From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
Normal
Functions
Red
of the
Blood
By
I
HE
WORDS
well
cells.
is not
essential
is cure
that
to
describe
The
word
by Dameshek4
spleen,”
but
he
known
whether
assume
that
pertain
spleen
it may
tion.
When
pulp,
spleen.3
the
the
heal
was
that
with
it means
characteristic
exists.
However,
the
spleen
the
the
have
been
that
situations.
injury
destroy
to
splenism
and
transplanted
with
and
has
been
Parabiosis
animal
in dogs
were
which
caused
with
one
distorted
hemolytic
with
cells
parabiotic
are not
by
the
disease
June
13,
1958;
spleen
accepted
for
the
the
the
splenic
short
which
relate
and
probably
spleens
Reed
Army
integrity
circulations
Other
of
of
technics
of splenic
years
the
the
a splen-
have
been
function,
as in every
results
of splenectomy
bartonella
spleen
was
but
upon
the
actually
Institute
infections
gone.5
Exassumption
two-thirds
Research,
Walter
of Hematology,
August
of
C.
Society
International
publication
399
the
is
func-
the
This
splenectomy
been
used
has
been
interpreted
by parabionts,6
I).
of
also
is intact.
Walter
of
spleen
function.
functions
of unsuspected
the protecting
rats
have
exchanged
in
us
functions
is a normal
appear
function,
field
For
presence
when
let
these
cell.
joining
In this
waiting.
of the
definitely
discussion
of
splenic
is
a healthy
vocabulary
of
maintaining
used,
in
activity
it is not
healing
splenic
without
whose
From the Department
of Hematology,
Reed Army
Medical
Center,
Washington,
Read at the VI (Boston)
Congress
1956.
Submitted
red
a word
the normal
functions
example,
when
the
normal
the
spleen
cells
it
describe
Now
certain
red
normal
but
syndrome
hematologists’
but
abnormal
those
hypersplenism
purposes
of
For
them-a
itself
too numerous
to mention.
there
are pitfalls
set and
periments
that
blood
some
is abnormal,
or
and
that
methods
used
to study
splenic
list. Ligation
of splenic
blood
vessels
supply.
ectomized
and
circulating
splenomegaly,
“normal
functional
caution,
that
for
a pathologic
hyperspienic
the
in 1907,2
considerably
of
the
a healthy
into
1913,1
to absence
mean
commission.
functions,
bacteria
may
of
introduced
normal
The
restrict
erythrocyte:
Of
heads
blood
itself.
of
toil
“splenism”
pathogenic
will
errors
vogue.
in
a lack
with
Hyposplenism
who
said
has added,
has
to
by
of
a long
Chauffard
that
is
intended
associated
daily
enjoyed
by Eppinger
to or related
coined
by
condition
sterling
and
honest,
spleen
first
due
is manifested
mark
omission
splenism
the
discussion
tried,
other,
of
a
usually
The
to the erythrocytes,
may
involve
abnormal
torn
to
be.
of the
errors
body.
is
it
removal
spleen’s
needed
have
usually
which
Hyperspienism
by
hypersplenism
is
function
to
CROSBY
Hypersplenism,
but
it describes
Hyperspienism
of splenic
blood
the
spleen.
used,
defined.
exuberance
H.
and
Relative
: A Review
which
may
have
been
used
a pattern
of changes
that
are
or atrophy
of the
is more
commonly
less
Cells
Waui
hyposplenism
Hyposplenism,
has come
to mean
Spleen
June
16,
1958.
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400
WILLIAM
per
cent
to
exclude
of their
red
the
cells
splenic
of the splenic
vein
physiologic
technics.
in
developing
first
normal
are
our
knowledge
of the
is
a
duction
of
this
activity
fragment
became
cells
necrotic
tissue
except
for
a few
At
When
the
k-rays,
an
stem
cell
From
studies
erythropoietic
evidence
transferred
to
human
These
control
sixth
at the
tissue
these
trabeculae,
parent
organ.1#{176}
the em-
of
appeared
and
organ.
have
been
apparently
obliterated
is
The animals
interpretation
and
the
of tissue
and
follicles,
erythroblasts
able
and
that
cells
by
to
provide
so treated
that
some
reproduces
is evident
of
piece
from
the
development
But
the spleen
animal,
the
surface,
with
promonth
month.
the
That
cells
marrow
of
The
an
spection
and
of proteins
be
live;
sort
the
of
differentiates.12
are
to
provide
are
three
for
present
which
of red
cell
by
enzyme
ways
to
the
bone
or
any
is largely
other
for
for
cell
substrate
potential
certain
of the
blood-forming
is a topic
on
a lack of valid
and
ambivalent
over
a cell
stream
withholding
the
not
the
organ
of erythropoiesis;
of red cell production
is the
make
blood
of
marrow
argue
a
is diseased.
is, of course,
to
is
organ
also
production
fashion
in
the
this
life
may
develop
in
is a normal
function
disorders
spleen
hypotheses
throughout
metaplasia
that
this
serious
the
in
reason
marrow
The
erythroblasts
altered
such
that
bone
housing.
survive
by
can
involve
orderly
retains
Myeloid
be said
erythropoiesis
The
is its
process
in
evidently
suspect
fall out. The
leaves
us our
together
There
The
the
fifth
When
donor
However,
tissue
it
time
the
the
an erythropoietic
marrow
spleen
diseases
must
friends
which
failing
in
a spleen
bone
spleens
blood
cells.
but it cannot
one
support
them.
bone
marrow
rate
this
After
transplanted.
system.
favors
the
the
of regenerating
that
blast.
spleen.
development
splenic
life.
capability.
Splenic
good
tion
intrauterine
absent
was
again
the
normal
a new
Present
normal
organs
of
of
capacity
to form
types
of anemia,
spleen.
was
the
At
spleen,
in the
erythroblasts
is
this
The
point
spleen
injection
the seeds
for
controls
die.
have
one
the
in
erythroblasts.9
a spleen
that is indistinguishable
grew
it repeated
the ontogenic
moment
are
part
During
the fifth fetal
give
rise
to so-called
mesenchymal
new
ligation
All of these
an important
demonstrated
during
of the
that
the
by
mesenchyme.
in the spleen
splenunculus.
same
to become
spleen.
a brief
is well
it is practically
the
red pulp,
sinusoids,
As the new
spleen
for
This
spleen
function
a functioning
is not
proliferated
bryonic
the
produce
and
collaterals.8
also played
tissue
of the spleen
has a long memory.
a portion
of it is transplanted
into
the
becomes
spleen
turn
designed
circulation
by
CROSBY
considered.
primitive
cells
is a normal
diminishes
the mesenchymal
is removed
and
new
in
cells
Experiments
portal
have
to he
of
minute.7
the
splenism.
spleen
function
which
of red
from
thwarted
methods
embryonal
spleen
derives
from
month
certain
fixed
mesenchymal
hemocytoblasts
each
blood
are quickly
Anatomic
function
Erythropoiesis
exchanged
venous
H.
one
120
is an
of
delivery
days.
putting
or
the
erythroproteins
that
can
The
manufacture
enzymatic
materials
which
informadata
to
pass
process
by
whose
providing
or
inhibitors.
in which
the
spleen
might
conceivably
exert
in-
control
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
SPLENIC
FUNCTION
over
AND
RED
(1 )
erythropoiesis.
The
synthesis
of hemoglobin
is no evidence
to suggest
crease
or
decrease
Hemolytic
of the
marrow,
that
the
be
due
may
but
spleen
exerts
that
progressive
the
marrow.
reticulocyte
to
stage
of
time
a red
is spent
ulocyte
count
Red
in
the
seen
the
young
turn
go
may
the
last
the marrow
peripheral
is
its
the
circulation.
Removal
cells
of the
The
days.
Perhaps
is so,
the
the
reticulocytes’
erythrocytes.
This
may
or may
not
as a
reticulocyte
half
of
peripheral
this
retic-
existence.
If
days
yet
pigment
seems
from
earlier
they
would
live two
count
would
be doubled,
but
to
This
cure
to
phenomenon
a hemolytic
production
is unchanged,
spleen
spleen
it pauses
this
of
cases
The
released
nucleus
two
day
some
(3 )
last
one day
reticulocyte
activity,
in
are
lost
believed
marrow
function.
has
marrow.
hyperplasia
might
When
unchanged,
red
bone
who
bone
marrow
would
not have
increased.14
in patients
when
splenectomy
fails
survival
the
erythrocytes
into
enzymatic
erythroid
marrow
a normal
cell
marrow.
only
in
an
upon
bone
young
red
to
the
of circulating
is doubled.’5
young
which
development
cell
amount
is not
cell’s
reflects
of
but
this
the
the
Ferrata,’3
effect
of
its
cause
of erythropoiesis.
inhibitory
wait
impede
this is a possibility,
there
( 2 ) The spleen might inunits
can
atrophy
the
or
While
do this.
spleen
control
at
to leave
and
the
the output
is sometimes
anemia.
age
hasten
erythropoietic
the
a normal
waiting
the cells were
in circulation
the
is not
When
might
of
by
to hypersplenism,
bone
spleen
number
this
401
CELLS
stromal
proteins.
that
spleen
can
induced
determine
the
or
the
disease
proposed
BLOOD
permit
indicate
is
the
unchanged,
reticulocyte
earlier
a splenic
count
delivery
control
of
the
of red
cell
when
the
delivery.
It has
been
reported
and
confirmed
splenic
vein
is ligated
so
into the vena
cava
rather
due
partly
It
has
to increased
been
that
than
that
hemolysis
explained
on
anemia
and
the
partly
basis
of
an
originating
in the spleen.
When
the splenic
system
and
liver
the hypothetical
hormone
hormone
it is not necessarily
a normal
one.
provoked
by
the
chronic
in rabbits
the spleen
is drained
through
the portal
passive
to
inhibition
which
the anemia
disappears
and anemia
never
develops
vein,
is transplanted
It has
after
than
been
ligated,
stated
splenectomy,
a release
from
cythemia”
that
and
splenic
is often
when
the
But in any
interpreted
as
an
effect
the
cell
of the
in patients
spleen
event,
reflecting
on
red
may
has
been
is
the
effect
that
is incident
be
marrow.4
from
upon
controls
the portal
is such
a
substance
to
the
elevated
ligation
vena
above
interpreted
hereditary
removed
phenomenon,
a splenic
mechanism
bone
with
hormone
through
If there
abnormal
into
is
hematopoiesis.8
when
the
collaterals
in dogs
when
the
directly
count
phenomenon
inhibition
seen
not
occur
monkeys.’9
as
the
the
to drain
emptying
anemia
inhibitory
blood
flows
is detoxified.
It may be an
the splenic
vein,
because
drain
the spleen
enlarge,
rather
of
hypothetical
congestion
occurs
by collaterals
system.5’16
This
as
cava.17
normal
manifesting
“Postsplenectomy
spherocytosis,
of
that
splenic
polybut
it does
normal
humans18
or from
when
it occurs,
should
not be
the
blood
bone
marrow,
volume
or
but
the
rather
red
cell
volume.
A splenic
effect
upon
maturation
of
the
red
cell’s
surface
can
be
demon-
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
402
WILLIAM
H.
CROSBY
in
-J
_1
Li
U
Li
(:1
4
20
TIME
Fic.
by
1.-Red
thin
strated
and
Singer,
the
their
red
many
are not
changes
cells
as it matures:
(2)
,.t2.
cholesterol
(1)
The
area.
the
as
an
of
their
(4)
splenectomy
total
surface
is normal
present,
but
of thin
cells
mature
and
do
by
the
process
appears2’
lose
volume
not
lose
and
of
spleen
controls
apparently
surface.
Because
reticulocytes
same
to some
are
slightly
than
red
cells
that
attrition
and
when
area
and
surface
sticky
and
in
cells
loss
acids
and
the
isoelectric
somewhat
than
are
p.2
to the
fatty
potential
250
sticky
before,
thinner.
but
They
change
is not an abrupt
area
of the cells already
replacement
after
splenectomy
fatty
acids.22
One
the
about
proportion
cells
reticulocytes
did
from
is larger
the
as they
extent
them
red
they
undergo
many
in diameter
and also
2. The
cells.
The
the surface
The
protect
essential
of zeta
to less
mature.
means
molecular
which
sur-
mature
decreases
in direct
of the
surface
area is the
to nonessential
to
Its
loss of water,
so the hemoThe
surface
of the cell also
diminishes
area
water
so much
to
an increase
1).
replaced
predominantly
charge
area
which
fig.
of lipid
to surface
ratio
of essential
cell
shield
concentration
of normal
(See
gradually
the surface.
zeta
potential
electrostatic
from
about
3.5
as it becomes
are
is composed
electrostatic
appear
on stained
smears
as thin
target
one. Loss of the spleen
does not increase
they
cell
is at
great
surface
Reflecting
the
volume
cells
become
mature
red cells
reticulum.
They
shrink
relative
changes
stickiness
red
1942.’
of a red
of lipid
The
increases.
cellular
the
amount
(3)
point
of the cell
reticulocyte
loses
but
normal
Most
of the loss of volume
is due
the cell becomes
more
concentrated.
surface
After
) . The
in the cell
enormously
acts
reticulocytes
to losing
(DAYS)
Dameshek,
surface
lipid
to the
Because
sticky.
As
in addition
changes
and
The
the
and
collisions.
in volume.
globin
in
to 135
most
of
contributes
SPLENECTOMY
( dogs
splenectomy
( Miller,
by splenectomy.2#{176}
rounds
the
after
cells.
of lipids,
arrangement
of
cells
target
AFTER
normal
surface
of this
the
a population
new
spleen
lipids.
population
was
The
as before
and
normal
function
maturation
stickiness
present,
proportion
so is the
of the
of
the
determines
red
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
SPLENIC
FUNCTION
to some
degree
AND
the
RED
time
BLOOD
403
CELLS
when
young
cells
are
released
from
the
effect
of the spleen
on the red cell surface
reticulocytes
may enter
the circulation.
The reservoir
function
of the spleen
refers
may
to the
sequestration
in the
of some
animals
pulp
and
expansile
and
cells
from
the
splenic
it is possible
active
animal
In
fight
an
way
extent.
capsule
Nevertheless,
are
parts
for
them
or run.23
the
of the
human
is not
spleen
are
muscle
expand
the
splenic
are the red
developed.
which
they
are
vein
cells
The
through
increases
incubated
their
Clarks2#{176} found
wandering
red
cells
them
that
extravasated
When
the
surface
too
them
which
qualities
in the
scrutinize
“culling
the
do
meet
not
and
of
red
since
the
The
certain
are
minimum
of
to
is transfused
average
may
the
into
red
cells
red
cells.
to any
great
is high.
cells
There
move
slowly,
are spent
in
may undergo
in the blood
saline
to red
of living
first
immune
than
18
its
to
attack
if it
encounters
sequestered
to
victim,
cells
a great
we
has undergone
This may be one
have
extent
may
some
of the
by
extravasated
hours,
The
has
water
cells
when
tissues,
the
freshly
depends
spleen
and to
abnormal.
spleen
a normal
almost
be
upon
suspect
that
change
to make
risks of stopping
in
The
Perhaps
this organ
to
those
which
erythropoietic
10 per
red
bone
cent
than
spherocytosis
cells.
the
15 days.
has
no
When
red
red
cells
this
is not
from
rapidly
from
spleen
the
hereditary
spherocytosis
the
example
of
such
the
in
are
pro-
reason
example
a patient
disappear;
blood
an
One
is a good
blood
cells
marrow
similar
it makes
of
When
In hereditary
but
ability
of
circulation
it produces
are marvellously
perfect.
Some
of the cells
hereditary
who
normally.28
the
from
of surviving
in the circulation.27
presence
of a normal
spleen.
recipient
less
a recipient
prematurely,
describes
remove
requirements.
misshapen
may
into
survive
the
destroy
survival
is transfused
human
of red
to hypotonic
at
them.
and
and the red cells
the marrow
is not
otherwise
behavior
ability
the
about
eats
phagocyte
duced
by the marrow
are incapable
for their
failure
to survive
is the
of is
red
when
of the
ml.
spleen
encounters
phagocytosis
function”
of the
passing
red cells
or
of the
spleen.
is an efficient
organ
size and shape.
But
deformed
are
after
and
cell
time
about
two days
the red cells
the erythrocytes
exposed
cells
But
stops
the
A mild
degree
of spherocytosis
spleen
have
taken
up a little
phagocyte
of the sequestered
red
to the passing
scavenger.
long
The
when
artery.25
in the
aside.
phagocyte
changed,
the surface
it appetizing
fragile
a
cells
enormously
or contract
fragility.
The
same
thing
happens
in a test tube.
By direct
microscopy
it shoulders
somehow
more
phagocytes.
again,
the
are
from
the splenic
red cells loitering
of red
or 40
in the
and of the 120 days
of a human
red cell’s
life,
the spleen.
During
periods
of splenic
sequestration,
certain
changes.
It is known,
for example,
that
from
which
fibers.
of erythrocytes
circulation
30
the
at
are
function
holds
not
age
against
an important
spleen
marrow,
the
proportion
perhaps
does
no
a large
them
the
concentration
splenic
to remove
This
adult
there
the
spleens
holding
average-size
In its normal
In its
The
circulation,
must
spleen.24
sinuses.
influence
their
same
donor
spherocytes
spleen
a spleen
destroys
behaving
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
404
WILLIAM
abnormally.
It
population
The
probably
sluggishly
in
slide
and
The
line
the
that
its
to the
of
blood
that
bar
In order
between
a normal
two
culling
If this
the
are
the
fashion
function
toward
hypertrophy
sinusoids.29
barrel
and
stream.
The
phagocytes.
staves
thickened
to
the
red
hyperfunc-
spherocytes.
pulp
and
Cells
enter
the
of
spherocytes
are
If
the
spherocyte
has
loitered
cells
Other
the
hemoglobin
filled
but
with
breakdown.
iron.
hemoglobin,
The
they
epithelial
cannot
hemosiderin
Not
and
while
of returning
the
iron
a child
in the
may
develop
a severe
pulmonary
parenchyma
The
cytosis
spleen
150
phagocytes
cords
seem
by
mg.
comparison
per
day
that
line
not
are damaged
phages
in the
to
dispose
some
The
“pitting
particle
much
as
fruit.
Like
meet
splenectomy
The
of
standard.
red
cell;
of
because
refers
a red
cell
stone
this
and
But
it takes
in
is an
taking
this
types
blood
contain
these
siderocytes
the
to
destroy
become
the
blood,
siderosis,
In hereditary
turned
over
phagocytes
grows
spleen
to
its
without
spheroby the
of
where
the
pulp
erythrocytes
one
they
finds
seem
siderotic
and
ability
cherry
example
of
action
when
the
instance
to
macrounable
becomes
remove
destroying
a
from
corrective
in certain
that
to
of
iron
accumulates
extravasations.3’
by any phagocyte,
hemosiderin
which
spleen
the
function,
circulating
supposed
able
pulmonary
diseases
spleen
dispose
when
the kidney
lung
the red cells
seem
completely
anemia
while
of repeated
hemolytic
the
the
of erythrocytes
the
disease,
of red
They
occurs
into the
phagocytes
red
iron.
plucks
culling
is returned
wandering
In other
conditions
cytoplasm
splenectomy
in the
was
the
iron
In the
to
are
efficiently.
the
is returned
to
are sometimes
able
tubules
readily
disposes
of its iron.
hemoglobin
iron
may
be
sinusoids.
function”
housewife
not
it
unused
a
offending
cells
such
the
inspector
After
In
for
from
an
body.
are
iron
of the
and
liable
to destruction
splenic
pulp
crusted
with
depot
the
hemosiderinuria
is extravasated
pulmonary
to the
to be so efficient.
of.32
a storage
them
of renal
of
iron-deficiency
as a consequence
of
the
of
all
cells
dispose
much
is spilled
into the urine.
Thus
handles
hemoglobin.30
When
blood
are picked
up by phagccytes.
These
incapable
is degraded
and the iron
organs
than
the spleen
the
which
must
in
the red
reused.
hemoglobin
of
are cytoplasm
of the phagocytes
to the circulation
the spherocytes
clls.
the
in
normal
restrained.
and attractive
to the phagocytes.
metabolism
is related
to its destruction
involved
In
move
lumen
changed
in iron
from
to be
of
and
fixed
are hyper-
pulp,
its surface
may be
The role of the spleen
Hemoglobin
erythroblasts
a
means
pulp
cells
is due
cells
that
destroy
shunted
into the
barrel-shaped
the way
to return
by
in the red
These
latter
the
between
“barrel
staves”
the sinus
wall.
in
are present
sinusoids.
these
are
erythrocytes
direction
easily
return
squeeze
accomplishes
spherocytosis.
indicate
circulation
thickness
behaving
phagocytes
walls
of splenic
in hereditary
it may
splenic
sinus
spleen
CROSBY
erythrocytes.
Wandering
form
the
trophic
the
a normal
abnormal
spleen
phagocytes.
phagocytes
lion
is
of
H.
the
without
spleen
cells
are
does
itself,
crushing
the
spleen
a solid
cell
the
behaving
found
not
as
that
do
destroy
the
action.
of hemolytic
granules
destroyed
anemia
a portion
of hemosiderin.
were
them
absent
as fast
from
as they
of the
For
the
many
blood
were
red
years
before
produced.
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SPLENIC
AND
FUNCFION
NORMAL
RED
BLOOD
405
CELLS
RECIPIENT
RED
SPLENECTOMIZED
RECIPIENT
CELLS
CELLS
SIDEROCYTES
z
z
4
Ui
SIDE
U)
-I
.J
Ui
U
ROCY
TES
Li
U)
U.
U)
z
4
___________________________
0
2
4
6
T:ME
Fic.
2.-Siderocytes
in the
siderocytes-same
donor,
cells indicates
the red cells.”
that
The
of
results
indicate
that
because
should
there
the
iron
of their
iron
remains
containing
any
activity.
the
the
the
the
of
cent
loss
of
of
red
plasmodia
known,
but
and
the
with
cells
not
sparing
20
without
per
loss
without
red
anemia
destroy
of the
cent
of
destroying
hemolytic
does
siderocytes
cells
and
transfusion.
counted.
siderocytes
affected
red
cells
after
splenectomy.
cells
are siderocytes
was
red-cell
bartonella
pitting
red
definitely
destroying
a spleen
But
and
organisms.
function
transfused
into
The red cells
to determine
cells,
red
sorts
as
the
The
the
granules
contained
inclusions
for
may
beBlood
recipients,
Heinz
siderocytes
the subject
count
neither
determined
iron
bodies,
reason
spleen
two
the
were
tagged
with
the rate
at which
the transfused
fell rapidly
in
cells
that
of red-cell
Howell-Jolly
of
demonstrated
iron granules.33
subject
the siderocyte
of observation.
In
that
the
many
nuclei,
have
their
At intervals
The
count
period
transfused
show
spleen
without
absence
of
numerous:
red
the
anemia
of the red
of siderocytes
splenectomized
the 24-hour
studies
be more
the
spleen
If it did,
transfusions
toward
these
after the
blood
were
great
These
blood
count
nonspherocytic
The
improvement
Forty
per
proportion
with
a spleen.
In
elevated
throughout
In
hereditary
a spleen
and one without
(fig. 2).
chromium
so that
it was possible
they were destroyed
in the recipient’s
there
siderocyte
from
HOURS)
of
unchanged.
with
spleen
a high
one with
radioactive
the
removed
case.’5
granules.
result
in some
is no improvement.
anemia
the
Transfusion
of
were
in
is not
a spleen.
Decline
granules
(
TRANSFUSION
of
day.
splenectomy
this
Experiments
havior
of the
by
same
the
AFTER
presence
24
‘
24
by
remained
case
was
their
were
them.
are
bodies,
radioremoved
apt
to
malarial
this
difference
is
not
be specific
not
for
siderocytes.
The
final
normal
function
of the
spleen
relative
to erythrocytes
is to destroy
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406
WILLIAM
CROSBY
H.
3
z
Ui
Ui
-I
aU)
NORMAL
RANGE
II
I
Ui
AVERAGE
1
1
2
4
DURATION
Fir..
3.-Effect
atrophy
of hemorrhage
develops
them
(luring
when
and
they
reach
Robertson34
mentation,
on
prolonged
they
formation
of stromal
red cell.
represents
Even
after
a reparative
Activity
of the
the
the
worn-out
is the
enzyme
systems
of the
Finch39
red
porated
into
iron,
so that
needed
the
was
has
cells.
red
any
and
red
found
When
cells.
iron
to be
the
red
cells
is
be
were
finally
Many
were
of the
this
the
cell
ago
Rous
destroyed
by
frag-
in the
spleen.
systems
decays36
and
also declines.
and the surface
that
the
at the
the
The
area
given
of
site
destroyed,
spleen
The
in the
presumaging
cell
increases.
is the
radioactive
element
an excess
hemoglobin
of red
almost
cell
all
to
the
graveyard
was
incor-
of nonradioactive
would
not
destruction.
of the
be
When
radioactivity
spleen.
deprived
of
this
hemolytic
function,
of deLangen’s
rabbits.4#{176} Each
day
enough
to keep
them
moderately
producing
or other
deficiency
years
enzyme
prosper.
Consider
the case
these
animals
were
bled
iron
Splenic
continues,35
and it probably
integrity
of the cell’s surface.
gradually
iron
Fe5#{176}
and
stored
1943”).
fragile38
and hence
more
susceptible
old red cells are finally
destroyed
in
isotopic
given
would
in the
spleen
of one
Then
the dogs
were
released
by degradation
therefore
radioactive
with
were
Lagen,
accumulated
to repair
the stroma
the stroma
relaxes
shown
Dogs
( de
cycle.
cells
fragments
The cell becomes
brittle,
mechanically
fragmentation.
The fragments
of the
of the
life
red
function
( MONTHS)
hemorrhage.
cell loses its nucleus
process
that maintains
ably
the enzymatic
ability
grows
thinner37;
apparently
spleen.
spleen
to
of a normal
lipids
4
of rabbit
dime
the
2
BLEEDINGS
that
that
10
DAILY
end
found
the
weight
anemia
proposed
and
OF
GM
f
I#{149}P
8
6
0.3
malnutrition.
On
this
it
seems
for many
anemic
regimen
their
not
months
without
spleens
to
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
SPLENIC
FUNCTION
became
atrophic
it is possible
of the
tion
AND
(fig.
to
red
3)
The
die
of the
because
of old
would
407
CELLS
pathogenesis
that,
would
spleen
BLOOD
.
compute
cells
of the
RED
be
of the
age.
almost
In
atrophy
bleeding,
such
an
is not
less
known,
than
animal
the
one
but
per
cent
hemolytic
func-
nonexistent.
SUMMARY
During
all
function.
(2
red
)
the
stages
Eight
of
of these
a red
cell’s
functions
the
turnover
red
and
(7 )
storage;
the
normal
been
an effect
upon
red cell production;
(3
cell surface;
(4 ) the reservoir
function;
iron
spleen
)
an
effect
the
a normal
erythropoiesis;
upon
maturation
“culling
function”;
(5 )
“pitting
exerts
(1)
considered:
(8 )
function”;
of the
(6)
destruction
of old
cells.
SUMMARIO
In
omne
le stadios
normalmente
(2 )
del
de
erythrocytos
de
es
(4 )
de
effecto
ferro;
e
(8 )
exerce
Erythropoiesis;
super
le matura-
( 5 ) elimination
( 7 ) “excision”
reservoir;
de
perfecte;
es normal
(1 )
(3 )
rob
metabolismo
alteremente
que
discutite:
erythrocytos;
(6 )
erythrocytos
le splen
tales
erythrocytos;
imperfecte;
ab
INTERLINGUA
erythrocyto,
Octo
le production
superficie
particulas
vita
IN
functiones.
super
del
rocytos
del
certe
effecto
lion
de
life
have
destruction
de
de
eryth-
ancian.
REFERENCES
1. Eppinger,
2.
H.:
Chauffard,
Zur
Paris 24:1201,
3.
Dameshek,
4.
-:
5.
Knutti,
W.
R.
Huff,
rats.
L.,
\Veinent,
den
Milz
Ono,
K.:
10.
Perla,
11.
Jacobson,
12.
Ford,
The
0.:
B.:
en ist,
was
en nicht
Med.
31:113,
Bantonella
50:1572,
Bull.
Klinische
die
enythnopoetische
\Tan
168:827,
1913.
Soc.
med.
Hop.
in
hacmat.
3:64,
1955.
splenectomized
bile
fistula
und
experimentelle
Untensuchungen
Tatigkeit
des
#{252}ber
Knochenmarks.
Berl.
Dyke,
I).
Anat.
C.:
K.:
Nature
of
Surgically
exchange
induced
in
parabiotic
splenogenic
anaemia
1951.
uber
Mikr.
ist. Bibi.
1955.
incidence
A.:
and
die
Entwicklung
10:573,
regeneration
L.
\Vchnschr.
Vaquez.
Acad.
161:56,
1950.
R. N. and Salomon,
Physiol.
U.
D.:
NI.
1914.
R.
Untersuchungen
Zellborsch.
kIm.
de
1935.
auf
51:1026,
8. Altman,
K. I., Watman,
in the rabbit.
Nature
9.
W.
Trantman,
J.
Am.
York
61:115,
and
Wchnschr.
R.
New
Hawkins,
Med.
Einfiuss
kim.
7.
Berl.
communication
Was
Bull.
and
H.
den
la
1907.
Exper.
Hirschfeld,
de
: Hypersplenismus.
E.
J.
den NIilzfunktion.
propos
Hypersplenism.
dogs.
6.
pathologie
M. : A
of autoplastic
Hematopoictic
den
menschlicher
Milz.
Ztschr.
f.
1930.
splenic
responses
to
transplants.
radiation
Am.
injury.
j. Path.
Ann.
12:665,
Rev.
Med.
1936.
7:345,
1956.
C.
E.,
fication
13.
Hamenton,
of
Ferrata,
A.
and
aplastiche.
14.
Crosby,
Am.
15.
-:
L.,
W.
H.:
Hereditary
E.
Barnes,
Fieschi,
The
A.:
Risultati
metabolism
Frenzel,
Klin.
Wchnschr.
B.:
of
H.
and
della
and
Cytological
splenectomia
nellen
anemia.
bile
pigmicnt
in
Blood
5:233,
1950.
Knochenmankhemmung.
1938.
F.:
identimielosi
1941.
hemoglobin
hemolytic
J.
Loutit,
1956.
e insegnamenti
Splenogene
17:1315,
W.
177:452,
23:979,
Arch.
18:112,
1955.
nonspherocytic
and
D.
Nature
Haematologica
J. Med.
16. Bock, H.
Beweis).
J.
radiation-chimaenas.
hemolytic
(Tierexpenimenteller
disease.
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
408
17.
WILLIAM
Campbell,
D.
18. Singer,
tomy
in man
Kreuter,
Crosby,
21.
Miller,
das
W.
B.,
24.
Ebert,
Banti,
and
of
Semaine
Clark,
E.
R.
and
Crosby,
38:41,
W.
and
Wyllie,
cells).
1914.
Blood
\V.
A.
Sheldon,
C.,
Crosby,
H.:
Rous,
W.
and
healthy
K.
stromna
I.,
of
Allison,
A.
K.
J.
Exper.
Finch,
C.
Finch,
Blood
Langen,
cells
Biol.
&
J.
Expen.
R.
and
Burn,
Bnit.
J.
no
reserves
de
Ia rate
erythrocytes:
seen
in
of
dans
their
living
blood
l’h#{233}mo-
removal
amphibian
of hemoglobin
by
Am.
larvae.
synthesis
dans
la
sph#{233}rocytose
in hereditary
h#{233}r#{233}ditaire.Rev.
to
various
Barlow,
lung;).
tile
Autoimmune
correlations.
spleen.
The
Blood
normal
fate
25:651,
1917.
and
Salomon,
K.:
Arch.
Biochem.
33:168,
N.
C.
P.:
circulation
of the
types
of
and
hemolytic
associated
J.
anemia.
Enzyme
Idiopathic
pulmonary
haemo17:25,
1948.
hemolytic
anemia.
II. Morphologic
Am. J. Path.
33:429,
1957.
12:165,
1957.
A.:
J.
Quart.
of
erythnocytes.
Incorporation
activity
Med.
I.
of
a-C’4
The
findings
acetate
in
the
into
1951.
as
a
fimnction
1955.
life cycle of the enythrocyte
and target
cell formation.
of
age
in
the
human
1:291,
J.
Stewart,
and
of
Med.
L.: The
hemolysis
Hegsted,
J. J. : A study
of the
Sung.
140:266,
1954.
significance
of hemoglobinemia
M.
the
H.:
Haemat.
mechanical
Med.
91:147,
C.
Bodiani,
erythnocyte.
B.,
5:983,
le role
extruded
as
reference
and
0.
and
S. and
man
Ann.
W. : The
Siderocytes
Watman,
A.,
normal
1951.
Robertson,
C.
W.
in
Chang,
mouse.
particular
V.,
Singer,
K. and Weisz,
problems
of splenic
osmotic
of
rouges
and
induration
Crosby,
V. H.:
clinico-pathologic
and
and
tile
erythrocyte.
Stewart,
target
Exper.
J. Haemat.
4:344,
1958.
Function.
London,
Cambridge
Brit.
that
fate
brown
animals.
Altman,
Soc.
1941.
globules
living
38:829,
(essential
34.
cells.
phagocytes,
des
of the
Med.
P.
of
Proc.
Med.
vie
Parpant,
& Clin.
33.
red
J. H. : The limit
13:273,
1952.
J.
Am.
with
H.
1943.
43:796,
production
circulation.
anh#{233}mopoi#{233}tique;
L. : The
‘iv. H. and Danieshek,
Crosby,
de
Milzexstirpation
( target
leptocytes
of Physiological
201:655,
tissue
Akeroyd,
spleen
Rappaport,
observations
40.
den
f. Chmrungie
1956.
0.,
the
32.
39.
lysolecithin.
1926.
H.
A.
in
siderosis
38.
splenec-
and
1913.
E.
A. : l)un#{233}ede
Whipple,
splenic
human
Sc.
and
anemia.
Schrumpf,
Lab.
37.
and
A. : Demonstration
Med.
Clark,
hemosideninunia,
36.
in
33:313,
capillaries
blood
35.
Einfluss
W. : Experimental
with
Architecture
E.
J.
med.
h#{233}mat.
11:140,
31.
Dameshek,
lipids
Stead,
Am.
hemolytic
30.
index
Gesellsch.
spherocytes
C. : Spl#{233}nom#{233}galie hemolytique
J. Anat.
29.
and
in the
1934.
Press,
V.
lymphatic
28.
den
deutsch.
of
interference
I. : Studies
mobilized.
lyse.
27.
following
hemolytic
1942.
J. : Features
R.
are
26.
K.
and
University
25.
iiber
Verhandle
pathogenesis
Singer,
49:42,
J.
Munn,
changes
cells,
1952.
Med.
Barcroft,
to target
Untensuchungen
Blutbild.
splenectomy
22.
observations.
W. : Hematologic
reference
CROSBY
1941.
202:171,
H. : The
E.
23.
H. : Unpublished
Dameshek,
particular
periphere
7:261,
by
W.
E. : Expenimentelle
auf
20.
Crosby,
E. B. and
with
J. M. Sc.
Am.
19.
and
K., Miller,
H.
M.,
Izzo,
fragility
M.
of dog
J.
and
Am.
Young,
enythrocytes
after splenectomy
and the
J. M. Sc. 210:301,
1945.
L.
E.:
tagged
Age
with
as
the
affecting
radioactive
iron.
1950.
M.,
Fluharty,
Kinney,
R.
G.:
T.
Iron
D.,
Thomas,
metabolism.
E.
The
I).,
Rath,
pathophysiology
C.
E.,
of
Haskins,
iron
D.,
storage.
1950.
D.:
Function
of
the
spleen
and
blood.
Acta
med.
scandinav.
115:271,
From www.bloodjournal.org by guest on June 16, 2017. For personal use only.
1959 14: 399-408
Normal Functions of the Spleen Relative to Red Blood Cells: A Review
WILLIAM H. CROSBY
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