803DR. T. G. BRODIE : THE PULMONARY CIRCULATION.

occurred there for many years, until one day a case was imported, andthe disease spread like wildfire, showing that the conditions for itsexistence were most favourable; and such instances might easily bemultiplied were it necessary. Besides, we know very well what diseasesewer air causes-it causes diarrhoea. Over and over again have I seenwhole households prostrated with diarrhoea, when air from a foul sewerhas leaked into the house, or air from a blocked-up sewer or soil-pipe has

found its way into the drinking-water cistern through the waste pipeand has fouled the water.

I therefore maintain that foul air contaminated by decomposinganimal matters is capable of producing mere diarrhoea and that whenit produces enteric fever it contains the poison of that disease, and thatthe arguments adduced to prove that this poison can be generated fromsuch decomposing matters independently of a previous case of thedisease are inadequate to do so; that in many of the cases where non-importation is supposed to have been all but proved it has not beeneven rendered a fair presumption, and therefore that in the presentstate of our knowledge we are not justified in saying that the disease ever arises de KOt’o.

The correctness of the views maintained in the above

paper has now been demonstrated by the discovery of thebacillus typhosus.

ABSTRACT OF

Three LecturesON

THE PULMONARY CIRCULATION, MOREPARTICULARLY IN RELATIONSHIP TOVARIATIONS IN CARDIAC ACTIVITY.

Delivered before the Royal College of Surgeons of Englandon Feb. 17th, 19th, and 21st, 1902,

BY T. G. BRODIE, M.D. LOND.,ARRIS AND GALE LECTURER; DIRECTOR OF THE CONJOINT LABOBA.-

TORIES OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON ANDOF THE ROYAL COLLEGE OF SURGEONS OF ENGLAND; AND

LECTURER ON PHYSIOLOGY AT THE LONDON SCHOOLOF MEDICINE FOR WOMEN.

PREVIOUS workers upon the circulation through the lungshave mainly confined their attention to a study of the

pressure changes in a pulmonary artery or vein in com-

parison with the pressure records in the aorta, and from theseoperations they have drawn conclusions as to the generalvariations of the circulation through the lungs. The close

relationship of the two sides of the heart to the pulmonaryvessels renders it, in most cases, a matter of considerable

difficulty to decide, from observations of pressure changesalone, whether or not any active change has taken place inthe pulmonary vessels. Hence the observations forming thesubject-matter of the main portion of these lectures havebeen conducted by Dr. W. E. Dixon and myself during thepast two years and took their origin from the application ofanother method-the plethysmographic-to the lung. Thismethod has already proved of very great value in the studyof the circulation in organs on the systemic circulation andhas also proved a most valuable means of studying thecirculation through the lungs under various conditions.The operation consists in first exposing the lower lobe of

the lung by the resection of two or three ribs. The lobe isthen thoroughly freed up to the root of the lung, and if theobject is to study the vascular changes one of two methodsis adopted. In our first experiments we prevented the entranceof air into the lung by gently compressing it before insertingit in the oncometer. In this way the lobe does not expandwith the ordinary air pressure used in artificial respiration.In a second series of experiments we first distended the lobeto its normal extent and then plugged the bronchus leadingto the lobe by a pledget of cotton-wool soaked in vaseline,inserted by means of a long probe passed down the trachea.The lobe was then fixed in the oncometer and its variations in

capacity recorded by connecting the oncometer to a pistonor bellows-recorder. We have always simultaneously regis-tered the aortic pressure by a mercury manometer. Theadvantages of the method lie chiefly in that it gives us atonce a record of the changes in amount of blood containedwithin the lungs, thus showing immediately the productionof an anaemia or congestion of the lung capillaries. Bycombining the information thus gained with the pressurechanges in the four chambers of the heart we can oftendefinitely determine the nature of the change that has been

produced in a more certain way than can ever be obtainedfrom records of the pressure changes only.

Variations in the flow of blood through the lungs may becaused by changes in the activity of the right heart or in theresistance offered by the pulmonary vessels and capillaries,and to this extent the problems offered for our study aresimilar to those so fully studied in the systemic circulation.Whereas, however, variations in the activity of the rightheart produce but small effects upon the flow through thesystemic capillaries, unless those changes be very pronounced,variations in the working of the left heart produce at oncemarked changes in the blood contents of the lungs. AsStolnikow has pointed out, the liver acts to a considerableextent as a blood reservoir on the systemic circulation, sothat the right heart may take a greater or less volume ofblood from the great veins without materially modifying the-systemic pressure. So the lungs play a similar part to theleft heart, acting as a reservoir in which blood may be storedif the left heart for some reason diminishes its output, andconversely contains a reserve of blood upon which the leftheart draws when its output increases. It is this very close

relationship to the two sides of the heart which makes thestudy of the pulmonary circulation of such difficulty and hasled many workers into considerable errors.

In these lectures we shall therefore discuss the various

experiments which we have performed in the following order o(1) the alterations in the pulmonary circulation due to purelycardiac changes ; (2) the alterations due to variations in thesystemic circulation, which may effect changes by alterationsin the output of the left heart or by modification in the flow-to the right heart; and (3) an examination of any changes.due to alterations in the resistance offered by the pulmonaryvessels.The blood-volume curve given by a lobe of the lung

in which the bronchus has been plugged in the mannerdescribed above gives the following features. There is asmall increase in volume at each inflation by the artificialrespiration apparatus of the remaining lobes of the two

lungs, and there is a very marked volume-pulse occurringwith each heart-beat. This volume-pulse is systolic in time.and is therefore due to the output from the right heart.Turning in the first instance to the effect of alterations in

cardiac activity upon the pulmonary circulation we mayfirst of all discuss the changes caused by excitation of theaugmentors and accelerators on the one hand and of theinhibitory fibres on the other. Stimulation of the acceleratorfibres which also usually causes augmentation, as a rule,leads to an increase in the volume of the lung and a rise inthe aortic pressure. The increased volume of the lungusually persists longer than the rise in aortic pressure. Ina few instances no increase in lung-volume is recorded andthese cases are usually accompanied by a, more marked rise inaortic pressure. Simultaneous records of the blood-pressurein the pulmonary artery and aorta show a marked rise in theformer which may or may not be accompanied by a rise inaortic pressure. From these results we conclude that thenerves chiefly affect the right side. The output from this.side usually shows a greater increase than that from theleft : hence the blood-volume of the lung is increased. Thevarious effects upon the aortic pressure show how variablethe action is upon the left heart.

Stimulation of the vagus also gives very interesting results.With weak stimulation, resulting in much slower beat, theaortic pressure falls gradually and a marked decrease in thevolume of the lung is recorded. A stronger stimulation,resulting in a much more marked fall in aortic pressure,leads to a quicker decrease in the lung-volume which, how-ever, is no more extensive. In these cases the right auriclepressure rises considerably, but the effect upon the leftauricle is much less marked. Hence we must conclude thatthe action of the vagus upon the heart is more particularlyfelt upon the right side. The diminution in volume of thelung can only mean a larger diminution in output of the

right ventricle as compared to that of the left.The next series of changes to be studied are those due-

primarily to an alteration in the systemic circulation. Ofthese we must distinguish two groups-namely, those iDwhich respectively a rise or a fall in the aortic pressure isproduced. These may exert an effect upon the pulmonarycirculation either through a change in the rate of flow ofblood into the right auricle or by affecting the output fromthe left heart. At present the latter of these two factorshas been chiefly studied.As the simplest case we may take the effect of restricting

804

the outflow from the aorta by partially or completely block-ing the aorta at the lower end of the thorax. Waller andlater observers have shown that the result of clamping theaorta is to cause a big rise in the aortic pressure, followedquickly by one in the left auricle. There is no rise in thepulmonary artery pressure unless the compression is kept uplonger than about 15 seconds. There is usually no effectupon the right auricle pressure. We have found that theeffect upon the lung as observed by recording its volume

changes is to produce a very marked congestion, themode of production of which is in the failure of the leftventricle to empty itself against the raised aortic pressure.In consequence of this fall in output from the left side theblood in the pulmonary veins cannot flow in normalquantities into the left auricle and is therefore accumulatedin the pulmonary veins and capillaries. There is no in-

competence of the mitral valves. A quite analogous seriesof changes is also observed when other procedures for raisingthe systemic pressure, apart from a direct action upon theheart, have been adopted, such as stimulation of the medulla,the vagi having been previously divided, stimulation of thedivided splanchnics, or stimulation of the upper surface ofthe spinal cord which has been divided in the lower cervicalregion.We next come to the effects produced by methods which

act upon the heart as well as the blood-vessels. Of theseone of the most important is suprarenal extract. This isknown to cause a large rise in aortic pressure due chiefly toconstriction of the peripheral arterioles ; but it also acts uponthe heart, whose rate is increased and output nearly doubled.The effect on the heart, however, is complicated, if the vagibe undivided, by a marked inhibition of the heart occurringmainly during the period of heightened aortic pressure. Theeffect of suprarenal extract upon the blood-volume of the

lung is to cause first a small diminution in volume, soonfollowed by a marked increase which persists during, and fora short time after, the rise in aortic pressure. Thus the maineffect is to produce a distinct congestion of the lungs. Theeffect upon the pulmonary blood-pressure is a rise to nearlydouble its original valve, commencing with, but lasting ratherlonger than, the rise in aortic pressure. The left auricle pres-sure at first falls, but rises rapidly when the aortic pressurehas reached a high point. The effect upon the right auriclepressure is a gradual and slight rise following the rise inaortic pressure. From these results we may conclude thatthe effects are mainly due to the action of the peripheralblood-vessels in causing the large rise in aortic pressure.They are, however, complicated by the action upon theheart. The increased output observed at first explains thepreliminary diminution in volume of the lung and the risein pulmonary pressure. The later effects are due to the risein the aortic pressure and the consequent inability of theleft ventricle to empty itself. The more reflex inhibitionthere is produced, the more marked, as a rule, is the

pulmonary congestion. These facts have an importantbearing upon the question whether suprarenal extract canbe advantageously used in hasmorrhage from the lungs.Certainly in the doses which we have employed, and withintravenous injection, our experiments strongly contra-indicate its employment for such a purpose. Whether asmaller dose, given by the mouth, so that the admittanceinto the circulation is much more gradual, can produce apulmonary constriction unaccompanied by a congestion isnow being investigated. Some further points in regard tothe action of the extract upon the pulmonary vessels aredescribed below-A drug of importance to us, in that it causes a fall in the

systemic pressure, is amyl nitrite. This is known to pro-duce its main effect by dilatation of the peripheral blood-vessels. The disadvantage against us here is that we are notquite certain of the details of its action upon the heart. Inthe cat a small dose of amyl nitrite sufficient to cause amarked fall in aortic pressure causes a large congestion of thelung, which takes place in two stages. There is a primary andmoderate increase in the blood-volume, followed by a slightdiminution, and this again is succeeded by the main volumeincrease, the nature of the record seeming to show that weare dealing with at least two different effects. The blood-pressure changes, so far as we have at present decided, haveshown only slight changes, the main one being a rise in theleft auricle pressure. The effect upon the pulmonary pressureis very slight and mainly in the direction of a late rise. Wethink, therefore, that the probable explanation of the con-gestion produced in the lung is a preliminary dilatation due

to the increased flow to the right side of the heart, followedby a later effect due to the action upon the heart which ismainly expressed upon the left side. This fails to emptyitself so completely and thus accounts for the rise in thepressure in the left auricle. In the dog the effect. is not

quite so striking. The changes are in the same directionbut are much less in degree. There is probably a muchbetter compensation in this animal than in the cat.

ARE THERE VASO-CONSTRICTOR NERVES TO THE PULMONARYARTERIES ?

This question has been already worked at by manyobservers ; but we need here only consider the facts broughtforward by Bradford and Dean and by François-Franck.All these observers came to the conclusion that thereare vaso-constrictor nerves. The evidence looked for byBradford and Dean was in one of three directions. First, arise in the pulmonary pressure out of proportion to the aorticpressure ; secondly, a rise in the pulmonary pressure with noaccompanying rise in the aortic pressure ; or, thirdly, a risein pulmonary pressure accompanied by a fall in aortic

pressure. In one series of their experiments they excitedthe vaso-motor centre in the medulla, having previouslydivided both vagi. This caused a large rise in the aorticpressure and a fairly well-marked rise in the pulmonarypressure. The spinal cord was then divided betweenthe sixth and seventh dorsal nerves and the stimulationrepeated. The aortic-pressure rise was now less thanbefore, but there was the same rise in the pulmonarypressure. Direct evidence was also sought by stimulation ofthe anterior roots of the upper dorsal nerves. This causeda rise varying in amount, but never very marked, in thepulmonary pressure, accompanied at times by a fall in theaortic pressure, at other times by a rise varying with differentanimals and with the nerve stimulated. From experimentssuch as these they concluded that the only explanation ofthe pulmonary rise is an active constriction of the pulmonaryarterioles.

François-Franck’s main method was to simultaneouslymeasure the blood-pressure in the pulmonary artery and inthe left auricle, and he considers that a rise in the former,accompanied by a fall in the latter, must mean pulmonaryconstriction. In his experiments he stimulated the sym-pathetic chain in the thorax from the sixth thoracic nerve upto the ganglion stellatum. The usual results he obtainedwere a rise in the pulmonary pressure, a fall in the pressureof the left auricle, and, as a rule, a fall in the aortic pressure.On some occasions he observed a rise in the aortic pressure.In some of his experiments he recorded the blood-volume ofthe lung by a plethysmographic method, and invariablyobtained an increase in volume as the result of the excitationof these nerves. This is an effect the reverse to that whichwe should a priori expect, and he supposes the result to bedue to the great distensibility of the pulmonary arteries. Ifthe arterioles are constricted over the whole lung the bloodwould be stored in the large vessels, and he supposes that theincrease in volume thus caused is more than sufficient to

compensate for the diminished volume in the capillaries andveins.Our criticism of the results of all these experiments lies in

two directions. First, the effects obtained are always verysmall, and all observers agree that the influence of thenerves on the blood-vessels can only be of slight degree. Butthe main objection to these experiments is that they havenot sufficiently excluded the action of the nerves upon theheart; and until this is done it is impossible to rely on ex-periments of this class. Bradford and Dean consider thatby taking into account those tracings only in which noapparent cardiac acceleration is to be seen any changesmust be due to an action upon the pulmonary blood-vessels.Roy and Adami, however, have shown that excitation of someof the sympathetic fibres running to the heart gives rise toaugmentation without acceleration, and many of our experi-ments have quite clearly corroborated this. If augmenta-tion takes place without acceleration the pulmonary pressurewill rise because the output from the right side is increased.The aortic pressure will also tend to rise because the outputfrom the left side is increased ; the pressure in the leftauricle will fall because the left ventricle is taking moreper beat ; and these are the effects which we think have inreality taken place in the records of these observers. The

only difficulty lies in explaining the fall in aortic pressurewhich they have commonly obtained. Bradford and Dean

experienced exactly the same difficulty and concluded that

805DR. W. ALEXANDER: THE EDUCATION OF EPILEPTICS.

their experiments were not sufficient to decide the cause oithis fall. That augmentation has taken place in many olFrdnçois-Franck’s experiments is quite clear from his owrtracings, for where he includes the volume-curve of the lungthere is always a quite marked increase in the volume-pulsewhich can only indicate an increased output from the rightheart.

Turning next to our own experiments we have stimulatedthe white rami communicantes of the upper thoracic nerves,the sympathetic chain itself, and the fibres from the ganglionstellatum. We have also attempted to exclude any possiblecardiac action by a preliminary division of all the branchesof the sympathet c that we could find running into the heart.We have, however, found that it is quite impossible to divideall these fibres without injuring those running to the root ofthe lung. We have also stimulated the fibres at theroot of the lung, but in this position we have onlyobtained completely negative results. The usual effectof stimulating the fibres leaving the ganglion stellatumis a fall in the volume of the lung, quickly followed

by an increase. In some cases we recorded an increasein the volume of the lung from the start, and in a fewcases, which, however, are very rare, we have observed adiminution in the volume of the lung during the whole timeof stimulation. Wherever we got a diminution in thevolume of the lung we invariably found an increased volumepulse, and simultaneously a rise in the aortic pressure. Wethink that the whole effect is best explained by the cardiacaugmentation which these results indicate, and that it is not

necessary to invoke any action upon the pulmonary vesselsfor their explanation. In those cases in which there is anincrease in volume of the lung from the start there is usuallyan increased volume pulse and the aortic pressure shows inmany cases practically no change, and lastly in those cases,the commonest, in which a preliminary diminution isfollowed by an increase in the volume of the lungthe increase in volume pulse is well marked, especiallyat first, and there is a decided rise in aortic pres-sure, followed by a gradual fall as the volume ofthe lung increases. Stimulation of the accelerator nerveitself, after it has left the ganglion stellatum, produces as arule an increased volume of the lung, with increased volumepulse. Hence we conclude that all the results that we haveobtained can also be explained in the simplest manner as ofpurely cardiac origin, and we therefore attempted to detectvaso-constrictor nerves, if any are present, by a differenttype of experiment. The nerves to be stimulated havingbeen isolated the animal was killed by bleeding ; the bloodwas whipped and was placed in a reservoir. Meanwhilecannulas were tied in the pulmonary artery and in the leftauricle. One lung was then ligatured at the root. Thecannula in the artery was then connected to the reservoirand blood perfused at constant pressure through the intactlung. The outflow was then recorded by a graphic method.We never obtained the least effect on stimulating any of thefibres leaving the ganglion stellatum, and hence we concludethat there are no vaso-constrictor fibres to the pulmonaryvessels. Experiments of this type, we think, would certainlyhave given us a positive result had such fibres been present,for it is easy to obtain such results with, for instance, thenerves to the vessels of a limb.

THE ACTION OF SOME DRUGS UPON THE PULMONARYCIRCULATION.

We have already stated the general effects of suprarenalextract upon the lung and pulmonary circulation. We havealso investigated the action of the suprarenal on the pul-monary arteries by direct perfusion. It gives us a verystriking result ; whereas perfusion of very dilute suprarenalextract through any of the systemic vessels causes theiralmost complete closure, the effect upon the pulmonaryvessels is in nearly all cases exactly the opposite-namely,a markedly increased rate of flow. Only in one instance havewe obtained constriction, and then the effect, though marked,was in no degree comparable to that which we should obtain,for instance, upon a limb. These experiments are, of course,of importance in considering whether suprarenal extract is ofvalue in haemorrhage from the lungs, but our conclusions upto the present must be somewhat guarded because our experi-ments have not yet sufficiently decided the action of smalldoses. With regard to the volume changes produced in thelung by suprarenal extract the dog again shows a difference from the cat. The changes, though in the same direction. arevery much smaller and the dilatation is more accentuated if

the vagi have been previously subdivided-a result which weshould naturally expect from the much greater and moreprolonged rise of aortic pressure that occurs under thesecircumstances.The action of nicotine is somewhat similar to that of

suprarenal extract, though, as it exerts less effect upon the

heart, its action being mainly confined to the peripheralblood-vessels, the results are rather simpler. Still, they arein the same direction-that is, to the rise in the aortic

pressure there follows a congestion of the lung and simul-taneously a rise in the pulmonary vein pressure and pulmonaryartery pressure.

Pilocarpine gives interesting results in that it tends to

produce systemic vaso-constriction, the effect of which is,however, obscured by the marked cardiac inhibition simul-taneously produced. If the cardiac inhibitory fibres be

paralysed by atropine, pilocarpine produces practically thesame results as nicotine. When given with the cardio-inhibitory mechanism intact it produces a great increasein the volume of the lung which is due to the cardiacinhibition. As this decrease in volume takes place it mustmean that the output from the left heart is less diminishedthan is that from the right heart. Muscarine produces thesame effects as pilocarpine.

THE EDUCATION OF EPILEPTICS.

BY WILLIAM ALEXANDER, M.D. R.U.L, F.R.C.S. ENG.,HONORARY SURGEON TO THE ROYAL SOUTHERN HOSPITAL, LIVER-

POOL; ACTING CONSULTING SURGEON TO THE HOME FOREPILEPTICS, MAGHULL.

TWELVE years ago the first step in improving the positionand comfort of epileptics in England was taken at Liverpoolby the establishing of the epileptic homes at Maghull.Previously to that time our epileptics, if they were poor"were consigned to the imbecile wards of the workhouse, andif they were rich they were looked after by relatives or byattendants, or were taken as boarders by people of variousclasses of life, who for a consideration relieved the parents oftrouble and responsibility without being always qualified forthe duties which they thus undertook. The condition of those-epileptics whose relatives were unable to engage caretakersand who did not wish to send them to the workhouse wasoften miserable in the extreme. The relatives were alwayskept in a state of constant anxiety and dread, and thepatients were frequently so confined to limited surroundingsand denied all liberty that it was no wonder that theybecame imbecile, stupid, or even insane. In spite of all the-precautions of anxious relatives and attendants dangerousand sometimes fatal accidents frequently occurred, andthe death of the unfortunate patient was too oftenconsidered a special providence and relief to all concerned.In the workhouses the patients were simply " herded " withthe imbeciles and the harmless insane inmates, without anyeffort being made for instruction, employment, or amuse-

ments. The primary objects of the establishment of thecolony at Maghull were to keep epileptic patients safe, to>

occupy and to train their bodies and minds, and to give themas muoh liberty as possible with due regard to their safetyand to the feelings and prejudices of their neighbours.These objects have been successfully carried out and to anunexpected extent. But it was found as the work of mentaland physical training progressed that the education of thepatients was often in a very backward state and required twobe.dealt with.

Defective education arose from various causes. In a con-siderable number of cases the patients were kept from schoolby order of their medical attendants, under the plea that the-brain mu-’t not be excited or that the patient must not be" bothered." The patient was allowed to do whatever wasmost agreeable-and education that necessitates " going to.school " is not generally agreeable to a large majority ofyoung children. The relatives, following up the professionaadvice to its logical conclusion, allowed the patients to do a.they liked in all other matters as well as in regard to educa-tion, and the little rascals soon found out that they coulricompel the relatives to give them whatsoever they wanted bysimulating the symptoms of the onset of an attack. Thi-.course of treatment of young epileptics cannot be too

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