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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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 beta -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.

                              
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Table 1.   Clinical and biochemical characteristics of 83 CIR, 67 CWL, and 14 CY

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
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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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Table 2.   Blood and plasma volumes in 83 CIR, 67 CWL, and 14 CY stratified according to gender



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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). triangle , Females; black-down-triangle , 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; triangle , CWL; diamond , 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). triangle , Females; black-down-triangle , 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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Table 4.   Hemodynamics of 83 CIR, 67 CWL, and 14 healthy CY stratified according to gender



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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; triangle , CWL; diamond , CY.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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 beta -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.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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