close

Вход

Забыли?

вход по аккаунту

?

Spleen studiesII. Microscopic observations of the circulatory system of living traumatized spleens and of dying spleens

код для вставкиСкачать
SPLEEN STUDIES
11, MICROSCOPIC 0BSERVATIOE;S O F THE CIRCULATORY SYSTEM OF
LIVING TRAUMATIZED SPLRFIK’B, AND OF DYING SPLEENS
NELVIN H. KKISELY
Bull Laboratory of Anatomy, The University of Chicago
INTRODUCTION
The first paper of this series (Knisely, ’36) described the
structure and some of the activities of the unstimulated splenic
vascular system. The observations are that the unstimulated
splenic vascular system of mice, rats and cats consists of preformed, lined, completely interconnected vessels. From the
structure alone one could easily conclude that the splenic
vascular system is ‘closed;’ but the usual concept of the
‘closed’ circulation is too limited to include the functioning of
the system, for the venous sinuses separate blood cells from
blood fluid. (Venous sinuses in filtering-filling phase retain
blood cells but are permeable to blood fluid. Red cells pass
through the walls of sinuses during other phases of their cycle
by individual penetration.)
In the first paper the question was raised, “Why cannot
everyone find the connections of arterial capillaries with
venous sinuses B ” The observations on unstimulated spleens
did not answer this question. Observations of the reaction of
the splenic vascular system to trauma and its agonal changes,
however, reveal the difficulty of demonstrating the finer vascular system of the spleen in fixed material.
‘Thia work was aided by a grant from the Rockefeller Foundation t o the
Biological Sciences Division of The University of Chicago.
The a d s t a n c e and counsel of Dr. R. R. Bensley, Dr. William Bloom, and the
other members of the staff of Hull Anatomical Laboratory, have been invaluable
in this work.
131
THE ANATOXICAL RECORD, VOL 65. NO. 2 A N D WPPLEMENT
MAY. 1936
132
MELVIN H. KXISELY
Kolliker in his article in Todd’s “Cyclopedia of Anatomy
and Physiology” (1847-1849) pointed out the danger of rupturing the fine splenic vessels by injection. On page 191 he
says,
How these smaller veins are connected with the very distinct
capillary network of the pulp I have not been able to find out ;
and I do not believe that either injection or inflation of the
vein or a microscopic examination will ever give any definite
conclusion hereto. F o r these vessels, often possessing but a
few little trabeculae f o r their coats are of such delicate texture that they tear by the slightest inechanical force while
by the microscope they cannot be distinguished from the surrounding constituents of the pulp.
Janosik (’03) who was able to demonstrate the fine vessels
of the spleen and their connections emphasized that the injection pressure must be as low as possible. He says on page
580,
Wenn man die Milz von der Arteria lienalis her und zwar bei
einem moglichst niedrigen Drucke injiziert, so kann man an
zahlreichen Stellen einen direkten Ubergang der kleinen
Arterien, welche insgesamt Endarterien sind, in kleine Venen
nachweisen. Um die Xalpighischen Korperchen herum findet
man fast immer Extravasate. Wenn man sich nur des
Rerlinerblaus ohne Zusatz irgend eincr Leimmasse bedient,
so sind die Extravasate sparlicher und hei der Katze finde ich
so ausgedehnte zusammeilhiingende Netze von wohlbegrenzten
und zwar mit Endothel ausgekleideten Bahnen, dass man an
ein vollstandig geschlossenes Rlutzirkulationssystem in der
Milz im Sinne von Sokoloff denken kann.
After describing the reactions of tlie splenic vascular system
to trauma and its agonal changes it is possible to discuss the
‘ampulla of Thoma. ’
The observations here reported were made using the same
transillumination method as was used to study the unstimulated splenic vascular system.
TRAUMATIZED SPLEEXS AND DYING SPLEENS
133
OBSERVATIONS
I . T h e reaction of the vascular system of living spleens of
mice, rats and cats t o s t i m d i produced by esperimeatal
manipulation
The splenic vascular system is much more sensitive, and
more reactive to the stimuli produced by experimental manipulation than is the circulatory system of any other organ I
have yet studied. If the surface of the living spleen is cut
slightly, two reactions take place immediately. First, great
numbers of the previously described physiological sphincters
contract. So many shut off the flow that sometimes one has to
look for a long time to find any moving blood in the parts of
the organ which are accessible for microscopic study. The
sheaths of Schweigger-Seidel are especially reactive and
powerful. They shut down more quickly and stay closed
longer than the other sphincters. Secondly, great numbers of
red cells pass out into the pulp partitions through the walls of
those sinuses that are in storage phase. (At times during the
passage of the red cells it appears as though the sinus had
contracted, increasing the pressure on its contents. However,
if there is a change in volume it is so small that i t cannot at
present safely be used as a criterion to determine whether or
not the sinus contracts, and in the absence of other criteria I
cannot now be certain either that it does or does not.)
The first red cells to pass through the sinus walls are distorted and then snap forward, showing that the membrane
lining the sinus is at first intact. The red cells come through
so fast, however, and the tissue around the sinuses is soon so
clouded that one can no longer see the sinus wall or study the
passage of erythrocytes through it. (This passage of red cells
out of sinuses is not at all like the escape of whole blood from
a small vessel during a microscopic hemorrhage.) The rapidity
of passage and the numbers which leave, seem to indicate that
the resistance of the sinus wall to the passage of red cells has
been altered.
134
MELVIN H. KNISELY
Observation of individual red cells which have passed into
pulp partitions following stimulation has as yet failed to
show that any of them are phagocytized or cytolyzed. They
ultimately return one by one to venous sinuses and pass in
through the walls. The last erythrocytes passing inward are
distorted and snapped forward just as they are in nnstimulated spleens.
After a variable period of time, sometimes within 30 minutes
later, the routine activities of the unstimulated spleen begin
haltingly to take place again. Usually the system does not
fully regain the smoothness and uniformity of action that it
had before being traumatized; as a rule, under these experimental conditions, there is still an excessive number of red
cells left in the pulp partitions at the end of 12 or 15 hours.
The latter seems to indicate that under some conditions red
cells can be in the pulp partitions for long periods without
being phagocytized.
This same set of changes, namely, clamping of sphincters
and passage of red cells into pulp partitions, occurs whether
the stimulation consists of cutting, pinching, scratching,
stretching, or twisting the spleen, the gastrolienal ligament,
or the vessels and nerves at the hilus. These reactions occur
if the spleen is touched with perspiring finger tips or with
metallic instruments which are at room temperature. Similar
reactions occur, but more slowly, if the temperature of the
Ringer's wash solution varies more than 1.5"C. from the
temperature of the abdominal cavity of the animal.
Thus it would seem that Barcroft and Stephens' report
( '27) that exteriorized spleens are insensitive to trauma,
needs further interpretation. Their criterion was that the
animal did not show signs of pain when the exteriorized spleen
was traumatized. The observations here reported show that
the vascular system of the spleen is very sensitive to tranma.
Here the criterion is the observed reaction of the living vascular system. These two sets of observations do not contradict
each other, for different criteria are used and, as is well
known, there are many visceral reactions which do not affect
consciousness.
TRAUMATIZED SPLEEXS AND DYING SPLEENS
135
From the variety of stimuli which initiate vascular reactions,
one can see why the living organ must be so vigilantly protected by careful manipulation when microscopic studies are
to be made. Owing to this sensitivity and reactivity, the first
spleens studied in this work were seen in the stimulated condition. Only by looking for source after source of stimulation,
and eliminating each when it was recognized, was it possible
to begin to study the vascular system of this organ while it
was free from such traumatic stimulation.
The greatest single obstacle in observjng the living unstimulated spleen microscopically, is the constant movement
imparted to it by the diaphragm. Every effort to hold it
still, even holding the stomach in a clamp, initiates the reactions to trauma. (Incidentally, those specimens are most
favorable for study that have relatively long gastrolienal
ligaments.)
It is entirely possible that the closing of large numbers of
sphincters and the migration of erythrocytes constitute a part
of the reactions of the system to unknown stimuli that reach
the organ during the normal lifetime of an animal. It is believed, however, that none of the stimuli listed are those to
which a spleen is subjected during an animal’s normal life.
Yet it is significant that such irritating processes almost invariably constitute a part of the preparation of a spleen for
injection, fixation by perfusion, or fixation by puncture or
immersion.
Such traumatic stimulation accounts for the presence of
some of the red cells found in the ‘cords’ of fixed and sectioned spleens. Indeed the clamping of the sphincters (especially of the sheaths of Schweigger-Seidel) throws light
upon several kinds of results obtained in splenic experiments.
For instance :
1. It accounts for the difliculty of injecting the splenic pulp
by way of the arterial system: a) Barcroft’s demonstration
( ’25)that the spleen of a dead animal has contracted to much
less than its physiological size, b) Robinson’s (’26) observation of the contraction of excised spleens, and c) Mall% statement ( ’00, p. 36), that “Their muscle walls (meaning the
136
MELVIN H. KNISELY
arteries) are also so powerful that it is practically impossible
to inject them completely in a contracted spleen.”
2. It is probably the reason why injection masses forced
into the splenic veins do not come out of the arteries. The
initial clamping of sphincters prevents the immediate intravascular transportation of the material, and the subsequent
pressure on the outside of the arteries of fluid that had escaped through the venous sinus walls collapses the arteries,
making it still more difficult for fluid to enter them.
Nisimaru and Steggerda (’32) kept spleens in a carefully
controlled constant temperature bath while injecting them, and
bogan their injections at low pressures. It is indeed significant that under these conditions material injected into the
veins came out through the arteries.
3. The clamping of sphincters may well account for some,
though not all, of the holes seen in the walls of the finer arterial
system of certain spleens fixed by injection. For consider the
alteration in the pressure relationships in the arterial system
which simultaneous clamping of great numbers of sphincters
brings about.
During the flow of blood in the arterial system of an unstimulated spleen there is a progressive decrease in pressure
from the large arteries to the arterial capillaries, due to the
friction of the moving blood on the vessel walls and the increase in total vascular cross section area. If one small
arteriole contracts tightly enough to obliterate its lumen, its
blood flow stops and the pressure in it, afferent to the constriction, rises until it equals that in the artery from which
the arteriole branches. In an unstimulated spleen some of the
branches of a given stem conduct blood while others are closed.
There is a rotation of access to the blood supply so that even
during the intermittent flow in terminal vessels, there is a
progressive decrease in pressure from large arteries to arterial capillaries. But, when large numbers of sphincters on
the latter simultaneouly close, the flow in them is stopped and
the pressure in the fine vessels increases, approaching as a
limit that in the main splenic arteries.
TRAUMATIZED SPLEENS AND DYING SPLEENS
137
It is but natural to assume that if the pressure head at which
an injection mass is being forced into an organ is that normal
for the large artery being injected, the pressure throughout the
arterial system therefore corresponds to the normal pressures
at each point in the system. But this is not necessarily (in
fact, seldom is) the case. The viscosity of the injection mass
and the rate of flow at each point are also factors affecting the
pressure throughout the vascular system. If the spleen is
injected when large numbers of sphincters are shut, the
pressure in the finest vessels can (previous to either rupture of
fine vessels or forcing sphincters open) be very nearly equal t o
the main pressure head at which the injection is being made.
Rupture of the more delicate vessels would permit the injection mass to enter the splenic pulp but it would leave holes
in the walls of the finest branches of the arterial system.
(Compare Kolliker’s statement of the delicacy of these vessels,
and Janosik’s that he demonstrated them when the injection
pressure was as low as possible.)
TI. Observatio%s om the rapid changes in the spleen durimg
t h e death of the animal
F o r a description of the changes taking place at death the
notes on mouse B8, a young animal having a thin spleen, may
be used. The activities proceeded too rapidly to be written by
the observer; they were recorded while being made by dictation to a stenographer. Each factor has been observed in rats
and cats, as well as in mice.
-Mouse B8. Previous to the death of the animal an area at
the junction of arterial capillaries and venous sinuses was
under observation. A venous sinus was emptying into a small
vein. White blood cells were visible in blood moving slowly
in the long straight capillaries of the pulp partitions. The
capillaries all showed the characteristic refractile lining mentioned in the previous paper. The animal had been opened
but a short time and the processes under observation were
those regularly seen in unstimulated spleens. Without warning, at 9.02 P.M., the heart stopped beating. Irregular respiratory motions continued.
138
MELVIN H. RNISELY
At the moment the circulation stopped erythrocytes began
to pass through the visibly intact linings of capillaries and
sinuses into contiguous tissue. As each one penetrated the
lining it was distorted and snapped forward. Red cells in
the marginal zone of the malpighian body and in pulp partitions went in all directions, each by itself. A large clear cell
shaped roughly like a prolate spheroid moved twice the
diameter of a red cell in 1minute. The red cells moved much
faster. Incidentally, at this time the intercellular spaces of
the pulp partitions probably were somewhat less than 7 p
in width for the red cells did not turn over freely in them.
At 9.05, as the animal made its last repiratory movement, I
was observing the subdivisions of an arteriole. Using the long
focus 40 X water immersion objective, 10 X oculars and a
green light filter I could see breaks appearing in the refractile
linings of the capillaries.
At 9.07 a 15 X ocular was substituted for one of the 10 X ’s
so that the field could be observed a t either 400 or 600 diameters. One erythrocyte was watched a few moments a t
600 X magnification. When the field was again surveyed at
400 diameters the number of red cells in the marginal zone
and pulp partitions had increased noticeably since 9.02, but
each one was traveling more slowly than before.
As breaks occurred in the capillary walls many highly refractile clear cells, some rounded, some irregularly starshaped, and all constantly changing form, appeared in the
field.2 Whether they became visible by moving into focus,
Since those observations were made Foot’s ( ’27) article ‘lOn the endothelium
of the venous sinuses of the human spleen” ha5 been brought t o my attention.
In addition t o studying fixed tissues he made hanging drop prepmations of sera@
spleen (from a spleen that was still warm) and examined them in a warm
chamber under the microscope. His in vitro observations are very pertinent to
the description of the dying spleen. Foot says, l‘h study of the living cells of
the spleen was not very illuminating, owing to the ditficnlty experienced in identifying them; many large cells were found t o be extraordinarily active, quite as
lively as fresh water amebae, but it could not be determined whether they were all
mscropha@s or whether some of them were not detached endothelium. Oells
showing the rod-like morphology of the latter were found, but they were not
actively motile.
. No membrane nor fragments thereof muld be found h
spite of careful searching.”
. .
TRAUMATIZED SPLEENS AND DYING SPLEENS
139
o r by alteration of their refractility in situ or by both methods
could not be determined. While these cells increased in
number the refractile borders of the capillaries disappeared.
The breaks in the capillary walls were real, for red cells
passing through them did not distort and snap forward; they
apparently met no more resistance than in progressing
through pulp partition tissue.
Then large clear irregular cells began to ingest red cells.
As a preliminary to the ingestmion,the red cell turned or was
turned, so that one flat side was closely apposed to the surface
of the ingesting cell. As many as three erythrocytes were seen
on one large cell ; then suddenly the red cells were inside the
phagocyte. The actual passage through the surface was too
fast to see. Phagocytic cells moved through the pulp partition tissue and acquired two, three or five red cells. One
was seen with seven in it. Those in this phagocyte then began
to turn darker and fragmented, until only two were left. The
cytoplasm of the phagocyte meanwhile acquired a dark
reddish-grey color. The processes of ingesting and breaking
up erythrocytes proceeded simultaneously so that any one
phagocyte seldom had more than from three to five red cells
visible in it, even though it could be seen to ingest two or
three times that number. By this time no vestige of capillary
walls was visible and even the end portions of the penicilli
branches were invisible for short stretches. By the time the
last capillary linings had disappeared, the number of phagocytes visible at any one time had reached its maximum.
The red cells in partly filled venous sinuses became arranged
in rouleaux. (In 4 years of watching circulation in many
organs of small laboratory animals, I have not yet seen
rouleaux formation in the living fEowi.ng blood, except under
known pathological conditions such as ether anesthesia, pressure or tension on the tissue, trauma, o r preceding the death of
an animal.)
From 9.11 on the rate of the agonal activities rapidly decreased to a few dow movements of phagocytes. All the
visible changes in the structure of the vascular system, the
140
MELVIN H. KNISELY
movement of red cells from vessels to tissue, and the intense
phagocytic activity took place in about 10 minutes ; most of it
much sooner.
Red cells pass through the lining of the sinuses and through
the positions previously occupied by capillary walls without
being distorted and snapped forward. At the end of the
agonal changes the sinus walls usually have a ragged appearance. Because the clouds of red cells surrounding the sinuses
make the changes in their walls more difficult to see than
those of capillary walls, they have been less frequently observed. So the conclusion cannot here be drawn that they
occur more rarely.
At the end of the death period there is less variation in
the diameters of the several venous sinuses of an area than
there is in the living. Few are as greatly distended as in an
unstimulated spleen, nor are the ones which were last in conducting phase as slender as they had been in the living organ,
and the corresponding pulp partitions are therefore more
nearly equal in thickness.
DISCUSSION OF OBSERVATIONS
Some of the agonal changes are more pronounced in one
spleen, some are more obvious in another. Every change is
usually seen in some degree. In these experiments the beginning of these processes has invariably been proof-positive
that the death of the animal was imminent.
These agonal changes are probably the source of many of
the conflicts in the reports of the structure of the finer splenic
vascular system. Consideration of the fact that the agonal
changes can be well on their way in 5 minutes and can have
gone to completion in 10 minutes, shows the probability that
in many cases of fixation by immersion the agonal reactions
have begun or gone to completion before the fixative has
reached the tissue. Tellyesniczky (’26 edition of Krause’s
Enzyklopodie der mikroskopischen Technik, p. 757) measured
the rate of diffusion of fixatives into pieces of immersed liver.
The slowest rate was 4 to 1mm. in 4 hours. The most rapid
TRAUMATIZED ST’LEEFS A 6 D DYIFQ SPLEENS
141
was 1 to 1.25 mm. in 1 hour. X y own measurements (using
Tellyesniczky ’s method) show that Romeis’ fixative penetrates
mouse spleen a little less than 3 mm. in the first half hour.
Mall (’00) makes a statement pertinent t o the question of
the adequacy of fixation by injection. He says, ‘‘If artificial
circulation is carried on through a spleen in which the muscle
is alive and contracted it is found that the spleen must be distended considerably before any fluid comes out the vein. This
usually takes a number of minutes after the artificial cjrculation has started.” I n fixation by injection (via artery or vein)
the physiological sphincters, traumatically stimulated by the
presence of the fixative in the larger vessels or by handling
of the organ, could easily stop the flow of fixative to the finer
vessels in the agonally reacting area, so that the fixative must
either 1) diffuse under pressure through the vessel walls
(which takes time), 2) force the sphincters open, or 3)
rupture fine vessels. If the vessels are ruptured by pressure
or if the agonal reactions have set in before fixation occurs,
the finer vascular system of the living unstimulated spleen is
no longer complete. Perfusion with saline previous to fixation
does not necessarily eliminate the danger of rupturing the
vessels.
Thus, beginning with the structure of the living unstimulated spleen, different combinations of variations of 1) the
number and positions of sphincters which contracted shut,
2 ) the tightness with which they closed, 3) the amount of
rupturing caused by injections, 4) the rates of progress of the
agonal changes in different spleens, and 5) the time the agonal
changes were in progress previous to the fixation of this
reactive tissue easily account for the ‘closed’ and all the ‘open’
and compromise circulatory system patterns that have been
described from sections of fixed spleens This accounts for
the fact that from one part of a fixed spleen a ‘closed’ pattern
may be described and from another part ‘open’ patterns, as in
Weidenreich’s (’01) classical study, for there is no reason to
believe that each of these variables operates equally in all
parts of a single spleen.
142
MELVIN H. KNISELY
The presence in fixed spleens of holes in the walls of capillaries, slits in venous sinus walls, open-ended capillaries, and
whole and fragmented red cells in phagocytes are not evidence
that the same features existed under the immediately previous
physiological conditions unless it is absolutely certain that the
fkation procedure employed does not itself cause changes in
the organ, and is rapid enough to prevent the initiation of the
agonal changes.
It seems probable that the freezing-drying technique (Gersh,
’32) by virtue of the possibility of freezing a whole live mouse
or an exposed functioning spleen instantaneously, will prove
suitable for studying spleens that have not undergone traumatic and agonal changes.
It may well be that some or all the phenomena seen in dying
spleens take place as reactions to stimuli which reach the
organ during an animal’s normal life. I feel that at present
we are in complete ignorance on this point because such
features have not yet been seen in living spleens and clearly we
cannot be certain that the fixation of the spleens which have
previously shown these features was adequate to prevent the
traumatic and agonal reactions.
Since it has been taught for so many years that the spleen is
“the graveyard of the red cells,” we must weigh carefully all
evidence of the splenic phagocytosis of whole red cells. Phagocytes have not yet been seen ingesting and cytolizing erythrocytes in living unstimulated spleens (Knisely, ’36). They are
phagocytized in dying spleens, and red cells and their decomposition products are not infrequently present in the
phagocytes of fixed spleens. Red cells can be either stationary
or moving in the pulp partitions for considerable time without
being phagocytized. Apparently splenic phagocytosia of
erythrocytes does not necessarily progress at a uniform rate
as is sometimes assumed.
DISCUSSION OF AMPULLA OF THOMA
One of the problems in this work has been the identification of the structures Mall named ‘ampulla of Thoma’ (Thoma
TRAUMATIZED SPLEENS AND DYING SPLEENS
143
1895 and 31al1, ’00 and ’02). Mall saw the connections of
ampullae with veins for in his 1900 paper (p. 33) he says:
“There are then marked channels or ampullae of Thoma, connecting the arteries with the veins, which can be demonstrated
by certain methods.”
Thoma showed that the distal end of the ampulla had a
mechanism which prevented injected material from entering
the veins, for he says (p. 48) :
Letzterer zeigt, wenn die Injectionsmasse nicht in die Venen
vordrang, haufig eine ampulltire Erweiterung, welche beweist,
dass der Druek der Injectionsmasse in dem Arterienendzweig
ein sehr hoher war, somit irgend welche Vorrichtungen
bestehen miissen, welche das Weiterschreiten der Injectionsmasse verhindern.
Since Mall’s papcrs were written, different authors have
used the term ‘ampulla of Thoma’ to designate various structures. For example, Robinson ( ’26) used the term to indicate
an exaggerated space in the splenic pulp tissue. He says (p.
352), “ F o r these reasons we believe that the ‘Ampulla of
Thoma’ is merely an exaggerated pulp space produced, no
doubt, by the concentration of blood flow at this point.”
MacNeal ( ’29) describes small ampullary dilatations at the
ends of several types of capillaries. Such pulp space dilatations as Robinson and XacNeal described have not been seen
in living spleens.
Tait and Cashin ( ’25, p. 424) equated the term ‘ampullae of
Thoma’ to the term ‘sheaths of Schweigger-Seidel.’ McNee
(’31) followed their usage.
But Mall (’02) clearly distinguished between the ellipsoids
and the ampulla of Thoma, for he says, “The ellipsoid of
Schweigger-Seidel continued to the end of the artery as a
small group of round cells and marks the beginning of the
Ampulla.” The structure of his ‘ampulla of Thoma’ cannot
be confused with that of the sheaths of Schweigger-Seidel. H e
says,
The first third of the ampulla is lined with spindle-shaped
cells which are directly continuous with the endothelial cells
144
MELVIN El. KBISELY
of the artery. The second third branches and often communicates with neighboring ampullae. The last third of the
ampulla is difficult to demonstrate but under certain conditions it can be injected as has been shown by Thoma and by me.
Mall also says, ‘‘Free communications between the ampullae
and veins have been seen from time to time by numerous investigators from W. Xiillcr to Helly, but no one has ever been
able to find them in great number nor free from extravasations.” And describing the connections of the structures Mall
calls ‘ampullae,’ he says,
If a spleen, made oedematous by injecting gelatin into either
the vein o r the artery or by filling the puly! with blood by
ligating the vein for half an hour, is injected through the
artery with some fine granular mass, like Prussian blue, it is
found that at the end of each arterial-capillary there are a
number of ampullae which communicate with the pulp spaces,
with one another, and with the veins.
Frequently, looking into a living unstimulated spleen, one
sees a somewhat elongated, cucumber-shaped structure, filled
with blood cells and appearing to have no efferent connection
with the venous system. Brief, uncritical observation of such
a structure could convince one that this is Thoma’s o r Mall’s
‘ampulla of Thoma.’ Each time that such a structure has
been carefully watched for a long time, a previously unohserved efferent sphincter has suddenly opened wide and the
structure has discharged its stored blood cells into an adjacent
venule. This structure, the static condition of which roughly
fits Mall’s description, proves by discharging that it is a
venous sinus in the storage phase of its activity. Such structures always proceed to repeat the regular venous sinus cycles.
Mall’s statement that efferent connections with venules have
been found from time to time but not in large numbers, supports the view that his ‘ampullae of Thoma’ were venous
sinuses because, in a fixed preparation, the only efferent connections that would be discovered are the patent ones. Under
most conditions more would be closed than open. Mall’s
statement that in a spleen distended with gelatin (or with
TRAUMATIZED SPLEENS A B D DYIKG SPLEENS
145
blood by ligating the veins) the ‘ampullae’ connect with the
gulp spaces, with one another, and with the veins, clearly describes the postmortem anatomical relationships of the individual sinuses constituting a multiple sinus system (compare
I, 11,I11 and I11a in fig. 2 of the first paper of this series).
Further, 3Call’s statement that the first third of the ampulla
is lined with “ spindle-shaped cells which are directly continuous with the endothelial cells of the artery” equates nicely
with Mollier ’s ( ’11) description of the spindle-shaped cells
lining the venous sinuses in his preparations.
Mall says, “The second third branches and often communicates with neighboring ampullae.’’ This sentence is an apt
description of the interconncctions of a multiple sinus system.
He says that the last third is difficult to demonstrate, but that
Thoma and he have been able to inject it. He states also that
the last third connects with a venule by a channel or channels
which have bridges of tissue across them. This latter statement rather accurately describes the ragged condition of some
sinuses’ efferent ends after the agonal changes have gone to
completion.
The fact that Mall’s fluid injection masses ‘extravasated’
through the walls of his ampullae also checks well with our
present knowledge of the permeability of the sinus wall io
blood colloids (Knisely, ’36).
From these considerations I am led to conclude that the
structures which Mall ( ’00) described and called ’ampullae of
Thoma’ were venous sinuses fixed in different phases of
physiological activity and in different stages of agonal disintegration.
After another series of researches (’02)’ during which Mall
injected spleens with, as he says, “ a great variety of mixtures
of asphalt, turpentine and granules” and gelatin, he concluded that “It seems as if the ampullae are only large holes
within the spongy pulp.” This is the same conclusion that
Robinson reached after injecting spleens from abattoirs and
autopsies with asphaltum in turpentine, hot lard, etc.
THE ANATOMICAL RI~CORD,VOL.
65, NO. 2 AND SWPPLJCMEXT
146
MELVIN H. KNISELY
SUMMARY
A variety of manipulative stimuli initiate two reactions in
living spleens : 1) Simultaneous complete contraction of a
great many physiological sphincters, particularly the ellipsoids
of Schweigger-Seidel, and 2) the passage of large numbers
of red cells from sinuses in storage phase into the pulp partitions. This explains 1) the difficulty of injecting the splenic
pulp by may of the arteries, 2) the reason why material injected into the veins does not come out the arteries, 3) the
presence of some of the holes in the walls of fine vessels of
injected specimens, and 4) the presence of part of the red
cells found in the pulp ‘cords’ in sections of spleens.
The agonal changes consist of 1) migration of red cells into
pulp tissue, 2 ) disappearance of portions of arterial-capillary
and capillary walls, 3 ) the appearance of irregularly shaped,
moving, constantly changing cells which rapidly ingest and
cytolyee erythrocytes, 4) the development of spaces in the
venous sinus walls large enough for red cells to pass through
without being distorted, and 5) the relaxation of distended
sinuses and stretched pulp partitions, which alters the tissue
so that the relative magnitudes of its parts are not the same as
in the functioning organ.
The most striking features of the agond changes are the
,instantaneousness of their onset and the rapidity with which
they go to completion.
The observations on the reactions of the spleen to trauma,
and the rapid agonal changes which take place in the organ
show why it is so difficult to trace the connections of the arterial capillaries with venous sinuses in fixed sections.
The term ‘ampulla of Thoma,, coined by Mall, was used by
Robinson to indicate large pulp spaces present in the tissue
after injecting foreign materials. It mas used by Tait and
Cashin, and later by &Nee, as a synonym for the terms ellipsoid, Capillarhiilsen, and sheath of Schweigger-Seidel.
Mall used it to designate the structures commonly known as
‘venous sinuses’ in the papers describing his early experiments. But in his 1902 paper, after injecting asphalt in
TRAUMATIZED SPLEENS A N D DYIFG SPLEENS
147
turpentine, etc., he applied the term ‘ampulla of Thoma’ to the
large pulp spaces he found, just as Robinson did 24 years
later, after similar treatment of the organ. The term ‘ampulla
of Thoma’ does not indicate a specific antttomical structure, but
has been applied to two real structures and to artificial dilatations produced by injection.
The observations reported in these two papers show the
activities and reactions of the splenic vascular system under
a limited set of conditions. 1 do not think that we can yet
safely conclude that the activities and reactions of the system
are necessarily similar under all other conditions.
LITERATURE CITED
BARCROFT,
J. 1923 Recent knowledge of the spleen.
Lancet, vol. 208, pp.
3 19-322.
BARCROIT,J. AND J. B. STEPHENS
1927 Observations on the size of the spleen.
J. Physiol., v01. 64, pp, 1-23.
FOOT,N. C. 1927 On the endothelium of the venous sinuses of the human spleen.
Anat. Rec., vol. 36, pp. 91-102.
GERSH, I. 1932 The Altmann technique for Bxation by drying while freezing.
Anat. Ree., TOI. 53, pp. 309-337.
;JANOSIK, J. 1903 Uber die Blutzirkulation in der Nilz. Archiv. f. mikr. Anat.,
Bd. 62, 8. 580491.
K~LLIKER,
A. 1847-1849 The article on the spltien in Todd’s Cyclopaedia of
Anatomy and Physiology, vol. 4, pp. 771-800. Longman, Brown, Green,
Longmans and Roberts, London.
KXISELY, M. H. 1936 Spleen studies. I. Microscopic observations of the circulatory system of living unstimulated mammalian spleens. Anat. Rec.,
VOI. 65, pp. 23-50.
MACXEAI,,W. J. 1929 The circulation of blood through the spleen pulp.
Archiv. of Path., vol. 7, pp. 215-227.
MALL, F. P. 1900 The architecture and blood vessels of the dog’s spleen.
Zeitsehr. f. Morphol., Bd. 2, S 1-42.
1902 On the circulation through the pulp of the dog’s spleen. Am.
J. Anat., 701. 2, pp. 315-332.
MCNEE,J. W. 1931 The Lettsonian Lectures on “The SpIeen: its structure,
functions, and diseases." Trans. Med. SW. of London, vol. 54, pp.
185-236.
XOLLIER,
5. 1911 Uebor den Bau der Capillaren Milzvene (Xilzsinus). Archiv.
f . mikr. Anat., Bd. 76, S. 608-657.
1932 Observations on the structure and funcNISIMAEU,
P. AND F. R. STEGGERDA
tion of certain blood vessels in the spleen. J. Physiol., vol. 74,
pp. 327-337.
148
MELVIN H. KNISELY
ROBINSON,
W. L. 1926 The vaseuhr mechanism of the spleen. Am. J. Path.,
VOI. 2, pp. 341-356.
TAIT, J. AND M. F. CASHIN 1925 Some points concerning the structure and
function of the spleen. Quart. J. Exp. Physiol., vol. 15, pp. 421-445.
TELLYESNICZKI,
I(. 1926 The article on ' 'Fixation, " in Krause 's Enzykklopiidie
der mikroskopisehen Technik, pp. 750-785. Urban and Schmarzenberg,
Berlin and Wien.
THOMA,R. 1895 Ueber die Blutgefiisse der Milz. Verhandl. der Anat. Gesellwhaft, Bd. 9, S. 45-52.
WEIDENREICR, F. 1901 Daa (3efZsssytem der Milz des Menschen. Arehiv. f.
mikr. Anat., Bd. 58, 8. 247-373.
Документ
Категория
Без категории
Просмотров
2
Размер файла
1 014 Кб
Теги
living, traumatized, dying, spleen, observations, microscopy, studiesii, circulatory, system
1/--страниц
Пожаловаться на содержимое документа