Vol. 275, Issue 6, R1878-R1884, December 1998
Dynamics of extracellular fluid volume changes during
hyperproteinemia
R. Davis
Manning Jr.
Department of Physiology and Biophysics, University of Mississippi
Medical Center, Jackson, Mississippi 39216-4505
 |
ABSTRACT |
The dynamics of fluid volume distribution
between the blood and interstitium during hyperproteinemia were studied
in 12 anephric, conscious dogs during several states of hydration.
After recovery from splenectomy and unilateral nephrectomy, plasma
protein concentration was elevated to 8.4-8.7 g/dl by daily
intravenous infusion of 330 ml of previously collected autologous
plasma for 11 days. The remaining kidney was then removed, and the next
day lactated Ringer solution equivalent to 10 or 20% of body weight
was infused intravenously. By the end of the 25-h postinfusion period,
Ringer infusion had increased circulating protein mass 20.9 ± 9.1%
(mean ± SE) in the 10% group (P < 0.05) and decreased it 10.5 ± 3.3% in the 20% group
(P < 0.05). The average increase in
blood volume and arterial pressure during the postinfusion period was
27.4 ± 2.5 and 20.7 ± 3.7%, respectively, in the 10% group
but only 17.8 ± 2.4 and 12 ± 1.6% in the 20% group (all
changes significant compared with respective control). The
relationship between blood volume and sodium space was similar to that
found during normoproteinemia, such that elevations in sodium space of
40-50% increased blood volume but greater elevations in sodium
space caused no further increases in blood volume. Overhydration during
chronic hyperproteinemia causes hypervolemia and hypertension, but, in
contrast to those in short-term studies, the increases in blood volume
and arterial pressure are not greater than those achieved during normoproteinemia.
blood volume; arterial pressure; interstitial protein; plasma
protein concentration; plasma colloid osmotic pressure
| |
INTRODUCTION |
ALTHOUGH HYPERPROTEINEMIA has been shown to occur in
several pathological conditions, including multiple myeloma,
sarcoidosis, lymphogranuloma, liver diseases, parasitic conditions, and
dehydration (2), few studies have been conducted on the factors
controlling the extracellular fluid volume in these conditions.
Short-term increases in plasma protein concentration or plasma colloid
osmotic pressure can cause large increases in blood volume and
decreases in interstitial fluid volume; however, it has been shown that chronic hyperproteinemia does not change blood volume or arterial pressure and increases interstitial fluid volume moderately (6, 8).
Therefore, the acute and chronic effects of hyperproteinemia on the
extracellular fluid volume are quite different.
Although much information has accrued on the effects of hypoproteinemia
on the extracellular fluid volume distribution and arterial pressure
(1, 7, 10), little is known about extracellular fluid volume
distribution in chronic hyperproteinemia and the resultant effects on
arterial pressure, especially during conditions of sodium and water
retention. A lack of understanding of factors influencing volume
distribution during hyperproteinemia has contributed to the
considerable controversy on whether crystalloid or colloid therapy is
best during volume resuscitation (4). It is not clear whether sodium
and water retention during hyperproteinemia will result in normal or
extremely marked increases in intravascular volume. Large increases in
blood volume could have serious hemodynamic consequences, resulting in
severe hypertension, pulmonary congestion, or pulmonary edema.
Therefore, the goal of this study was to examine the dynamics of
distribution of extracellular fluid volume and arterial pressure during
chronic hyperproteinemia and overhydration. Studies were performed in
anephric, conscious dogs which, before nephrectomy, were made
hyperproteinemic by daily intravenous infusion of previously collected
autologous plasma for 11 days.
| |
METHODS |
Animal preparation and experimental protocol.
Experiments were conducted on 12 conscious, anephric dogs with a mean
body weight of 27.1 ± 1.3 kg. The project had the approval of the
local Institutional Animal Committee. All dogs were splenectomized and
had chronic arterial and venous catheters implanted. During the first
surgical procedure, the spleen and the right kidney were removed
through a midline abdominal incision. Also at this time, chronic
catheters were implanted in the aorta and inferior vena cava through
the femoral artery and vein. Aseptic technique was used in all surgical
procedures, and atropine sulfate (1 ml of 0.4 mg/ml im; Elkins-Sinn,
Cherry Hill, NJ) was administered before surgery. Anesthesia was
induced with sodium thiopental (25 mg/kg iv Pentothal; Abbott, North
Chicago, IL) and was maintained with a mixture of methoxyflurane
(Penthrane, Abbott) and oxygen. Appropriate gas
concentrations were delivered to the dogs through an endotracheal tube
connected to an Ohio Medical Products anesthesia machine
(Kinet-O-Meter). The catheters were tunneled subcutaneously and exited
the back between the dog's shoulders for protection. During a 10- to
14-day period of recovery after surgery, the dogs were trained to lay
quietly in their cages. Water was provided ad libitum throughout the experiment.
Plasma was collected by plasmapheresis during the next 25 days for
later intravenous infusion. During the plasmapheresis procedure, 1,600 U of heparin (1.6 ml of 1,000 U/ml) were administered intravenously, and 250 ml of blood was allowed to flow unimpeded from the arterial catheter into a 300-ml transfer pack (Fenwal) into which 1,000 U of
heparin had been initially added. Next, the blood was centrifuged for 5 min and the plasma was removed, placed in another transfer pack, and
immediately frozen. A volume of lactated Ringer solution equal to the
volume of plasma removed was mixed with the remaining erythrocytes, and
the mixture was returned to the dogs by intravenous drip. On some days,
the procedure was repeated for collection of a second volume of plasma.
Over the 25-day plasmapheresis period, plasma was collected 26-28
times. After the plasmapheresis period was completed, a 17-day recovery
period was allowed before the beginning of the experiment.
During the experimental period, the plasma protein concentration of the
dogs was elevated over a 12-day period by infusing by intravenous drip,
in 1 h, ~330 ml of previously collected autologous plasma. On
day
11 of the plasma infusion, the dogs
were anesthetized as before and the remaining left kidney was removed
through a separate flank incision. The dogs recovered rapidly from the
surgery, because thiopental and methoxyflurane anesthesia were used.
During the morning after nephrectomy, a number of control measurements were taken for 3 h and ~330 ml of autologous plasma was intravenously infused. At the end of the 3-h period, lactated Ringer solution, warmed
to body temperature, was intravenously infused in the amount of 100 ml/kg in the 10% group and 200 ml/kg in the 20% group at an average
rate of 29.6 ± 0.6 ml/min. The anephric control group received no infusion.
During the plasma collection period, sodium intake was maintained at
~75 meq/day by feeding the dogs 894 g/day of P/D prescription diet
dog food (Hills Pet Products, Topeka, KS) to which 45 meq of sodium
chloride (5 M NaCl) was added. During the 12-day plasma infusion
period, sodium intake was maintained at 75 meq/day by intravenous
infusion of ~330 ml/day of previously collected autologous plasma,
which contained ~45 meq of sodium, and the dogs were fed 894 g/day of
P/D prescription diet dog food (Hills Pet Products) without any
additional sodium added to the food.
Experimental measurements and instrumentation.
The dogs were housed in metabolic cages and were fitted with a Statham
P23 AC or P23 ID transducer at the level of the heart. An infusion tube
and the transducer wires exited the dog pens through protective tubing.
The infusion tube was connected to a Sage model 375 A pump, which was
used to infuse the lactated Ringer solution. The transducer wires were
connected to a Grass model 7D recorder that was connected in turn to a
digital computer. Every minute throughout the day, the computer sampled
arterial pressure 500 times in a 3-s period and the average was stored on a computer disk (11). Central venous pressure was measured with a
Statham P23 BC transducer that was connected to the Grass recorder.
Venous pressures were determined while the dogs lay quietly in their cages.
Blood volume and sodium space were measured using the dilution
principle. Blood volume was measured by dilution of
51Cr-tagged red blood cells (NEN,
Boston, MA) (7, 8, 13). The red blood cells of a 20-ml sample were
tagged the day before the infusion day with 100 µCi of
51Cr (7, 8, 14). A 7-ml blood
sample was withdrawn through the arterial catheter for background
radioactivity determination. Then 10 ml of chromated red blood cells
and 2 ml (10 µCi) of 22Na (NEN)
were injected through the venous catheter. Blood samples of 7 ml were
drawn through the arterial catheter at 5, 20, and 40 min and 1, 2, 3, 4, and 5 h after the infusion to determine the dilution volumes. It was
assumed that no chromated red blood cells were lost from the
circulation during the control period in the first 5 h of the
experimental period. The validity of this assumption was confirmed by
the stability of the blood volume of the control group. Control values
of blood volume and sodium space were determined from the sample
withdrawn 3 h after injection (7, 8, 14). Overhydration was then
produced by infusing the lactated Ringer solution as previously stated.
Two hours after the conclusion of the infusion, 20 ml of blood was
withdrawn and the red blood cells were labeled with 200 µCi of
51Cr. Just after the 24-h
postinfusion sample, 10 ml of these cells were intravenously injected,
and 20 min and 1 h later, blood samples were withdrawn for
determination of blood volume. Regression lines relating blood and
sodium space were determined using the curve-fitting algorithm from
Sigma Plot (Jandell Scientific, Corte Madera, CA).
Plasma volume was calculated considering blood volume and large-vessel
hematocrit (7, 8, 13), and total intravascular protein mass was
calculated from the product of plasma volume and plasma protein
concentration. Plasma protein concentration was measured with an
American Optical (Buffalo, NY) refractometer.
Statistical analysis was performed by first determining overall
significance with a two-way ANOVA for repeated measures (3 groups and
time as the repeated measure). Second, if the two-way ANOVA showed
significant changes, significance of the individual experimental times
was determined with a one-way ANOVA. Post hoc analyses were performed
with Dunnett's test for multiple comparisons with a control (3). The
data were considered to be statistically significant if
P < 0.05. All data are expressed as
means ± SE.
| |
RESULTS |
Experiments have been performed examining the distribution of
extracellular fluid volume and the changes in arterial pressure during hyperproteinemia.
Plasma protein concentration responses to hyperproteinemia and
overhydration.
As shown in Fig. 1, after hyperproteinemia
was produced by daily intravenous infusion of autologous plasma for 12 days, plasma protein concentration averaged between 8.4 and 8.7 g/dl in
the anephric control group, the 10% group (which received 100 ml/kg infusion of lactated Ringer solution), and the 20% group (which received 200 ml/kg of lactated Ringer). The two-way repeated-measures ANOVA showed that the group × time interaction was significantly different for plasma protein concentration after the Ringer infusion (P < 0.0001). The average
postinfusion plasma protein concentration decreased markedly in both
the 10 and 20% groups (P < 0.05 for each group compared with control group); however, the average decrease
in plasma protein concentration was greater in the 20% group than in
the 10% group (P < 0.05). The
minimum value of plasma protein concentration was reached at 5 min
postinfusion and equaled 6.3 ± 0.1 g/dl in the 10% group
(P < 0.05 compared with respective control) and 5.9 ± 0.1 g/dl in the 20% group
(P < 0.05), and plasma protein
concentration in the anephric control group was not significantly changed at this time.
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Fig. 1.
Responses of plasma protein concentration (PPC) to intravenous infusion
of lactated (Lac) Ringer solution in conscious, anephric dogs during
hyperproteinemia. The 20% group received 200 ml/kg of
Ringer, 10% group received 100 ml/kg of Ringer, and anephric
control group received no infusion; n = 4 for each group. Data are means ± SE.
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Responses of blood volume to hyperproteinemia and overhydration.
As shown in Fig. 2, blood volume increased
in the 10 and 20% groups during lactated Ringer infusion. In the
anephric control group, blood volume did not change significantly
during the entire postinfusion period. The two-way repeated-measures
ANOVA showed that the group × time interaction was significantly
different for blood volume after the Ringer infusion
(P < 0.0001). In addition, blood
volume significantly increased in the 10% group during the 25-h
postinfusion period and averaged 127.4 ± 2.5% of control (P < 0.05 compared with control
group). In the 20% group, blood volume averaged 117.8 ± 2.4% of
control during the postinfusion period
(P < 0.05 compared with control
group). The average increase in blood volume in the 10% group was
significantly greater than that in the 20% group during the
postinfusion period.
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Fig. 2.
Responses of blood volume to intravenous infusion of lactated Ringer
solution in conscious, anephric dogs during hyperproteinemia. The 20%
group received 200 ml/kg of Ringer, 10% group received 100 ml/kg of
Ringer, and anephric control group received no infusion;
n = 4 for each group. Data are means ± SE.
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Responses of sodium space to hyperproteinemia and overhydration.
The two-way repeated-measures ANOVA showed that the group × time
interaction was significantly different for sodium space after the
Ringer infusion (P < 0.0001). Figure
3 shows that sodium space increased
significantly in both the 10 and 20% groups during the entire
postinfusion period (P < 0.05 compared with control group). The average postinfusion sodium space of
the 20% group was significantly greater than that of the 10% group.
The individual sodium spaces of the anephric control group did not
change significantly compared with the respective control throughout
the entire postinfusion period except for a small increase after 24 h.
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Fig. 3.
Responses of sodium space to intravenous infusion of lactated Ringer
solution in conscious, anephric dogs during hyperproteinemia. The 20%
group received 200 ml/kg of Ringer, 10% group received 100 ml/kg of
Ringer, and anephric control group received no infusion;
n = 4 for each group. Data are means ± SE.
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Responses of mean arterial pressure to hyperproteinemia and
overhydration.
Figure 4 shows that the individual arterial
pressures of the anephric control group did not significantly change
from the respective control value throughout the entire postinfusion
period. The two-way repeated-measures ANOVA showed that the group × time interaction was significantly different for mean arterial
pressure after the Ringer infusion (P < 0.02). Arterial pressure increased markedly in the 10% group after
lactated Ringer infusion and averaged 120.7 ± 3.7% of control
(P < 0.05 compared with control
group) during the entire postinfusion period. Arterial pressure also increased in the 20% group during lactated Ringer infusion and averaged 112 ± 1.6% of control (P < 0.05 compared with control group) during the entire postinfusion
period. The average difference in postinfusion arterial pressure in the
10 and 20% groups did not reach significance.
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Fig. 4.
Responses of mean arterial pressure (%control) to intravenous infusion
of lactated Ringer solution in conscious, anephric dogs during
hyperproteinemia. The 20% group received 200 ml/kg of Ringer, 10%
group received 100 ml/kg of Ringer, and anephric control group
received no infusion; n = 4 for each
group. Data are means ± SE.
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Circulating protein mass responses to hyperproteinemia and
overhydration.
As seen in Fig. 5, circulating protein mass
in the anephric control group did not change significantly throughout
the postinfusion period. The two-way repeated-measures ANOVA showed
that the group × time interaction was significantly different for
circulating protein mass after the Ringer infusion
(P < 0.0001). The average circulating protein mass of the 10 and 20% groups did not differ significantly from the control group, but the average postinfusion decrease in intravascular protein mass was greater in the 20% group
than in the 10% group (P < 0.05).
Figure 5 shows that the circulating protein mass in the 10% group did
not change significantly for the first 5 h of postinfusion; however, by
25 h postinfusion, the circulating protein mass increased 20.9 ± 9.1% (P < 0.05 compared with
respective control). In the 20% group, by 25 h postinfusion, circulating protein mass had decreased 10.5 ± 3.3%
(P < 0.05 compared with respective
control).
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Fig. 5.
Responses of circulating (Circ) protein mass (%control) to intravenous
infusion of lactated Ringer solution in conscious, anephric dogs during
hyperproteinemia. The 20% group received 200 ml/kg of Ringer, 10%
group received 100 ml/kg of Ringer, and anephric control group received
no infusion; n = 4 for each group.
Data are means ± SE.
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Central venous pressure responses to hyperproteinemia and
overhydration.
The two-way repeated-measures ANOVA showed that the group × time
interaction was significantly different for central venous pressure
after the Ringer infusion (P < 0.002). Figure 6 shows that after lactated
Ringer infusion, the average postinfusion central venous pressure
increased in the 20% group (P < 0.05 compared with control group) but not in the 10% group. The
average postinfusion difference in venous pressures in the 10 and 20%
groups did not reach significance. Central venous pressure of the
anephric control group did not significantly change during the entire
postinfusion period. However, individual central venous pressures of
the 10 and 20% groups were increased significantly throughout the 25-h postinfusion period compared with their respective controls.
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Fig. 6.
Responses of central venous pressure to intravenous infusion of
lactated Ringer solution in conscious, anephric dogs during
hyperproteinemia. The 20% group received 200 ml/kg of Ringer, 10%
group received 100 ml/kg of Ringer, and anephric control group received
no infusion; n = 4 for each group.
Data are means ± SE.
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Distribution of extracellular fluid volume during normoproteinemia
and hyperproteinemia.
Figure 7 illustrates the changes in the
relationship between sodium space and blood volume during
normoproteinemia and when plasma protein concentration was chronically
increased. Data plotted are paired sodium spaces and blood volumes
during the first 5 h of the postinfusion period for groups that
received 10 and 20% of their body weight of lactated Ringer solution
and had either normal or high plasma protein concentration. The normal
plasma protein concentration curve in Fig. 7 (9) shows that blood volume increased as sodium space increased as long as the sodium space
was elevated <40-50%. Greater expansions of extracellular fluid
volume resulted in no further increases in blood volume. The high
plasma protein concentration curve is very similar to that of the
normal plasma protein concentration curve and also shows that increases
in sodium space >40-50% resulted in no further increases in
blood volume. Also, for an unexplained reason, the individual sodium
spaces of the high protein group, as seen in Fig. 7, lay
within a narrower range than those in the normal protein group.
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Fig. 7.
Relationship between sodium space and blood volume in dogs with normal
(A) and high
(B) PPC. Data for normal-PPC group
are included for comparison (9).
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The regression of the normal plasma protein concentration curve is
blood volume is 
284.7 + 7.320 (sodium space) 4.404 × 10
2 (sodium
space)2 + 8.915 × 105 (sodium
space)3,
r2 = 0.68. The
high plasma protein concentration curve is blood volume is
1,217 + 28.34 (sodium space) 0.1977 (sodium
space)2 + 4.544 × 104 (sodium
space)3,
r2 = 0.639. The
plateaus of the two curves were statistically compared (in terms of
blood volumes) between 20 and 300 min postinfusion in the 10 and 20%
groups with either normal or high plasma protein concentration. The
average increase in blood volume during this time period in the normal
plasma protein concentration group was 23.8 ± 0.1%, and the
increase in the high plasma protein concentration group was 21.3 ± 0.1% (P not significant). Therefore,
a chronic increase in plasma protein concentration did not increase the amount of volume retained in the vasculature during overhydration.
| |
DISCUSSION |
Although it is well known that short-term increases in plasma colloid
osmotic pressure can cause large shifts of fluid into the vasculature
(4, 12), the control of the distribution of extracellular fluid volume
during chronic hyperproteinemia is poorly understood. During
overhydration in the present study in hyperproteinemic dogs, blood
volume increased as long as the increase in sodium space was
<40-50%. However, when sodium space increased more than this,
all the additional infused fluid escaped into the interstitium and
there were no further increases in blood volume. Therefore, the blood
volume-sodium space relationship in the present study in dogs with high
plasma protein concentration was very similar to the relationship found
in a previous study performed by Manning and Guyton (9) in dogs with
normal plasma protein concentration, as shown in Fig. 7. The maximum
increase in blood volume as described by this relationship was not
significantly different in the normoproteinemic and hyperproteinemic
dogs. This might be counterintuitive, because short-term increases in
plasma colloid osmotic pressure can cause large increases in blood
volume (4, 12). However, there are changes that occur during
chronic hyperproteinemia that may prevent blood volume from changing
and thus maintain the distribution of extracellular fluid volume.
To understand why the distribution of extracellular fluid volume is
similar during normoproteinemia and hyperproteinemia requires an
examination of the Starling capillary forces (12). These forces control
the movement of fluid across the capillary membrane and thus have a
major impact on fluid volume distribution. The balance of Starling
capillary forces is determined by the differences between capillary and
interstitial hydrostatic and colloid osmotic pressures. In the absence
of other changes, an increase in plasma colloid osmotic pressure should
cause an influx of fluid into the vasculature and thus increase blood
volume. In short-term studies, this is certainly true (5), and
intravenous infusion of colloids is an effective acute expander of
vascular volume (4). However, as it has been previously shown, the
long-term effects of hyperproteinemia on blood volume are quite
different from the short-term effects, such that chronic
hyperproteinemia causes no change in blood volume (8).
One reason why blood volume does not increase during chronic increases
in plasma protein concentration is the accompanying increase in
interstitial protein concentration (8). It has been previously shown
that chronic hyperproteinemia, achieved by daily intravenous infusion
of previously collected autologous plasma for 9 days, caused no change
in blood volume even though plasma protein concentration increased from
a control value of 6.9 ± 0.2 to 9.3 ± 0.2 g/dl and plasma
colloid osmotic pressure increased 10 mmHg. During this time, prenodal
lymph protein concentration, an index of interstitial protein
concentration, increased from a control value of 1.6 ± 0.2 to 5.1 ± 0.1 g/dl on day
9 of plasma infusion and the
calculated colloid osmotic pressure of this lymph increased 10.7 mmHg.
Therefore, the transcapillary colloid osmotic pressure changed little
during chronic hyperproteinemia because of extravasation of protein
into the interstitial fluids. Therefore, maintenance of the
transcapillary colloid osmotic pressure gradient may play a major role
in preventing blood volume changes during chronic hyperproteinemia (8).
In the present experiment, the value of blood volume during the control
period was close to that measured in the previous study on
hyperproteinemia (8). Therefore, interstitial fluid colloid osmotic
pressure likely increased in the present study in a fashion comparable
to that of the previous study, thus preventing hypervolemia.
As noted before, blood volume in the present study increased during
overhydration as long as the increase in sodium space was
<40-50%. There are several factors that could explain why further increases in sodium space caused no additional increases in
blood volume. First, plasma protein concentration
decreased in both the 10 and 20% groups because of hemodilution in
both groups and a decrease in circulating protein mass in the 20%
group. Therefore, a decrease in plasma protein concentration and plasma colloid osmotic pressure in both groups resulted (9), which would have
allowed more fluid to leave the circulation (12). Second, the increase
in blood volume in the 10 and 20% groups increased arterial pressure,
which could have increased capillary hydrostatic pressure, which could
have in turn increased transcapillary fluid flux. In addition, the
increase in central venous pressure that occurred in both the 10 and
20% groups could have further increased capillary hydrostatic pressure
and thus increased transcapillary fluid flux, which would limit the
degree of increase in blood volume.
Blood volume increased more in the 10% group than in the 20% group
after lactated Ringer infusion. This could have been responsible for
the slightly greater increase in arterial pressure in the 10% group.
The greater increase in blood volume in the 10% group could have been
due to a decrease in circulating protein mass in the 20% group and the
increase in protein mass in the 10% group. An additional factor that
could have contributed to the smaller increase in arterial pressure in
the 20% group compared with the 10% group is that the high central
venous pressure in the 20% group could have caused the Frank-Starling
relationship of the heart to operate at a nonoptimal point, thus
attenuating the increase in cardiac output in this group.
The present study and previous studies on hypoproteinemia by Manning
and Guyton (7, 10) indicate that the distribution of extracellular
fluid volume is highly dependent on the transcapillary colloid osmotic
pressure gradient, as originally predicted by Starling (12). The unique
finding in the present study and in other studies performed on
hyperproteinemia is that chronic elevations in plasma protein
concentration result in increases in interstitial fluid protein
concentration, and interstitial fluid colloid osmotic pressure and the
resultant transcapillary colloid osmotic pressure gradient change
little. Therefore, blood volume changes little during overhydration in
hyperproteinemia and the distribution of extracellular fluid volume is
unaltered from that of normoproteinemic animals.
Perspectives
Considerable controversy has recently occurred over whether crystalloid
or colloid therapy is best for volume resuscitation (4). The present
experiment and previous experiments from this laboratory may shed some
light on this controversy.
The present experiment clearly demonstrates that chronic increases in
plasma colloid osmotic pressure do not increase blood volume after
infusion of an isotonic electrolyte solution. On the other hand, dogs
that had their plasma protein concentration decreased to 2.5 g/dl by
plasmapheresis had their kidneys removed and were overhydrated using
the same protocol as in the present experiment (7). The
blood volume-sodium space relationship markedly shifted down the blood
volume axis (7), and, at any given sodium space, the blood volume was
much lower in hypoproteinemic dogs than in either normoproteinemic or
hyperproteinemic dogs. Thus a chronic decrease in plasma colloid
osmotic pressure decreased blood volume and significantly impacted the
blood volume-sodium space relationship. Therefore, severe chronic
hypoproteinemia prevents any expansion of blood volume during
intravenous infusion of a balanced electrolyte solution.
The loss of blood by hemorrhage is always accompanied by a loss of
plasma proteins. If, under these conditions, plasma protein concentration decreases below 3 g/dl, infusion of an electrolyte solution will cause only a short-lived increase in blood volume. Therefore, colloid infusion (either alone or accompanied by red blood
cells) would be necessary to bring blood volume back to normal. In
conclusion, for successful volume resuscitation, administration of
colloids is necessary in patients with severe hypoproteinemia, but
increasing colloid osmotic pressure above normal does not increase
blood volume except on a short-term basis.
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ACKNOWLEDGEMENTS |
I thank Ivadelle Heidke for typing the paper.
| |
FOOTNOTES |
This research was supported by National Heart, Lung, and Blood
Institute Grants HL-51971 and HL-11678.
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: R. Davis Manning, Jr., Dept. of
Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505.
Received 17 March 1998; accepted in final form 17 August
1998.
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Am J Physiol Regul Integr Compar Physiol 275(6):R1878-R1884
0002-9513/98 $5.00
Copyright © 1998 the American Physiological Society
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Abstract
Introduction
