Central and noncentral blood volumes in cirrhosis:
relationship to anthropometrics and gender
Søren
Møller1,
Jens H.
Henriksen1, and
Flemming
Bendtsen2
Departments of 1 Clinical Physiology and
2 Gastroenterology, Hvidovre Hospital, University of
Copenhagen, DK-2650 Copenhagen, Denmark
 |
ABSTRACT |
The size of the central and arterial
blood volume (CBV) is essential in the understanding of fluid retention
in cirrhosis. Previously, it has been reported decreased, normal, or
increased, but no reports have analyzed CBV with respect to gender and
lean body mass. The aim of the present study was by means of an
optimized technique to reassess it in a large group of patients with
cirrhosis compared with healthy controls and matched controls in
relationship to their body dimensions and gender. Eighty-three patients
with cirrhosis (male/female, 60:23), 67 patients without liver disease (male/female, 22:45), and 14 young healthy controls (male/female, 6:8)
underwent a hemodynamic investigation with determination of cardiac
output, central circulation time, and CBV determined according to
kinetic principles. Related to gender, CBV was lower in male cirrhotics
(1.48 ± 0.30 liter) than in matched and young controls
(1.68 ± 0.33 and 1.72 ± 0.33 liter, respectively;
P < 0.05-0.01). No significant differences in CBV
were seen between female cirrhotics and controls. Absolute and adjusted
CBVs were lower in the females than in men with cirrhosis
(P < 0.001), and men with cirrhosis had lower absolute
and body weight-adjusted CBVs than matched controls (P < 0.01). Normalized values of CBV (%total blood volume) were
significantly lower in patients with cirrhosis (25 ± 4%) than in
matched controls (31 ± 7%) and young controls (28 ± 4%;
P < 0.02). CBV correlated significantly with anthropometrics, including lean body mass (r = 0.68-0.82; P < 0.0001). In conclusion, the CBV of
patients with cirrhosis was lower than that of controls when adjusted
for body dimensions and gender. There are significant gender
differences, and signs of underfilling are more pronounced in male than
in female patients. The results emphasize the importance of adjustments
of blood volumes for anthropometrics and gender.
central circulation time; hyperdynamic circulation; lean body mass; peripheral vasodilatation; portal hypertension; systemic vascular
resistance
 |
INTRODUCTION |
IN PATIENTS WITH CIRRHOSIS,
peripheral and splanchnic arterial vasodilatation leads to a
hyperdynamic circulation with increased cardiac output (CO) and
heart rate and an abnormal distribution of the blood volume
(4, 19). The total blood and plasma volumes are increased
and abnormally distributed with an increase in the noncentral or
peripheral blood volume (2, 12, 21, 23, 30). The size of
the central and arterial blood volume (CBV), which represents the
effective blood volume where baro- and volume receptors are located,
has been the subject of debate (7, 23, 31). According to
the peripheral arterial vasodilatation theory, central hypovolemia
leads to a baroreceptor-induced activation of fluid-retaining
mechanisms and the development of ascites (4, 26). The
alternative overflow theory holds that central and peripheral
hypervolemia leads to spill-over of fluid into the peritoneal cavity
and thereby the formation of ascites (15). When kinetic
principles were applied, earlier results from our laboratory (5,
6) suggested that the CBV was contracted in patients with
cirrhosis correlating with the severity of the liver disease and the
portal pressure. In contrast to these findings, the results of Wong et
al. (32, 33) on the size of the thoracic blood volume as
assessed by radionuclide angiography showed higher values in patients
with cirrhosis than in controls. Hence, the size and pertinent
variables that determine the size of the CBV is still under discussion.
Because humans differ with respect to corpulence, gender, and age, the
question is how anthropometric data should be adjusted for
comparability. Formerly, adjustments were made with respect to body
weight, ideal body weight, body surface area, and body mass index.
However, no studies have analyzed CBV with respect to gender and lean
body mass. Dual energy X-ray absorptiometry permits quantification of
the lean body mass, and this may represent an additional parameter for
adjustment of blood volumes and flow.
We have now improved the CBV assessment technique by independent
determination of CO and central circulation time (CCT), and the aims of
this study were to assess the distribution of blood volumes and flow in
a large group of cirrhotic patients compared with healthy controls and
patients with diseases not related to the liver with respect to body
dimensions and gender for evaluation of the comparability.
 |
MATERIALS AND METHODS |
Study population.
The study population consisted of 83 consecutive patients (23 female
and 60 male) with biopsy-verified cirrhosis; 67 patients had a history
of alcohol abuse; that is, a consumption exceeding 50 g/day for >5 yr.
They had abstained from alcohol for at least 1 wk before the study and
had no signs of withdrawal symptoms at the time of the study. Fourteen
patients had nonalcoholic cirrhosis, classified as either posthepatitic
or cryptogenic, and two patients had a combined etiology. According to
the modified Child-Turcotte classification (3), 15 patients belonged to class A, 36 to class B, and 32 to class C. The
presence of slight or moderate ascites was confirmed by ultrasonography
or paracentesis. Thirty-five patients had ascites; they were receiving
diuretics and had been put on a sodium-restricted diet. Forty-two
patients received a daily diuretic dose of spironolactone (50-200
mg), nine received furosemide (40 mg), and 30 patients received
furosemide (80 mg). Additional cardiovascular medication was prescribed
for 21 patients and included
-blockers, calcium-channel blockers,
thiazides, and digoxin. None of the patients had hepatic encephalopathy
above grade 1 or had experienced recent gastrointestinal bleeding.
One control group without liver disease consisted of 67 patients (45 females and 22 males), who were referred for a hemodynamic investigation to exclude circulatory disorders, mainly intestinal ischemia or renovascular arterial hypertension. These patients were treated with diuretics and other cardiovascular drugs including vasodilators (nitrates, calcium-channel blockers).
A second control group consisted of 14 young healthy volunteers (8 females and 6 men) with no known disease; their mean age was 28 yr.
None was receiving medication.
Patients and controls participated after giving their informed consent
according to The Helsinki II Declaration, and the study was approved by
the local ethics committee for medical research in Copenhagen (journal
no. KF 01-294/99). No complications or side effects were encounted
during the study. Clinical and biochemical characteristics of the
patient and control groups are shown in Table
1.
Catheterization.
Patients and controls underwent a hemodynamic investigation in the
morning after an overnight fast and at least a 1-h rest in the supine
position. Catheterization of hepatic veins and femoral arteries was
performed as described elsewhere (16). Under local analgesia, a Swan-Ganz catheter size 7-Fr was guided to the hepatic veins via the femoral route under fluoroscopic control. A small indwelling polyethylene catheter (5-Fr) was introduced into the femoral
artery by the Seldinger technique, with the tip of the catheter located
at the aortic bifurcation. Pressures were measured directly by a
capacitance transducer (Simonsen & Weel, Copenhagen, Denmark). The mean
arterial pressure (MAP) was determined by electronic integration of the
pressure signal. Right atrial pressure (RAP) was determined as the mean
pressure over a period of 15 s. The hepatic venous pressure
gradient was determined as wedged minus free hepatic pressures. Zero
reference was the midaxillary level, and the pressures were measured in
millimeters of mercury. Hepatic blood flow was determined by the
indocyanine green constant infusion technique (11).
CO was measured by the indicator dilution technique after a bolus
injection of 150 kBq of 125I-labeled human serum albumin
(IFE IT. 205, Institute of Energy Technique, Kjeller, Norway) into the
right atrium, followed by arterial sampling. Systemic vascular
resistance (SVR; expressed in
dynes · s · cm
5) was assessed as 80 × (MAP
RAP/CO); the pressure was expressed in millimeters of
mercury and CO in liters per minute. Heart rate was determined
by electrocardiography. The mean indicator transit time (CCT)
represents the mean indicator sojourn in the central vascular bed
(14). CCT was determined independently of CO by a
quantitative injection of 0.5 MBq 99mTc-labeled human serum
albumin (Vasculocis CIS Bio International, Griff sur Yvette, France)
from a catheter depositing directly into the right atrium, followed by
automatic arterial sampling for 60 s as recently described
(8).
CBV was assessed in accordance with the kinetic theory, as CO
determined by 125I-labeled human serum albumin multiplied
by CCT determined by 99mTc-labeled human serum albumin
(14). The coefficient of variation of duplicate
determinations of CBV is <9% (6). The plasma volume was
measured as the injected amount of 125I-labeled serum
albumin divided by the plasma concentration of radioactivity 10 min
after injection. The total blood volume was determined from plasma
volume and hematocrit with correction for plasma trapping as plasma
volume/(1
0.89 × hematocrit). The noncentral blood volume
(non-CBV) was calculated as the difference between the total blood
volume and the CBV. The ideal body weight (kg) was estimated as
[height (cm)
100]
1/4[height (cm)
150] (16). All volumes and flow were adjusted with
respect to gender, body weight, body surface area, ideal body weight,
and lean body mass. The lean body mass was measured by dual energy
X-ray absorptiometry. A Nordland XR 36 (Nordland Medical Systems, Ford
Atkinson, WI) whole body X-ray densitometer was used. This instrument
uses a rectilinear scanner, which runs at medium speed to detect the differences in the density of a subject lying on the scan table (17). Body mass index was calculated as body weight (kg)
divided by height squared (m2). The circulating plasma
renin concentration was determined in a subset of 20 patients with
cirrhosis by a commercially available two-site immunoradiometric assay
(IRMA; DGR International, Marburg, Germany). The IRMA is a
noncompetitive assay in which renin in the sample is sandwiched between
two antibodies. The first antibody is immobilized to the coated bead,
and the other is radiolabeled for detection. Renin present in the
samples is bound by both antibodies to form a sandwich complex. The
amount of bound renin present is directly proportional to the amount of
renin present in the sample.
Statistics.
Data are presented as means ± SD. Statistical analyses were
performed by one-way ANOVA with Tukey's correction or by the
Kruskal-Wallis ANOVA on ranks with Dunn's correction. Bivariate data
were analyzed by unpaired Student's t-test or the
Mann-Whitney U-test. Correlation analyses between
stochastically independent variables were performed by the Spearman's
rank correlation test. Regression analyses were performed by linear
regression. Multivariate linear regression analysis was performed by
the backward stepwise regression technique. A P value <5%
was considered significant.
 |
RESULTS |
Characteristics of patients and controls are shown in Table 1.
With respect to anthropometrics, body weight was higher in the young
controls than in the patients with cirrhosis and controls without liver
disease. Moreover, controls without liver disease had a lower body
weight than had patients with cirrhosis. Similarly, body surface area
and body mass index were lower in the controls without liver disease
and higher in the young controls compared with those of patients with
cirrhosis. With respect to lean body mass, young controls had a higher
value compared with controls without liver disease, whereas there was
no significant difference when compared with patients with cirrhosis.
Age was significantly higher in the controls without liver disease and
significantly lower in the young controls compared with patients with
cirrhosis. Gender distribution was significantly different, with
relatively more females in the group of controls without liver disease
(P < 0.01). Patients with cirrhosis had significant
portal hypertension (hepatic venous pressure gradient: 15 ± 6 mmHg) and impaired liver function (Table 1).
Distributions of blood and plasma volumes are presented in Table
2 and Fig.
1 in relationship to gender and
severity of liver disease, respectively. In the total population of
patients with cirrhosis, the absolute CBV value was 1.38 ± 0.32 vs. 1.31 ± 0.39 and 1.43 ± 0.34 liter, respectively,
in controls without liver disease and young controls (P = 0.33). In general, absolute CBV was lower in females than in males
(76, 68, and 70% of male CBV in cirrhotics, controls without liver
disease, and young controls, respectively; P < 0.005)
and lower in male cirrhotics than in male controls (88 and 86% of CBV
in controls without liver disease and young controls, respectively;
P < 0.01). When adjusted for body weight, CBV was
reduced in patients with cirrhosis (19.8 ± 3.4 ml/kg) compared
with controls without liver disease (22.8 ± 6.4 ml/kg;
P < 0.02) but not compared with CBV of young controls (19.3 ± 3.2 ml/kg). When adjusted for ideal body weight and body surface, no significant differences were found between the groups. But,
when related to gender, CBV was lower in the female individuals and in
the cirrhotic patients (Table 2). Adjustment for lean body mass showed
CBV to be significantly lower in the total group of patients with
cirrhosis (31.2 ± 10.3 ml/kg) than in the controls without liver
disease (35.1 ± 8.2 ml/kg; P < 0.05), and there was a general trend toward higher values in females. Relative values of
CBV (CBV/total blood volume) × 100% were significantly lower in
patients with cirrhosis (25 ± 4%) than in the controls without
liver disease (31 ± 7%; P < 0.001) and young
controls (28 ± 4%; P < 0.05). The relative CBV
tended to be higher in male than in female controls, whereas there was
no difference between male and female cirrhotic patients. Within the
group of patients with cirrhosis, there was no significant difference
in CBV between the individual Child-Turcotte classes [Child class A,
1.44 ± 0.21 liter; Child class B, 1.33 ± 0.30 liter; and Child class C, 1.42 ± 0.37 liter; not significant
(NS)]. The correlations among CBV on the one hand and body weight,
ideal body weight, body surface, body mass index, and lean body mass on
the other are shown for the individual groups in Table
3. Corresponding regression lines are
shown in Fig. 2. There was a significant
relationship between CBV and anthropometrics. A backward stepwise
linear regression analysis revealed that lean body mass
(P < 0.001) and, secondarily, body surface area
(P < 0.001) predicted CBV most accurately.
Furthermore, CBV correlated significantly with the total blood volume
(Table 3). The circulating renin concentrations were significantly
higher in the cirrhotic patients, 228 ± 606 vs. 8 ± 4 ng/l
in the young controls (P < 0.001). However, we did not
find a significant relationship between CBV and the renin
levels.

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Fig. 1.
Central and arterial blood volume (CBV) in the patient
group according to Child classifications A, B, and C, in controls
without liver disease (CWL), and in young controls (CY). CBV is given
in absolute values (A) adjusted for body weight
(B), ideal body weight (IBW; C), body surface
area (D), and lean body mass (LBM; E).
, Females; , males. Dots and bars
represent means ± SD.
|
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Table 3.
Correlations between volumes and flow and patient characteristics
relating to body size in 83 CIR, 68 CWL, and 14 healthy CY
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Fig. 2.
CBV in relationship to anthropometrics: body weight (A),
IBW (B), body surface area (C), and LBM
(D). , Cirrhotic patients; ,
CWL; , CY. For correlation coefficients, please see
Table 3.
|
|
Non-CBV, total blood volume, and plasma volume were all significantly
increased in patients with cirrhosis compared with controls without
liver disease and young controls (P = 0.01 to 0.001, Table 2 and Fig. 3). In general, the
volumes were higher in males but were affected differentially by
adjustment for body dimensions, as seen in Table 2. The non-CBV tended
to be higher in the young controls than in the controls without liver
disease (P < 0.05; Table 2). When adjusted for lean
body mass, the plasma volume was significantly more expanded in Child
class B and C patients than in Child class A patients
(P < 0.05; Fig. 3).

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Fig. 3.
Noncentral blood volume (non-CBV) in the patient group,
according to Child classifications A, B, and C, in CWL and in CY. CBV
is given in absolute values (A) adjusted for body weight
(B), IBW (C), body surface (D), and
LBM (E). , Females; , males.
Dots and bars represent means ± SD.
|
|
Patients with cirrhosis and young controls exhibited a hyperdynamic
circulation with increased CO and cardiac index, compared with controls
without liver disease (P < 0.05). CO was generally higher in males (Table 4). We found no
significant differences in the CO of the individual Child classes. CBV
correlated to the degree of hyperdynamic circulation with respect to CO
(r = 0.53; P < 0.0001) and heart rate
(r =
0.31; P < 0.005) but not to the degree of arterial hypotension. The differences between patients and
controls without liver disease and young controls were more pronounced
when CO was adjusted for anthropometrics. The stroke volume was
generally higher in males and significantly higher in male cirrhotic
patients (P < 0.01). Comparably, the CCT was shorter
in the cirrhotic patients than in the controls without liver disease.
However, there were no differences with respect to cirrhotic patients
and young controls. Patients with cirrhosis exhibited marked
vasodilatation, as reflected by reduced SVR, compared with controls
without liver disease. Again, no significant difference was seen with
respect to cirrhotic patients and young controls. Although some
individuals in the group of controls without liver disease received
nitrates, none of them had hemodynamic signs of vasodilatation. In
patients with cirrhosis, CBV correlated significantly with SVR
(r =
0.49; P < 0.001) and indicators
of liver dysfunction such as alanine aspartate aminotransferase
(r =
0.29; P < 0.01), coagulation
factors II, VII, and X (r = 0.25, P < 0.05), and galactose elimination capacity (GEC; r = 0.40; P < 0.001; Fig. 4)
but not with the Child-Turcotte score. We found a significant
correlation between the CBV and hepatic blood flow (r = 0.40; P < 0.005) but not between CBV and the hepatic
venous pressure gradient.

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Fig. 4.
Correlations between CBV on the one hand and the systemic vascular
resistance (SVR; A), hepatic blood flow (HBF; B),
and galactose elimination capacity (GEC; C) on the other.
, Cirrhotic patients; , CWL;
, CY.
|
|
 |
DISCUSSION |
The main finding of the present study is that overall the CBV in
patients with cirrhosis is reduced or normal or relatively low compared
with that of controls without liver disease and young healthy subjects.
When related to gender, it is only reduced in male cirrhotic patients.
Females have lower CBV compared with males. CBV correlates
significantly with anthropometrics, such as lean body mass, and markers
of hepatic function (hepatic blood flow and GEC), whereas a
relationship to portal pressure was not demonstrated in the present
patient population.
The estimated CBV includes the blood volume in the heart cavities,
lungs, and the central arterial tree (14). This volume may
largely be equivalent to the so-called effective blood volume, which
represents the central vascular compartment where volume and
baroreceptors are located (13). The size of the CBV in
cirrhosis has remained controversial. A reduced CBV would indicate
central underfilling consistent with the peripheral arterial
vasodilatation theory (28). Absolute measurements of the
CBV in patients with cirrhosis have not been performed by others by the
same technique. However, the effective blood volume has been assessed
by measurements of the sympathetic outflow and activity of the
renin-angiotensin system (9, 22, 24). Indirect assessment
of the effective blood volume may be more physiological, because it
determines the activity dependent on the stimulation of receptors
located in the central vascular area (29). A few animal
studies have been performed in rats with portal hypertension induced by
partial portal vein ligation (1). In this experimental
model, with kinetic principles, the CBV was similarly reduced. However,
no studies of the CBV have been performed in experimental models of cirrhosis.
In contrast to previous reports from our group (6, 16),
the overall CBV in the total population of cirrhotic patients in the
present study was either normal or relatively low compared with that of
controls. Several explanations can be given relating to the applied
technique and the selection of patients and controls. The CBV is
determined as the CO multiplied by the CCT, both of which are now
independently determined by the use of 125I-labeled albumin
and 99mTc-labeled albumin, respectively. The CCT is now
determined with the indicator substance installed within the catheter.
This reduces the transit time slightly by ~0.2-0.5 s, but the
procedure is identical in patients and controls and will not give
substantial differences in the CBV of the individual groups. A fact
that is also reflected by an almost unaltered absolute CBV value of
1.38 liter in the cirrhotic patients of the present study compared with the 1.39 and 1.49 liter previously published (6, 16, 20). In contrast, the CBV of healthy controls (1.31 liter) and controls without liver disease (1.43 liter) is significantly lower than
the normal values previously published (1.81 liter) (6). An explanation for this discrepancy may be sought in a different gender
distribution. Whereas the gender ratio between the previous and present
cirrhotic patients is the same [males/females, 0.40:0.38 (NS)], those
of the control groups are different (males/females, 0.33:2.05; controls
without liver disease; P < 0.01; and males/females, 0.33:1.33 young controls; P < 0.1). In the male
controls, the absolute CBV was 1.68 and 1.72 liter, respectively,
compared with 1.48 in the cirrhotic males (P < 0.05-0.01). No differences in CBV were found between female
controls and female cirrhotics. These results emphasize the importance
of gender when comparing different study populations. Mismatching
between the groups in terms of age may complicate comparison of the
CBV. Thus the controls without liver disease were somewhat older, and
the young controls were younger than the cirrhotic patients. However,
we found no correlations between the CBV and age in any of the groups.
Differences in nutrition may also affect the CBVs. Some of the controls
without liver disease were emaciated because of abdominal discomfort
and clinical suspicion of intestinal ischemia. Part of these
differences can be dealt with by correction for anthropometrics.
However, this procedure may introduce another problem with relatively
high CBV values when adjusted for body weight and lean body mass in those patients with a very low body weight. When the control group without liver disease was matched for body weight by excluding controls
with a very low body weight, no significant changes were found in the
adjusted CBV values (data not shown). The higher CBV values in females
after adjustment for lean body mass probably reflects a differential
distribution of lean and fat body mass in males and females. Another
caveat with respect to the matching procedure relates to the young
controls, whose arterial blood pressure is lower and CO relatively
higher than those of controls without liver disease and of our previous
controls (6, 16). This means that with respect to
hemodynamics, the young controls resemble more cirrhotic patients.
Accordingly, we found no significant differences in the central
hemodynamics and SVR of these groups. Some of our controls without
liver disease were given a meal before determination of the CBV, which
may change distribution in the direction of a higher splanchnic blood
volume and hence a lower CBV. According to the peripheral arterial
vasodilatation theory, vasodilatation may contribute to a decreased CBV
(26, 28). Because the SVR was lower in our young healthy
controls than that previously reported (6), a more
pronounced vasodilatation in the present young controls may, at least
in part, explain their lower CBV. Psychological factors may also play a
role in the younger volunteers. Ideally, controls should completely
match cirrhotic patients for age, gender, fasting, and body weight, but
this would be impractical in terms of recruiting elderly volunteers as
controls. Lastly, it should be emphasized that we found no evidence of
an increased CBV in any of the cirrhotic patients.
CBV correlated significantly to indicators of liver dysfunction, such
as alanine aspartate transferase, coagulation factors, and GEC.
However, we did not find a significant association between CBV and the
degree of portal hypertension as previously reported (6).
Neither did we find a significant difference in the CBV of the
individual Child classes or patients with and without ascites. This
could theoretically be due to differences in the patient populations,
but in the main, we found no major differences in the composition of
our patient group and those described in previous reports. There could
be differences in the administration of the amount and the type of
diuretics, but, as reported earlier, we found no significant difference
in the CBV of patients treated with (1.38 ± 0.36 liter) and
without diuretics (1.38 ± 0.28 liter). A plausible
explanation is that many patients in Child class A are not truly
preascitic but have previously been treated with diuretics. If a recent
ultrasound examination has shown absence of ascites, the patient may be
classified as a Child A patient, but from a hemodynamic point of view
may still behave as a Child class B or C patient. In the present study,
we did not find a significant relationship between the CBV and the
degree of portal hypertension, as reported previously (6).
The degree of portal hypertension in the total patient population (15.0 mmHg) was comparable with the values previously reported (14.8 mmHg).
However, over the last decade, patients with cirrhosis and portal
hypertension have been more intensely treated with
-blockers and
nitrates, albumin, paracentesis, and cardiac drugs, a fact that may
blur an association to portal pressure.
The strong significant relationship between volumes and flow on the one
hand and antropometric data on the other emphasizes the importance of
relating hemodynamics to body dimensions. As seen in Table 3, the blood
volumes, including the CBV, correlated with body weight, ideal body
weight, body surface, body mass index, and lean body mass, which
stresses that at least one of these should be taken into consideration
when comparing hemodynamic data of individual groups. Results of the
multivariate analysis indicate that lean body mass and body surface
area best predict CBV and should be preferred for purposes of normalization.
The difference between the current and previous findings in the
absolute CBV values of the total patient populations is most likely
explained by an effect of the different distribution of gender in the
patient groups (6, 16, 20). However, the relative CBV was
significantly lower in the cirrhotic group and a normal volume may be
relatively reduced if the capacity of the vascular bed is enlarged. A
key feature is that the effective blood volume is physiologically
reduced and activates volume and baroreceptors, as reflected by the
increased sympathetic nervous activity and activated
renin-angiotensin-aldosterone system (9, 25, 27). This is
also supported by the finding of an increased arterial central
compliance in patients with cirrhosis, as recently reported by our
group (8, 10, 18). Our results confirm increased renin
concentrations in cirrhosis, whereas we were unable to detect a
significant relationship with CBV. In the present study, the
significant, indirect relationship between the CBV and SVR indicates a
relationship between the peripheral arterial vasodilatation and the
size of the CBV. However, there is a trend toward a more increased CBV
in patients with pronounced arterial vasodilatation. In addition, we
found an inverse correlation between the degree of hyperdynamic
circulation, as reflected by the increased heart rate, and the CBV. The
direct relationship between CO and CBV and the relationship between SVR
and CBV should be interpreted with caution owing to a relatively high
degree of covariation between these variables.
In conclusion, the overall CBV in patients with cirrhosis is reduced or
normal, especially in males. The results emphasize the importance of
adjustments of CBV for anthropometrics and gender. The effective blood
volume may be only relatively reduced in the supine position and
overtly underfilled in the upright position. The results of the present
study agree with the peripheral arterial vasodilatation theory.
 |
FOOTNOTES |
Address for reprint requests and other correspondence: S. Møller, Dept of Clinical Physiology and Nuclear Medicine, 239, Hvidovre Hospital, DK-2650 Hvidovre, Denmark (E-mail:
soeren.moeller{at}hh.hosp.dk).
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. Section 1734 solely to indicate this fact.
First published February 26, 2003;10.1152/ajpgi.00521.2002
Received 10 December 2002; accepted in final form 13 February 2003.
 |
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