Mechanisms of Fluid and Electrolyte Retention

in Experimental Preparations in Dogs

II. With Thoracic Inferior Vena Cava Constriction
By JAMES 0. DAVIS, P H . D . , M.D., AND DAVID S. HOWELL, M.D.

Cardiovascular and renal hemodynamic function, nitrogen, electrolyte, and water balances, and
circulating eosinophils have been studied before and during the formation of aseites produced
by thoracic inferior caval constriction. The data show a striking decrease in the renal and fecal
excretion of sodium (Na) and an elevation in fecal potassium (K) output. An analysis of pos-
sible factors which might effect the reduction in renal Na excretion demonstrates that neither
a low cardiac output nor a depressed glomerular filtration rate is the primary factor.

T
HE PRESENT STUDY is concerned were made after the meal to determine whether
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with the renal mechanisms of salt and
water retention during the formation of
experimental ascites. In animals exhibiting
chronic fluid retention, the extracellular fluid
volume expands as a result of more complete
reabsorption of sodium by the kidney tubules.1"4
In this important respect, dogs with experi-
mental ascites1"7 are similar to patients with
cardiac failure8"10 and decompensated hepatic
cirrhosis.11 Study of the mechanisms involved
in such animals may provide information
pertinent to the retention of fluid and electro-
lytes in clinical states.
Previous study of acute and chronic experi-
mental pericarditis2 failed to suggest a direct
effect of venous hypertension on the kidney or
to indicate a correlation between the rate of
glomerular filtration and electrolyte excretion.
Alterations in electrolyte balances and the
low Xa and high K pattern of fecal electrolyte
excretion during acute and chronic peri-
carditis suggested altered adrenocortical func-
tion.
In addition to the factors studied in experi-
mental pericarditis,2 the present report includes
data on the relation of cardiac output and
postprandial glomerular filtration rate (GFR)
to salt retention during ascites formation.
Measurements of glomerular filtration rate
From the Laboratory of Kidney and Electrolyte
Metabolism, National Heart Institute, National
Institutes of Health, Public Health Service, Federal
Security Agency, Bcthesda, Md.
Received for publication Doc. 1, 1952.
171
the increase from the postabsorptive to the
postprandial level is as great and lasts as long
in dogs accumulating ascites as in the normal
dog. These data are important because the
daily peak of salt excretion occurs during the
postprandial increase in GFR in the normal
dog2' 12 whereas Na excretion is very low in the
postprandial state. Eosinophil counts were
made in an attempt to further the evaluation
of adrenocortical function. Water exchange
and the response to a water load have also
been measured.
METHODS
Ascites was produced in trained female mongrel
dogs by constriction of the thoracic inferior vena
cava to one-third to two-thirds its original diameter.
Cardiac output was measured by the direct Fick
procedure in unanesthetized dogs in the postabsorp-
tive state. Oxygen consumption was determined
with a Blaloek dog mask attached to a Tissot
spirometer. Expired air was collected for a four-
minute period and analyzed in duplicate for the
percentage of oxygen and carbon dioxide with a
Haldane apparatus. Mixed venous blood was ob-
tained from the right ventricle by passing a poly-
thene catheter through a no. 15 needle via the
external jugular vein. Arterial blood samples were
obtained by direct puncture of the femoral artery.
Blood samples were drawn under oil into heparinized
syringes, and oxygen content was determined in
duplicate by the manometric method of Van Slvke
and Neill. External jugular and femoral venous
pressures were measured with a saline manometer;
all other pressure measurements were made with a
Statham strain gauge and a D'Arsonval galvanom-
eter.
Circulation Research, Volume I, March 195$
 172 FLUID AND ELECTROLYTE RETEiYTION

Total peripheral resistance was calculated from The dogs were kept in metabolic cages except at
the formula, the end of each hour when urine and blood samples
were obtained; water was allowed ad libitum.
PM X 980 X 13.6
T The three-hour renal excretory response to a
Vt
gastric or intravenous water load was determined
where Pm denotes mean arterial pressure in mm. Hg in the postabsorptive state. Water (-10 cc. per
and Vt - cardiac output in cubic centimeters per kilogram) was given by stomach tulie; gastric.

4.0 DOG # 5
CARDIAC OUTPUT
(L./MIN.) 3,5

3.0
• :. •

t
,
c
U n
LJ
CR 70 •230
AND •200
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C
PAH" 60
(CC./MIN.) : I7O

PLASMA PROTEIN 8.0 7.9 7.0 5.0 3.8 6.9

(GM.%)
FEMORAL

U L
OAA
VENOUS PRESSURE C\J\J
(MM. WATER) 100 •

FEMORAL 150
ARTERIAL (-•-)
AND RIGHT 100
VENTRICULAR(—)
PRESSURES 50
(MM. HG.)
0

27
BODY WEIGHT •

(KG.) 25 -

23 -
i
3 I 2 NO-HIGH
ASCITIC FLUID •

THORACIC
REMOVED (L.) 2 PROTEIN DIET
IVC CONSTRICTION
1
25 30 5 10 159 2 0 301 5 10 15 20 25 30 5 10 15
MARCH APRIL MAY JUNE JULY
FIG. 1. Cardiovascular and renal hemodynamic function after thoracic inferior caval constriction. Ascites
failed to develop following the first constriction so the ligature was tightened at a second operation. Experimental
values are plotted above and below horizontal lines which represent the average of three control determinations.
Femoral arterial and right ventricular pulse pressures are indicated by the stippled areas.

second. Mean femoral arterial pressure was calcu-
lated from the pressure curve by integration.
Postabsorptive measurements of GFR and renal
plasma flow (RPF) were made by determining the
clearance of creatinine (COR) and para-aniino-
hippurate (CPAH) respectively by use of a constant
infusion of CR and PAH in normal saline at a rate
of approximately 0.3 cc. per minute. For the post-
prandial studies, GFR was estimated hourly for 8
to 12 hours after the meal; CCR was determined
following a single subcutaneous injection of CR.
drainage was performed 40 minutes after water
administration to determine the completeness of
absorption. The volume of unabsorbed water was
measured and the fluid was replaced immediately.
For the intravenous water test 25 cc. per kilogram of
water were infused during a 40-minute period.
For the eosinophil counts, a mixture of propylene
glycol and phloxine was used in the proportions
suggested by Speirs and Meyer." All other ex-
perimental procedures and chemical methods have
been described elsewhere.1
 JAMES 0. DAVIS AND DAVID S. HOWELL 173

The dogs were fed a synthetic diet containing SO
Cal. per kilogram per day, 0.2 Gin. per kilogram per
day of nitrogen, and 4 mEq. per kilogram per day
of Na during the control interval and during the
experimental period until protein depletion was
T-1S24 dye space were conducted in dogs 1 to 3.
Eosinophils were counted in dogs 2 to 6. Water
exchange and the response to a water load were
determined in a group of normal dogs as well as in
clogs 1 to 10.

DOG #1 THORACIC IVC CONSTRICTION

r 55
CR' 50 • • 1
(CC./MIN.) 45
40 ; 1
11
11
C 1 I
PAH 125
(CC./MIN.) IOO

. . .11
45
FF
1 1 1
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33
1 • .
70
PLASMA __
PROTEIN 53
(GM.%) ^

BALANCE
(GM./DAY) +6

FEM0RAL(-*-)l25
VP
0
+3

+9
E.J.(~)AN D 200
ti" ft!

— —
w mmm •

(MM. WATER) 5 0
1
— • — •

FEMORAL 200
ARTERIAL 150
PRESSURE l 00
0
(MM.HG.) °
ASCITIC FLUID , N-10.8 N-18.5
REMOVED % '.
(U
(N-GM.)
f
0
5
| ASCITES N-6.0
OPERATION
1
10 15 20 25 30 5 10 15 20 25 30 4
1
9 14
N-7.0N-69
II 1 1 1I1 1
19 24
NOVEMBER DECEMBER JANUARY
FIG. 2. The effect of thoracic inferior vena cava constriction on renal function, protein metabolism, and cardio-
vascular pressures. Values for CCH, CPAH, FF, and plasma protein are plotted as solid columns above or below a.
line which represents the average control value. Seefigure4 for the convention used in plotting X balance. The
stippled areas indicate the variation in systolic and diastolic arterial pressures with respiration. E. J. and V. P.
represent external jugular and venous pressure respectively. Ascitic fluid N is not included in the plot of N
balance but total N removed by paracentesis is shown above the columns for ascitic fluid.

established. A high protein and a low salt diet was RESULTS

given to effect protein repletion.
Different clogs were used for different aspects of
the study. In dogs 1 to 5, postabsorptive measure-
ments of GFR, RPF, plasma Na, and plasma pro-
tein were made. GFR and Na excretion were deter-
mined in the postprandial state in clogs 4 and 5.
Determinations of cardiac output and intracardiac
pressures were made in dogs 5 and 6; femoral
venous and arterial pressures were measured in
dogs .1, 2, 3, 5, and 6. Studies of metabolic balances,
plasma K and chloride (Cl), hematocrit, and
Cardiovascular Hemodynamics. Following
constriction of the thoracic inferior vena cava,
femoral venous pressure increased 10 to 15 cm.
of water above the control level and ascites
developed (figs. 1 and 2). External jugular,
right auricular, and right ventricular pressures
were not appreciably altered. A reduction in
systolic and pulse pressures occurred in two
 174 FLUID AND ELECTROLYTE RETENTION
of the six animals (see fig. 2), but mean femoral
arterial pressure remained unchanged or in-
creased slightly. Cardiac output remained at
the control level after caval constriction in
dog 5 (fig. I) whereas a marked reduction
occurred in dog 6. In this animal, a second
operation was performed and the ligature
loosened to reduce the degree of constriction.
Subsequently, cardiac output and total periph-
eral resistance returned to the control level,
arterial pressure remained unchanged, and
of the average control value; FF remained
elevated. This fall in renal function occurred
concurrently with protein depletion which
resulted from removal of large quantities of
protein by abdominal paracentesis (figs. 1 and
2).
In order to test the hypothesis that reduced
renal function was the result of protein de-
pletion, a low salt and a high protein diet was
fed (figs. 1 to 3). On this regimen, protein
repletion was rapidly effected; CCR returned

No INTAKE i
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9 J-6CH-J
M.EQ./DAY \
100

No
/i.EQ./MIN.

PLASMA
PROTEIN
GM.%

CR
CC./MIN.

2 14 18 21 23 24 29 30 57 58 84 100 104 129

CONTROL PERIOD DURI-NG ACITES FORMATION

FIG. 3. Relation of postabsorptive and postprandial GFR to renal Na excretion (EN») before and during ascites
formation. Values for postabsorptive CCit are shown as adjacent black columns which are plotted above and
below the horizontal line representing the average of nine control periods. Hourly measurements of postprandial
CCH are shown by the open areas plotted from the same horizontal line; Na excretion during corresponding
periods is plotted as adjacent black columns. The vertical arrows which precede experimental values for KN,»
and postprandial CCH indicate the time of feeding. After protein repletion, Na intake was increased from 9 to
60 mEq. per day so that plasma Na and, consequently, the filtered load of Na returned to the control level or
above.

femoral venous pressure fell. However, venous
tension below the constriction remained suffi-
ciently high (10 cm. of water above the control
level) for the continued formation of ascites.
Postabsorptive Renal Clearances. During the
first 7 to 10 days following caval constriction,
GFR remained at the control level or increased
slightly while RPF fell (figs. 1 to 3); conse-
quently, filtration fraction (FF) was elevated.
After the initial phase, GFR fell 20 to 30
per cent below the control level and RPF
showed a further decline of 25 to 50 per cent
to the control level (dogs 1, 2, and 4) or above
(dog 3), and CPAH returned to the level ob-
served before the onset of protein depletion.
In dog 5 (fig. I), protein repletion was not
completely accomplished, and renal function
failed to reach the control level. The results
suggest a causal relationship between protein
depletion and reduced renal function.
Relation of Postprandial GFR lo Na Ex-
cretion. In addition to the postabsorptive
measurements of renal function, GFR was
estimated for 8 to 12 hours after feeding; in
 JAMKS O. DAVIS AND DAVID S. HOW ELL 175

dogs 4 (fig. 3) and 5. To establish the pre-
prandial level of renal function, postabsorptive
measurements were made within a few days
of each group of postprandial determinations.
Before ctival constriction, GFR increased be-
tween 20 and 40 per cent after ingestion of
food and remained elevated for several hours
I I 1 I
in GFR which was similar in magnitude and
duration to that observed during the control
period; however, postprandial Na excretion
was never greater than 5 ^Eq. per minute.
In dog 4, protein depletion was accompanied
by a fall in postprandial as well as post-
absorptive GFR and subsequent repletion
\ I I I [ I I I I

DOG #1 THORACIC IVC CONSTRICTION

C :
CR
(CC./MIN.) 50
40

0
Downloaded from http://circres.ahajournals.org/ by guest on January 22, 2018

No
BALANCE 30
(M.EQ./DAY)
60

Cl
BALANCE 30
(M.EQ./DAY)
60
K 0
BALANCE
(M.EQ./DAY) 10

20,
WATER of
EXCHANGE
(L)

BODY
18
WEIGHT 16
(KG.)
14
ASCITIC 3
FLUID 2 ( ASCITES I
REMOVED
(L)
I
0
OPERATION
i i
31 5 10 15 20 25
i
I
i 11
30 5 10 15
I
I • I20 25 30 4 9 14 19 24
NOVEMBER DECEMBER JANUARY
FIG. 4. Changes in Ccit, metabolic balances, and body weight following constriction of the thoracic inferior
vena cava. The convention for the plot of the balance data is as follows: (1) intake was plotted downward from
the zero line, (2) output was plotted upward from intake line, (3) solid bUick areas represent total balance, and
(-1) cross hatched ureas indicate fecal electrolyte excretion. Consequently, solid black area above the zero line
indicates negative balance and black area below the zero line represents positive balance. Fecal Na excretion
was too low to plot during ascitcs formation and ascitic fluid elcctroU'tcs are not included in plots of balance
data.

(fig. 3). Na excretion increased from the
postabsorptive level of 5 to 10 nE(\. per minute
to as high as 100 ^Eq. per minute after the
meal (fig. 3).
During the immediate postoperative period
and after protein repletion, ascites formation
was accompanied by a postprandial increase
resulted in a rise in GFR both before and after
feeding. In dog 5, both postabsorptive and
postprandial values for GFR decreased during
protein depletion and Na excretion following
the meal was as low as in dog 4. As in the case
of the postabsorptive measurements, post-
prandial GFR failed to return to the control
 170 FLUID AND ELECTROLYTE RETENTION

level in dog 5 because protein repletion was
not complete.
Metabolic Balances, Plasma Electrolytes,
Water Metabolism, Hemoglobin, Hematocrit,
T-1824 Dye Space, and Eosinophil Counts.
Na, Cl, and water balances were markedly
positive following caval constriction (fig. 4).
Since surgical trauma results in alterations in
electrolyte and nitrogen (N) balances, changes
seen before the appearance of ascites may have
day; during ascites formation fecal Na output
was never above 2.0 mEq. per day (dogs 1 to 3).
Urinary K excretion was reduced whereas a
marked elevation in fecal K output occurred
(fig. 4); total K balance was positive. Plasma
K was slightly elevated throughout the experi-
mental period. Calculations showed no evidence
for movement of Na into the intracellular
compartment and K into the extracellular
space. Changes in Cl balance occurred at the

c
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0
o
so-

URINE _°___? _
OUTPUT so •»- r --J

(CC./KG./DAY) * * a
I
10

100 >
RESPONSE - * - * •
TO WATER 75
LOAD (%) 8 o
50 b ° _
\}
25[r
DOG A B C D E F , , I 2 3 4 5> 7 8
NORMAL EXPERIMENTAL
Ki(i. 5. Daily urine output and the three-hour renal excretory response to a water load administered by
stomach tube in normal clogs and in dogs with ascites. The values for urine output are the average for sev-
eral weeks. Solid symbols represent values obtained in normal dogs while open circles show results dur-
ing aseites formation. The broken horizontal lines have been drawn to emphasize the lack of overlapping
between open and solid symbols

been partially related to the effect of the
surgical procedure. After ascites appeared,
the peritoneal cavity served as the principal
depot for retained fluid and electrolytes (fig.
4), and renal tubular reabsorption of Xa was
almost complete throughout the experimental
period.
Although the principal reduction in Na
excretion was renal, fecal Na output was also
decreased (fig. 4). Control values for fecal
Na excretion ranged from 4.5 to 8.5 mEq. per
same time and in the same direction as altera-
tions in Na balance.
Water exchange was increased following
caval constriction (fig. 5) although water
balance was always positive and isotonicity of
body fluids was maintained during normal
Na intake. (4 mEq. per kilogram per day)
On a low Na diet (.5 mEq. per kilogram per
day), plasma Na consistently declined to
levels of 130 to 135 mEq. per liter. The three-
hour renal excretory response to a gastric
 JAMES 0. DAVIS AND DAVID S. HOWELL
water load of 40 cc. per kilogram was impaired
(fig. 5). Normal dogs excreted 80 to 95 per cent
of administered water but dogs with ascites
excreted only 40 to 65 per cent of the water
load. Part of this delay in excretion may be
related to incomplete absorption since 17 to
37 per cent of the water load was recovered
by gastric drainage performed 40 piinutes
after water administration. However, a defect
in excretion was present since only 28 to 62
per cent of the intravenous water load was
excreted.
Hemodilution occurred during the early
postoperative period; hemoglobin and hema-
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tocrit fell while an elevation in T-1824 dye
space occurred. Later in the course of the
experimental period, protein depletion re-
sulted; hemoglobin and hematocrit continued
to decline while T-1824 dye space remained
unchanged in dog 1 and increased 15 to 20
per cent in dogs 2 and 3.
Since the low Na and high K pattern of
fecal electrolyte excretion suggested an altera-
tion in adrenocortieal function, circulating
eosinophils were enumerated and N balance
was measured. A postoperative drop in eosin-
ophils occurred, but the number of circulating
eosinophils returned to the control level and
remained within normal range throughout the
period of ascites formation. The response to
epinephrine and adrenocorticotropic hormone
(ACTH) was not detectably altered during the
experimental period. N balance was positive
in the presence of adequate protein intake and
ascites accumulated regardless of the state of
protein metabolism (fig. 2).
DISCUSSION
Hepatic venous congestion appears to be
essential to the formation of ascitic fluid with
a high protein concentration. This type of
ascites is permanent unless hepatic venous
pressure declines.2' 5r 7 The necessity of a
congested liver or splanchnic area for ascites
formation is indicated by the finding that
partial ligation of the inferior vena cava below
the hepatic venous outflow produces hind leg
edema but no ascites.5> u These data and
personal observations that a transient ascites
with a low protein concentration follows con-
177
striction of the hepatic portal vein implicate
the liver rather than the splanchnic area.
Of vital importance in the pathogenesis of
ascites is the retention of salt and water by
the kidney. The extracellular fluid volume
expands as a result of more complete renal
tubular reabsorption of Na and water. The
factors effecting this alteration in renal tubular
transport of Na have not been defined. A
direct effect of elevated venous pressure on the
kidney has been ruled out by the results of
Volwiler and co-workers5 and Hwang and
associates14 who failed to obtain chronic fluid
retention following constriction of the ab-
dominal inferior vena cava superior to the
renal veins. The possible influence of adrenal
venous congestion has also been excluded by
placing an abdominal caval ligature superior
to the adrenal venous tributaries (personal
observations).
The observations reported show that the
formation of ascites is not related to a drop in
cardiac output. Ascitic fluid formed in dog 5 in
which cardiac output remained unchanged.
In case 6 in which cardiac output was initially
reduced, ascites continued to accumulate after
the ligature was loosened although cardiac
output returned to the control level.
Extensive measurements of GFR demon-
strate that a reduction in GFR is not the
primary factor leading to salt retention.
Values for postabsorptive and postprandial
GFR were observed at the control level or
above in the presence of almost complete Na
retention. It should be emphasized that under
the present circumstance of alterations in
protein metabolism, measurements of post-
absorptive GFR provided a satisfactory index
to changes in postprandial GFR.
In an attempt to further the evaluation of
adrenocortieal activity, circulating eosinophils
were counted. While an eosinopenic response
is no longer considered definitive evidence of
adrenocorticotropic activity, the negative
findings failed to indicate increased adreno-
cortieal hormone secretion from stimulation of
the adrenal cortex by ACTH. Additional ob-
servations are needed to clarify the relation of
the adrenal cortex to the pathogenesis of
ascites.
 178 FLUID AND ELECTROLYTE RETENTION
SUMMARY AND CONCLUSIONS
1. Following constriction of the thoracic
inferior vena cava, femoral venous pressure
became elevated and ascites appeared. Cardiac
output remained at the control level or de-
creased but no correlation between the level
of cardiac output and salt retention was ob-
served.
2. During the early part of the experimental
period, both the postabsorptive and post-
prandial rate of glomerular filtration remained
unchanged or increased whereas RPF de-
creased. Later, during protein depletion, post-
absorptive and postprandial GFR fell below
the control levels and RPF showed a further
Downloaded from http://circres.ahajournals.org/ by guest on January 22, 2018
decline. Renal function was restored during
protein repletion. These findings suggest a
causal relationship between protein depletion
and reduced renal function.
3. Marked Na retention occurred while
postabsorptive and postprandial GFR was at
the control level or above. This evidence
demonstrates that a mechanism other than a
low GFR was operative.
4. A striking reduction in fecal Na and
urinary K excretion occurred; fecal K output
was elevated.
5. The number of circulating eosinophils
was not detectably altered.
6. Water exchange was increased whereas
the renal excretory response to a water load
was reduced.
ACKNOWLEDGMENTS
We are indebted to Dr. Robert \V. Bei-liner for
suggestions and criticisms during the study and to
Dr. James L. Southworth and Alfred Casper for
performing the surgery. Vicla Slawson, Karen
Lundegiiiird, Jeanne Brown and James Burch
rendered technical assistance.
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2 14
DAVIS, J. 0., LINDSAY, A. E., AND SOUTHWORTH,
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STAMLER, J., GOLDBERG, H., GORDON, A., WEIN-
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SCHILLING, J. A., MCCOOKD, A. B., CLAUSEN,
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 Mechanisms of Fluid and Electrolyte Retention in Experimental Preparations in Dogs: II.
With Thoracic Inferior Vena Cava Constriction
JAMES O. DAVIS and DAVID S. HOWELL

Circ Res. 1953;1:171-178

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doi: 10.1161/01.RES.1.2.171
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Copyright © 1953 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7330. Online ISSN: 1524-4571

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