND E. A. STEAD, JR.

(From the Medical Clinic of the Peter Bent Brigham Hospital and the Department ofMedicine, Harvard Medical School, Boston)

(Received for publication April 29, 1942)

Many of the blood vessels of the extremities areunder reflex control. Numerous stimuli, such ascooling the body, pain, loud noise, or deep inspira-tion, produce reflex vasoconstriction. Heatingthe body causes reflex vasodilatation. The factthat either pre- or post-ganglionic sympathectomyeliminates these vasoconstrictor and vasodilatorresponses demonstrates that the sympatheticnerves contain the efferent limb of the reflex arcfor both types of response (1, 2). These vaso-motor reflexes which are mediated through thesympathetic nerves could be explained equally wellby either of the following hypotheses: (a) thatvasoconstriction is an active process resulting fromreflex sympathetic stimulation, and vasodilatationis a passive phenomenon resulting from inhibitionor lack of sympathetic activity; (b) that bothvasoconstriction and vasodilatation are activeprocesses resulting from reflex activity. The lat-ter hypothesis assumes that part of the reflexvasodilatation results from inhibition of activevasoconstriction, but that vasodilatation beyondthat point is an active process resulting from re-flex stimulation of the vasodilator nerves. Thishypothesis gained support from the demonstrationthat the sympathetic nerves to the extremities con-tain both adrenergic and cholinergic fibers. Thenerves supplying the sweat fibers are cholinergic,but anatomically they form a part of the sympa-thetic system. Might it not be possible that vaso-dilator, cholinergic fibers also coursed through thesympathetic ganglia and nerves?

Lewis and Pickering observed that heating thebody was the most satisfactory means of causingneurogenic vasodilatation in the extremities ofboth normal subjects and patients with Raynaud'sdisease, and that this response to body heatingoccurred only in the presence of intact sympatheticinnervation (1). They noted that in normal sub-jects whose skin temperature had previously been

lowered by exposure in a cold room, blocking theulnar nerve caused vasodilatation and warming ofthe anesthetized fingers. In two of their patientswith Raynaud's disease, block of the ulnar nervedid not cause the fourth and fifth fingers to warm.Heating the body produced normal vasodilatationin these fingers. They concluded: "To sum up,it is found in cases of Raynaud's disease exposedto suitable room temperature that ulnar anesthesia,with its inhibition of vasoconstrictor tone, fails torelease the vascular spasm, but that under thesame conditions, warming the body relaxes thevessels. The last effect occurs through sympa-thetic paths, failing to occur after sympathectomy,but as it is not due to simple inhibition of vaso-constrictor tone, being, in fact, prevented by anes-thetization of the mixed nerve, it must be attrib-uted to active vasodilatation." These experimentsare not conclusive because no evidence was ob-tained to show that the block of the ulnar nervehad actually inhibited the vasoconstrictor impulsesto the vessels supplying the fourth and fifth fin-gers. It has been found that it is not always safeto rely on anesthesia alone as a sign that all sym-pathetic fibers to the area are blocked (3). Lewisand Pickering (1), estimating changes in bloodflow from changes in skin temperature, were un-able to obtain evidence of vasodilator nerves innormal subjects. They believed that these nega-tive experiments were not conclusive becausechanges in blood flow are not always reflected bychanges in skin temperature. They pointed outthat the loss of vasoconstrictor tone raised thetemperature of the part to such a degree that fur-ther active vasodilatation had little chance of caus-ing a further rise in skin temperature.

Grant and Holling (3) studied the blood flowin the forearm during intensive body heating.They found that the blood flow increased, andthat this increase was dependent on the integrity

665

J. V. WARREN, C. W. WALTER, J. ROMANO,AND E. A. STEAD, JR.

of the sympathetic nerves. Local nerve block,however, caused the anesthetic skin to becomepale and cool. "Moreover, if the skin is firstflushed and warmed, and kept so by heating thebody, and a cutaneous nerve is then blocked (thecirculation to the hand being arrested), the areathen becomes anesthetic and ceases to sweat, palesand cools." These authors concluded that thereare two means of defense against a rise of bodytemperature. "The first is brought into actionby relatively gentle heating and consists chieflyof a dilatation of the arteriovenous anastomosesin the extremities, caused by inhibition of vaso-constrictor tone. The second is added when theheating is more intense and consists mainly of ageneral dilatation of the cutaneous vessels associ-ated with sweating, both of which are caused bystimulation of the sympathetic nerves." Theseexperiments, too, suggest that the sympatheticnerves carry vasodilator fibers, but they are notconclusive. No data are given to show that novo-cainization of the peripheral nerves had producedcomplete sympathetic paralysis. Lack of sweat-ing of the anesthetized skin was noted, but recentinvestigations have shown that sweating may bemarkedly decreased without interfering with otherfunctions of the sympathetic nerves (4). Theauthors point out that the circulation in the fore-arm is considerably increased immediately aftersympathetic ganglionectomy, and they are unableto account for the difference between the effectof blocking a mixed nerve to a part of the limband the effect when the sympathetic nerves sup-plying almost the whole limb are blocked.

The fact that heating the body produces agreater blood flow in the normal extremiity thanin the extremity which has been sympathectomizedfor some time cannot be used as evidence for theexistence of vasodilator nerves (1). It has beenrepeatedly shown that there is an increase in tonein vessels deprived of their sympathetic nerve sup-ply. If the comparisons between the blood flowin the normal and in the sympathectomized ex-tremities are made after several days, the com-pensatory changes in the sympathectomized partmake interpretation of the results difficult. Thepoint at issue is whether, immediately after sympa-thetic section, the blood flow in the normal ex-tremity can be increased by reflex stimulation to

a level above that in the sympathectomizedextremity.

It is possible to study the problem of whethervasodilator fibers are present in the sympatheticnerves supplying the extremities by determiningthe blood flow in the upper extremity before andafter novocainization of the sympathetic gangliasupplying the part. The novocain blocks bothvasoconstrictor and vasodilator stimuli. If vaso-dilatation is a passive process resulting from inhi-bition of reflex vasoconstriction, then blocking allvasoconstrictor impulses will cause as great a de-gree of vasodilatation as can be produced throughreflex response to heating the body. On the otherhand, if the sympathetic nerves' carry both vaso-constrictor and vasodilator fibers, paralysis of bothof these will produce some increase in blood flowbecause of removal of the vasoconstrictor im-pulses, but it will not produce as great an increasein blood flow as will reflex vasodilatation fromheating the body, because the vasodilator impulseswill also be blocked.

METHOD

These experiments were carried out on a normal, paidvolunteer. The blood flow in the hand and forearm wasmeasured by plethysmographic methods (5, 6). Whenthe blood flow in the forearm was determined, the cir-culation to the hand was occluded by a tourniquet, distalto the forearm plethysmograph (7, 8).

The subject sat upright in a chair with the arms rest-ing on a table in front of him. The parts to be studiedwere placed in the plethysmograph and surrounded bywater of the desired temperature for at least 30 minutesbefore the experiment was started. Control flows weretaken.

The sympathetic ganglia supplying the right upper ex-tremity were then paralyzed by the paravertebral injec-tion of novocain. The spinous processes of the 7th cer-vical and upper 5 dorsal vertebrae were marked with askin pencil and scratches were made 4 cm. lateral to eachspinous process. The skin over the region was then dis-infected, and wheals were raised by injecting 1 per centprocain hydrochloride into the skin surrounding eachscratch. A 3 inch, No. 22 gauge needle was insertedinto the wheal opposite the 3rd spinous process, and ad-vanced perpendicular to the skin, toward the lower borderof the rib, until it impinged in the general region of thetubercle. After contacting the rib, the needle was with-drawn slightly, a 2 cc. syringe full of 1 per cent procainwas attached, and the needle was advanced slowly in atransverse plane at an angle of about 30 degrees to thesagittal plane of the body. Procain was infiltrated alongthe inferior margin of the costovertebral joint, the neck,and the head of the rib, so that there was no lasting

666

BLOODFLOW IN THE HANDAND FOREARMAFTER PARAVERTEBRALBLOCK

TABLE I

Summary of the experimental data on the hand

Temperature of water in Blood flow in cc. per minuteplethysmograph per 100 cc. of tissue

Remarks

Right Left Right Left

Resting .300 C. 300 C. 1 1 Room temperature: 210 C.Body exposed.

Reflex vasodilatation induced by im-mersing legs in hot water at 430 C. 300 C. 300 C. 8 11 The subject is warm all

over and has begun tosweat. Vasodilatation isnot complete.

After right paravertebral block.Heating of legs continued. 310 C. 310 C. 32 0-? On the left, the vasocon-

strictor effect of pain hasovercome the vasodilatoreffect of heating the body.There is no vasoconstric-tor effect on the right be-cause of the paraverte-bral block.

After recovery from paravertebralblock. Heatingoflegscontinued.. 310 C. 310 C. 13 13 Blood flow in both hands

gradually rising as heat-ing of the bodv continues.

Temperature of water surroundingright hand raised to 430 C. Heat-ing of legs continued .430 C. 310 C. 34 19 Full vasodilatation in the

right hand from a combi-nation of local heat andheating the body did notproduce a significantlygreater blood flow thanwas produced by block ofthe sympathetic ganglia.

discomfort. The needle was inserted until it struck thebody of the vertebra. In each instance, the patient de-scribed paresthesias along the intercostal nerve as theneedle was advanced the last 1 or 2 cm.

The 4th and 5th intercostal spaces were needled insuccession, and then the 2nd and the 1st. Finally, aneedle was inserted opposite the 7th cervical spine in adirection parallel to the needle in the first space. Be-cause of the position of the patient, the upper 3 needleshad to be angulated downward slightly as they skirted theneck of the ribs. Ten cc. of alkaline procain (9) wereinjected slowly in each interspace. After sympatheticparalysis developed, as evidenced by vasodilatation andthe development of Horner's syndrome on the injectedside, the needles were removed.

Reflex vasodilatation was produced by immersing thelegs in hot water (430 C.). Heating the body does notproduce maximal vasodilatation in the hand when thewater in the plethysmograph is maintained at 300 C. (8).Therefore, when the full degree of vasodilatation whichcould be induced by heat was desired, the part underobservation was surrounded by hot water. When thewater was in contact with the skin, as in the handplethysmograph, the temperature was kept at 430 C.When the water was separated from the skin by a thinrubber membrane, as in the forearm plethysmograph, thetemperature was maintained at 460 C.

RESULTS

Blood floz in the hanzds. The data from thisexperiment are summarized in Table I. In thispaper, the blood flow is recorded as cc. of bloodflow per minute per 100 cc. of tissue enclosedwithin the plethysmograph. With the tempera-ture of the water in the plethysmographs at 300and the arms, chest, and lower extremities ex-posed, the blood flow in each hand was 1 cc. perminute per 100 cc. of tissue (Figure 1-A). Roomtemperature was 210 C. The lower extremitiesbelow the knees were then immersed in water at430 C. Body heating by this means was con-tinued throughout the entire experiment. Partialreflex vasodilatation occurred and the blood flowin the hands increased, rising to a level of 8 cc. inthe right, and 11 cc. in the left (Figure 1-B). Atthis time, normal vasomotor activity, which is de-pendent on the integrity of the sympathetic nerves,was demonstrable in both hands (Figure 2-A).The sympathetic ganglia supplying the right upperextremity were then paralyzed by right paraverte-

667

J . V. WARREN, C. W. WN-ALTER, J. ROMIAN-O, AN-D E. A. STEAL), JR.

A

ROOM COOL WATER 300C.RIGHT 1 C.C.LEFT 1 C.C.

HEATING BODY WATER 300C.RIGHT 8C.C.LEFT 11 C0C.

B RIGHT5 0.0.

J LscI LEFT

5 C.C.

HEATING BODY

RIGHTLEFT

RIGHT 430C.LEFT 3 1°C0

34C.C.1 9 C.C.

AFTER RT. PARAVERTEBRALBLOCKWATER 3f1C.

RIGHT 32 C.C.LEFT 1 C.C.

F11(. 1. Bl) IAM)1i .o IN iE RIo(,lT ( UPPliER) .AN\D) LEFTi- 1 HA\i) [N05,;Recorle(l ill cc. of 10lood pier miiiiute pier 1011 cc. of hanl. A..K ulitrol. B'odly expiosed,

oomi teml)erature 210 C., water in plethysillogral)h at temlerature of 31K C). B. Afterimmersing lower legs in water at a temperature ol 430 (C The hlood flow lias increasedin bothi lianids. C. Legs still in water at 430 C. Water ahout right lianid at temlierature01 430 C. Blood flow increased in hboth lianids hut greater in the one surrounided hv thehot water. D. Alter righlt lparavertelbral block. \\ater al)out 1t)th hands at temperatureof 31° C. Note that blocking the sympathetic nerves produces as g-reat ani increase in1loo0( flow as the comlbination Of local lheat anidl lheatinig the h)o-d- ( Figure 1- ). The paillp)roduce(l hv insertin(g the needles for the paravertel)ral hlock has causedl marke(d v a-so-constriction in the lI ft hliam(l.

biral iinjection olf novocain. The pulse waves inthe rig,ht hand showe(l a marked ilncrease in size,alld tile VaSOIllI)tor actiVity \-ilichI Was l)resenlt lbe-fore the 1)lhck dlisal)l)eare(l coiimpletely ( Figure2-B) A (leel) breath, or pincinlg tile skill, 110

longer l)p (ituce(i vasocoi1striction i n the r-ighlt halndll.There x-as a miiarkedl Horner s svil(ldrome oi1 theright. Tile skin of the riglht face anld( arm +waswar\ m anid flushed, an1(l the veins, ftill. Tilere w-as

n:o sweatilng. Note that the left hian(I ilow sIhowedn) sl)oipitanleous variatiolis ill voltiime, lbtt for a dif-ferelnt r-eason. The )aill callsed ) p)tittinlg tileilee(Iles inl pllace for tue l)paraertel)ral block liladprodutced geiieralized vaasoco(lstrictioill in all p)arts

of tile skill exceplt \-ilere tile sy pill)atiletic ilerves;ila(l leeli plaralyze(l. The skill of tile left arm wasc)old( ail(i clanilill. Tile v-essels of tile left biand(1were fnliv conlstrictedl, ail(d tile 1)100(1 flow, vXervslow. Tlle vasoconstrictor effect of paini liad COill-

pletely o-er-come the vasodlilator effect of hleatillgthe bo0d. Tile blood flow inl tile riglit Ilaid(I asnlow 32 cc. (Figuire 1 -D ); that ill tile left Ilaind wastoo0 loW to lbe mlleasturedi for So(lle illilltites, lbt it

gradluialiv il1crease(d as tile effects of tile p)ainl (le-cr-ease(l. As tile effect of tile novocain wore off,tile lioodi flo in tile riglt ilaild gradtiallv (le-ci-ease(l. Becantse of the continltie(d body lleatiilg,tile i)ioo(l fl ill botil lilai(is reille(i sonlewlhat

668

BLOOD FLOW\ IN- TIIE HIAN-D AND FOREARMAFTER I'ARAV-ERTEBRAL BLOCK

A B

RIGHT

LEFT

CONTROL AFTER NOVOCAIN- BLOCKOF RIGHT

SYMPATHETIC GANGLIAFic(;. 2. NASOTORRESPONSESIN TIlE RIGHT ( UPPER) A\N) LrFT (I 0¾ Fi H \Ni)S

A. Control. Normial vasomotor activitv in both biands. B. After rigbt iarav-ertel)ral block. The ar-terial pulsations are very- marked in the riglt biand. aniiI tbere is 11n eVidence 0foat\ iiim()to!- ractivitv.Tlbere is imiarke(d vas con:,striction in tbe left band(I because o0 tbe lain cause(l by inserting tbe niee(llestjri tbe block.

ali(ve the level p)rslet hefore the 1)1(c)k. Spon-tanelleoS vasI(ln)tO( activity was now p)resent in

1)htIl hanlds.This pmrtio i of the experiment (lenlonstratedi

that the b)1od0 flow in the rig,hit hand. alreadv inI-crease(l l)v reflex vasoillatati(on fromii heatincg thebody, was tuirthier inicreasetI by blocking all thesympathetic nerves to the l)art. It w-as olviouts.h(owever, that coml)lete v-asodilatationi w-as niotPresent in the lhandI l)efore the paraverteblral blo()ck.It hias been dlemilonistrated thiat, in the hand. comn-plete vasodilatation is niot l)rodticedl 1v leatin,gthe body if the teml)eratture of the water surround-iimg the lhanid is imiainitainied at 302 C. ( 8). Themaximal -asodlilatatioln that cani be indulticed 1bhe,at will oCccur if the \water is miiainitaiinedl at a

tenpl)erature of 432 C. Therefoire, in ord-(ler- to

conipare the effect of l)arav-ertel)bral b)1ick with theftlll v-as (lilator effect otf heat, it wvas nlecessary to

raise the teml)erattire of the water stirrotild(lilng,-the righlt lhani(l.

The w-ater albmit the right biaid(I was lheatedl to432 C., that abmtit the left hand remiiainied at 31'C. Twenty minuites later- blood(Xx flows x-ere re-cor(le(l in both hands ; that in the rViht was 34 cc.

that in the left, 1() cc. Tl1e blood flow in the leftlhandCI lha(l r-i-sen becatise of the cOiinliitiel body lheat-ilng aPrO)ltcedl by having 3 extremiiities immiiiierse(lin x-ater at 43 2 C. The fl-iw in the righlt lhand(Ilhadl increased above that in the left lhanid becauseof the combined effect of local lheat and bo)dyheating. It is significant that tlis co(mbl)ination

TABLE II

S1umary of experimental observations oil rig/it forearm

'Iemiiperature of waterin plethysmograph:

Blood flow in cc. perminiute per 100 cc.

of tissue

RestingA\fter right paraxertebrdl block.

Recovery stae..I emperaiture of -water snrroundill(n

right forearm raised to 460 C..

31V C.31: cC. 1 2

31

4 6: C. 1 2

Room temperatnre: 22- C.Block satisfactorv, as sh own by- hot.

dlrv rig,,ht hand wvith ralpi(d bloo(d

flo -. TIhe left hand( was c moIstand c(old(.

T'he temiiperatLnre was ralised to 46: C.rather than 430 C. because- in theforearm plethysimograph the wvateris separated froiim the skin by a thinrUbber imiemiibrane.

Remark:

669

J V. WNARREN., C. W. WVALTER, J. ROMANO., A-ND E. A. STEAD. JR.

A

CONTROLWATER 31'CFLOW 2 C C

B

7L5 c.c

C

AFTER PARAVERTEBRAL BLOCKWATER 31-C. WATER 46° CFLOW 12 C.C. FLOW 12 CC.

II. 3. lio.()( 1F.o\\- IN111N Rio lIT F1om1.\i\

Recor(le(d as cc. per iillnlte per 100 cc. of lorearlni. Circulati WI to the biail(Ioccltd(le(l. A. Conitrol. \Water in plethysmlogralpl at 31 CC. 13. Aiter para-vertebral block. Water in pletvhIsmograph at 31 C. Note marked increase inblood flob. C. After- water in the plethysmiilog-raphl la(l bieen at tnlp)eratlire (f460 C. fo0- tfo(rty minuttets.

of local a(l l)bodv lheating(, catisedI IIo oreater vaso-

dilatationi in the riglht lhaln(d tlhani did bllocke of the

svml)athetic nerve supl)l)l. It was, tlherefore, coin-

cluide(d that there were nlo vasoldilatllr fillers in the

sVm11l)athetic nerves stl)p)lving the hialndl, because

remlloval of all smpl)athetic inpl)tlses l)rod(ltce(l cimll-

plete vaso(lilatatioll.Blood flow In tlitl forcurm. Becatise the vas-

ctilar reactions (of the forearmii differ sollmewhat

fromii those of the lhand(l (7, 8, 10), it was still pos-

sible that the sympathetic fibers stip)p)lving the

forearimi milighit colntaini vasodilatolr fibers. Tlhere-

fore, at aniother timie, the response of the vesselsof the forearmii after blocking of the svnmpathetic

nerve supply \vas sttl(lie(l (Table II).The suibject sat tupright in a clhair, with the riglht

forearmii in a plethvsmograph. The water in the

plethysmograp1h X-as ittainitaiite(I at a tenllperatureof 31 ' C. The resting )lood( flow-\- was 2 cc. per

intite per 100 cc. ot torearml. The smpl)atheticnerves to the right tip)l)er extremllity XN-ere tlhel)1lckedl l)b the ptaravertebral injecti( I (If llmv caill.T'his p)r(ou(ltlCed a marked HIriel-'s ,syndlrome (i1the rigilt. The skin Itf the righit face aid(I riohitarll becllme warilnl flitsiseel. an(l (lry. hrie veilnswere ftull. The skin of the remainder (If the Ia dvx-as plale, col(ld anld covere(r wVith l)ersl)iration froi i

the pain which was p)rodlulced b)y p)tutting thenee(lles in place lor the injection. The Mlood flowin the righlt forearm wvas 12 cc. after the bl:ck.As the effect of the ov cain ffre(1ff the 1)1(1flow rettirne(d te the colntrol leXel. 'I'lhe tem)pera-ttire (If the water in the plethsmllograph was tlhenlraise(d te) 46° C. FhIorty miinitites later the bloodflow in the forearni was 12 cc. As in the lhand(l.paralysis olf the symp)athetic nerves lhadl proelice(das great vasodilatatiul1 as (li(l the application otfhlcal lheat. It was ]IOt conisi(lere(d necessary to

670

BLOODFLOW IN THE HANDAND FOREARMAFTER PARAVERTEBRALBLOCK

determine the blood flow after body heating be-cause it has been shown that the application oflocal heat to the forearm produces more completevasodilatation than is obtained from heating thebody (8).

COMMENT

This investigation was carried out on only one

subject. In each set of experiments, data were

collected before, during, and after the paravertebralblock. Because of the nature of the investigation,it was possible to make repeated observationsduring each phase of the experiment. It is feltthat this type of carefully planned experiment, inwhich the subject serves as his own control, is

more valuable than less complete observations on

several subjects.Other investigators have not produced as great

a degree of vasodilatation from paravertebralblock as they have from heating the body (6, 11).They made no attempt, however, to determinewhether the injection of novocain had completelydestroyed all evidences of sympathetic activity.Their results are comparable to those obtainedby us while the effect of the novocain was wearingoff. Partial block produces some increase inblood flow, but not as much as is caused by bodyheating. It has been previously shown that themajority of the vessels in the hand are fully dilatedby local heat (8). The fact that blocking sympa-

thetic impulses to the hand produces as completevasodilatation as does heating the part indicatesthat most of the vessels in the hand are under theinfluence of the sympathetic nervous system. Aswill be pointed out below, the forearm differs fromthe hand in this respect.

In the forearm, blocking of the sympatheticganglia caused an increase in blood flow to thesame level as that produced by local heat. It isknown that in the forearm, local heat produces as

great, or greater, vasodilatation as that producedby heating the body (8). Neither local heat, nor

a combination of local heat and body heating, pro-

duces maximal vasodilatation in the forearm (8).Exercise causes much greater vasodilatation thanoccurs as a reflex response to heating the body, or

than was produced in this subject by block of thesympathetic nerves. This indicates either that, incontrast to the hand, many of the vessels of theforearm are not under the control of the sympa-

thetic nervous system, or that heat is not an ade-quate stimulus for producing reflex vasodilatationin the forearm. Experimental observations haveshown that heating the body is the strongestknown stimulus for reflex vasodilatation of thevessels of the forearm. The vasodilatation in-duced by arterial occlusion, exercise, and epineph-rine is not reflex in origin. As the vessels of theskin of the hand have been shown to be undersympathetic control, it is logical to assume thatthe vessels of the skin of the forearm are alsounder sympathetic control, and that the differencein the reaction of the vessels of the hand and ofthe forearm to heat and sympathetic block is ex-plained by the greater mass of muscle in the fore-arm. These observations suggest that the sympa-thetic nervous system plays little part in regulat-ing the blood supply to the muscles.

Grant (12) has demonstrated that the localvascular effects of exercise are independent ofthe sympathetic nerves. Kunkel, Stead, andWeiss (8) concluded that local heat to the fore-arm caused much greater dilatation in the vesselsof the skin than in the vessels of the muscles.They noted that though the resting blood flowcould be greatly varied by raising or lowering thetemperature of the water surrounding the fore-arm, vigorous exercise of the forearm producedapproximately the same increase in blood flowabove the resting level. It has also been shownthat arterial occlusion produces a much greaterblood flow in the forearm than occurs after reflexdilatation from heating the body, or from a com-bination of body heating and local heat to the fore-arm (8, 10). This again is in sharp contrast tothe findings in the hand and foot, where localheat produces more nearly maximal vasodilatation.The reactive hyperemia in the forearm producedby the release of arterial occlusion is not alteredby sympathectomy (10).

Patients with destruction of a lateral portion ofthe medulla oblongata, from thrombosis of theposterior inferior cerebellar artery, frequentlyshow partial sympathetic paralysis. In certain ofthese patients, the vessels of the extremities on theside of the lesion are not able to constrict fullywhen the body is cooled, but they dilate normallywhen the body is heated (4). They resemblecases of unilateral peripheral sympathectomy in

671

J. V. WARREN,C. W. WALTER, J. ROMANO,AND E. A. STEAD, JR.

that the involved hand is the warmer one whenthe body is exposed in a cool room, but they differfrom the unilateral sympathectomy in that warm-ing the body produces as great an increase in bloodflow in the involved hand as it does in the normalhand. The induction of this type of paralysis ofvasoconstriction without disturbance of vasodilata-tion would be ideal in the treatment of Raynaud'sdisease. Heretofore, there have seemed to be twoequally plausible explanations for this dissociationbetween vasoconstriction and vasodilatation: (a)that the sympathetic nerves to the extremitiescontain both vasoconstrictor and vasodilator fibersand that the medullary lesion destroyed the centralconnections of the vasoconstrictor fibers withoutinjuring the tracts concerned with vasodilatation;(b) that the sympathetic nerves contain only vaso-constrictor fibers, vasodilatation being simply in-hibition of vasoconstriction, so that partial de-struction of the' central connections of the vaso-constrictor fibers interfered with the active processof vasoconstriction without disturbing the passivevasodilatation resulting from inhibition of vaso-constriction. The experimental data reportedhere indicate that the latter is the correct explana-tion. It is of interest that with the medullarylesion the remaining connections of the vaso-constrictor nerves are sufficient to prevent thevessels of the extremities from exhibiting the in-crease in tone which follows either pre- or post-ganglionic sympathectomy, though they are notcapable of producing normal vasoconstriction oncooling the body. Therefore, inhibition of vaso-constriction still allows full normal vasodilatationto occur.

SUMMARYANDCONCLUSIONS

(1) On two occasions, the sympathetic gangliasupplying the right upper extremity of a normalsubject were injected with novocain by the para-vertebral route. The blood flow in the hand andforearm was measured before, during, and afterthe anesthetization.

(2) Complete absence of any vasomotor ac-tivity in response to sensory stimuli or deep in-spiration indicated complete paralysis of the sym-pathetic ganglia supplying the right hand. Thesympathetic paralysis produced a striking increasein blood flow. After the effect of the novocain

had passed away, the right hand was immersed inwater at a temperature of 430 C. Local heatproduced the same increase in blood flow in theright hand as had sympathetic paralysis.

(3) The fact that acute sympathetic paralysisproduces nearly maximal dilatation in the hand in-dicates that most of the vessels supplying thehand are under control of the sympathetic nervoussystem.

(4) The fact that complete blocking of sympa-thetic ganglia produces full vasodilatation in thehand demonstrates that inhibition of sympatheticactivity is sufficient to explain the vasodilatationwhich occurs in the hand when the body is heated.There is no necessity for postulating that the sym-pathetic nerves to the hand contain vasodilatorfibers.

(5) In the forearm, paravertebral novocainiza-tion of the sympathetic ganglia caused a six-foldincrease in blood flow. A similar increase inblood flow was produced by immersing the fore-arm in hot water (460 C.). This indicates thatremoval of all sympathetic impulses to the vesselsof the forearm produces as great a rise in bloodflow as does heating the part. Inhibition of vaso-constriction adequately explains the increase inblood flow which occurs when the body is heated,and there is no need to assume that the sympa-thetic nerves to the forearm contain vasodilatorfibers.

(6) The fact that neither heating the forearmnor injection of the sympathetic ganglia withnovocain produces maximal dilatation in the fore-arm indicates that many of the vessels of the fore-arm are not under control of the sympatheticnervous system. It is suggested that the vesselsof the skin of the forearm are under the controlof the sympathetic nervous system, and that thoseof the muscle are not.

This investigation was carried out with the technicalassistance of Miss Rosamond Piotti, S.B.

BIBLIOGRAPHY

1. Lewis, T., and Pickering, G. W., Vasodilatation inthe limbs in response to warming the body; withevidence for sympathetic vasodilator nerves inman. Heart, 1931, 16, 33.

2. Bolton, B., Carmichael, E. A., and Stiurup, G., Vaso-constriction following deep inspiration. J. Physiol.,1936, 86, 83.

672

BLOODFLOW IN THE HANDAND FOREARMAFTER PARAVERTEBRALBLOCK

3. Grant, R. T., and Holling, H. E., Further observa-tions on the vascular responses of the human limbto body warming; evidence for sympathetic vaso-

dilator nerves in the normal subject. Clin. Sc.,1938, 3, 273.

4. Stead, E. A., Jr., Ebert, R. V., Romano, J., andWarren, J. V., Central autonomic paralysis. Arch,Neurol. and Psychiat., 1942, 48, 92.

5. Lewis, T., and Grant, R. T., Observations upon reac-

tive hyperemia in man. Heart, 1925, 12, 73.6. Freeman, N. E., The effect of temperature on the

rate of blood flow in the normal and in the sym-

pathectomized hand. Am. J. Physiol., 1935, 113,384.

7. Grant, R. T., and Pearson, R. S. B., The blood cir-culation in the human limb; observations on thedifferences between the proximal and distal partsand remarks on the regulation of body tempera-ture. Clin. Sc., 1938, 3, 119.

8. Kunkel, P., Stead, E. A., Jr., and Weiss, S., Bloodflow and vasomotor reactions in the hand, fore-arm, foot, and calf in response to physical andchemical stimuli. J. Clin. Invest., 1939, 18, 225.

9. Walter, C. W., The basis of successful parenteraltherapy. U. S. Nav. M. Bull., 1941, 39, 249.

10. Wilkins, R. W., and Eichna, L. W., Blood flow tothe forearm and calf. 1. Vasomotor reactions:role of the sympathetic nervous system. Bull.Johns Hopkins Hosp, 1941, 68, 425.

11. Prinzmetal, M., and Wilson, C., Nature of peripheralresistance in arterial hypertension with specialreference to vasomotor system. J. Clin. Invest.,1936, 15, 63.

12. Grant, R. T., Observations on the blood circulationin voluntary muscle in man. Clin. Sc., 1938, 3,157.

673