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White blood cell and platelet counts could affect whole blood viscosity

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Blood viscosity is correlated with cerebral blood flow and cardiac output, and increased viscosity may increase the risk of thrombosis or thromboembolic events. The relationship between hematocrit and viscosity is well-known, however, the relationships between white blood cell (WBC) or platelet count and viscosity were not fully studied. The aim of the present study was to determine the influences of platelet count and WBC count on blood viscosity. One-hundred and 13 subjects with different hemoglobin, WBC and platelet count were enrolled into the study. The variables measured included serum fibrinogen, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), complete blood counts including hemoglobin, hematocrit, platelet count, red blood cell (RBC) count, WBC count, whole blood and plasma viscosity. The relationships of these variables with whole blood or plasma viscosity were analyzed. Serum fibrinogen, cholesterol, triglyceride, HDL and LDL did not correlate with whole blood viscosity. Not only hematocrit, hemoglobin and RBC, but also WBC and platelet count, could affect whole blood viscosity. On the other hand, none of the variables could affect plasma viscosity. All the blood cell components, but not the plasma proteins detected above, could affect whole blood viscosity. When patients are with high leukocytosis and thrombocytosis, impaired blood viscosity should also be considered to obtain appropriate clinical management.
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B
lood viscosity is correlated with cerebral blood
flow
1
and cardiac output,
2
and increased viscosity
may increase the risk of thrombosis or thromboembolic
events.
3
Hematocrit and hemoglobin are among the
many factors that influence blood viscosity. Other fac
-
tors such as white blood cell (WBC) count and platelet
count are less evaluated. We hypothesized that WBC and
platelet count might also affect blood viscosity. In the
present study, we planned to evaluate the influence of
different levels of red blood cell (RBC), hematocrit, he
-
moglobin, WBC and platelet count on blood viscosity.
METHODS
One-hundred and 13 patients who visited the hema
-
tology clinic with different hemoglobin, WBC and platelet
counts were enrolled into our study. Iron deficiency ane-
mia, pancytopenia, polycythemia vera, essential throm-
bocythemia, idiopathic thrombocytopenic purpura, mye-
lodysplastic syndrome, aplastic anemia and thalassemia
composed most of the disorders. All patients with multi
-
ple myeloma, Waldenstrom macroglobulinemia and cir
-
rhosis of liver with reverse albumin/globulin ratio were
excluded as they would have high plasma viscosity and
might affect our results. After having signed informed con
-
sent, these patients were measured for serum fibrinogen,
cholesterol, triglyceride, high-density lipoprotein (HDL),
low-density lipoprotein (LDL), complete blood counts
(CBC), whole blood and plasma viscosity. Whole blood
and plasma viscosity were measured by a digital vis
-
cometer (Brookfield Engineering Lab, Stoughton, MA,
USA). CBC were measured by an automated hematology
analyzer (Sysmex SE9000, Toa Medical Electronics,
394
J Chin Med Assoc
2004;67:394-397
Chao-Hung Ho
Division of Hematology, Department of
Internal Medicine, Taipei Veterans
General Hospital; National Yang-Ming
University School of Medicine, Taipei,
Taiwan, R.O.C.
Key Words
hematocrit;
plasma viscosity;
platelet count;
white blood cell count;
whole blood viscosity
Original Article
White Blood Cell and Platelet Counts
Could Affect Whole Blood Viscosity
Background. Blood viscosity is correlated with cerebral blood flow and cardiac out
-
put, and increased viscosity may increase the risk of thrombosis or thromboembolic
events. The relationship between hematocrit and viscosity is well-known, however,
the relationships between white blood cell (WBC) or platelet count and viscosity
were not fully studied. The aim of the present study was to determine the influences
of platelet count and WBC count on blood viscosity.
Methods. One-hundred and 13 subjects with different hemoglobin, WBC and platelet
count were enrolled into the study. The variables measured included serum
fibrinogen, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density li
-
poprotein (LDL), complete blood counts including hemoglobin, hematocrit, platelet
count, red blood cell (RBC) count, WBC count, whole blood and plasma viscosity.
The relationships of these variables with whole blood or plasma viscosity were ana
-
lyzed.
Results. Serum fibrinogen, cholesterol, triglyceride, HDL and LDL did not correlate
with whole blood viscosity. Not only hematocrit, hemoglobin and RBC, but also
WBC and platelet count, could affect whole blood viscosity. On the other hand, none
of the variables could affect plasma viscosity.
Conclusions. All the blood cell components, but not the plasma proteins detected
above, could affect whole blood viscosity. When patients are with high leukocytosis
and thrombocytosis, impaired blood viscosity should also be considered to obtain ap-
propriate clinical management.
Received: February 13, 2004.
Accepted: July 1, 2004.
Correspondence to: Chao-Hung Ho, MD, Division of Hematology, Taipei Veterans General Hospital,
201, Sec. 2, Shih-Pai Road, Taipei 112, Taiwan.
Tel and Fax: +886-2-2875-7106; E-mail: chho@vghtpe.gov.tw
Kobe, Japan); serum cholesterol, triglyceride, HDL,
LDL, were determined using the SMAC-II Analyzer
(Technicon, New York, USA). Kruskal-Wallis test was
used to analyze the results. Pearson correlation matrix
was used to assess the relationship between the values.
RESULTS
Table 1 shows the mean and range of different vari
-
ables in the 113 subjects. Figs. 1 and 2 show the relation
-
ships of whole blood viscosity with RBC, hemoglobin,
hematocrit, log-WBC and log-platelet count in these sub
-
jects. These figures demonstrate that there was significant
relationship between whole blood viscosity and RBC, he
-
moglobin, hematocrit, log-WBC and log-platelet count
(p < 0.001, < 0.001, < 0.001, = 0.005 and 0.016, respec
-
tively).
We then divided the patients into 3 subgroups ac
-
cording to their levels of whole blood viscosity in order
to see the difference in each variable. Group A included
58 patients with whole blood viscosity £ 3.0, Group B in
-
cluded 39 patients with whole blood viscosity 3.01-4.0
and Group C, 16 patients with whole blood viscosity >
4.0. Table 2 shows the means of the variables in these 3
subgroups. Hemoglobin, hematocrit, RBC, WBC and
platelet counts were significantly different in the 3 sub
-
groups of patients with different whole blood viscosity
395
August 2004 WBC, Platelet Count and Viscosity
RBC (M/UL)
012345678
0
1
2
3
4
5
6
7
r=0.639
p<0.001
Hb (g/dl)
0 5 10 15 20
WBV (cps)
0
1
2
3
4
5
6
7
r=0.695
p<0.001
Hct (%)
0 10203040506070
WBV (cps)
0
1
2
3
4
5
6
7
r=0.706
p<0.001
WBV = Whole blood viscosity
Fig. 1. The relationship between RBC, hemoglobin, hematocrit and whole blood viscosity.
Table 1. Mean of different variables in 113 subjects
Male Female Total
Mean ± SD (Range)
Age (year) 72.0 ± 11.6 (25-87) 57.4 ± 18.7 (15-89) 66.3 ± 16.3 (15-89)
Hemoglobin (g/dL) 10.5 ± 3.4 (5.2-19.2) 9.1 ± 3.0 (2.9-14.7) 9.9 ± 3.3 (2.9-19.2)
Hematocrit (%) 32.2 ± 10.4 (14.7-59.1) 28.3 ± 8.0 (10.9-44.3) 30.7 ± 9.7 (10.9-59.1)
Red cell count (´ 10
12
/L) 3.70 ± 1.31 (1.52-6.89) 3.71 ± 1.09 (1.79-6.69) 3.70 ± 1.22 (1.52-6.89)
MCV (fL) 89.0 ± 11.2 (63.4-121.1) 78.0 ± 14.2 (52.1-102.5) 84.7 ± 13.5 (52.1-121.1)
White cell count (´ 10
9
/L) 6.4 ± 6.7 (0.91-46.4) 13.9 ± 49.6 (1.77-334.6) 9.3 ± 31.4 (0.91-334.6)
Platelet count (´ 10
9
/L) 202 ± 200 (1-784) 292 ± 353 (3-1935) 237 ± 272 (1-1935)
Fibrinogen (mg/dL) 382 ± 114 (190-650) 342 ± 88 (106-501) 367 ± 272 (106-650)
Cholesterol (mg/dL) 160 ± 45 (50-254) 173 ± 49 (91-313) 166 ± 47 (50-313)
Triglyceride (mg/dL) 126 ± 121 (29-941) 113 ± 50 (33-234) 121 ± 99 (29-941)
Whole blood viscosity 3.16 ± 0.88 (1.53-6.05) 2.81 ± 0.60 (1.69-4.21) 3.03 ± 0.80 (1.53-6.05)
Plasma viscosity 1.31 ± 0.28 (0.40-1.99) 1.27 ± 0.18 (0.95-1.85) 1.30 ± 0.24 (0.40-1.99)
(p < 0.005, < 0.005, < 0.005, = 0.005 and 0.016, respec
-
tively, Kruskal-Wallis test). On the other hand, MCV,
fibrinogen, cholsterol, triglyceride, HDL and LDL (data
of the latter 2 not shown) were not significantly different
among them. Thus, whole blood viscosity was affected
significantly by hemoglobin, hematocrit, RBC and WBC
counts, but unaffected by fibrinogen, cholesterol, tri
-
glyceride and platelets.
We further divided the patients into 3 subgroups ac
-
cording to their levels of plasma viscosity. Group D in
-
cluded 41 patients with plasma viscosity £ 1.2, Group E
included 41 patients with plasma viscosity 1.2-1.4 and
Group F, 26 patients with plasma viscosity > 1.4. No sig
-
nificant difference was found in any of the variables in
these 3 subgroups (p all > 0.05). Thus, no variables af
-
fected plasma viscosity.
DISCUSSION
Blood viscosity is known to have close relationship
with blood flow. Increased viscosity may increase the
risk of thrombosis or thromboembolic events. Blood vis
-
cosity can be divided into whole blood viscosity and
plasma viscosity. These 2 viscosities can exert different
influences in different situations. For example, in the ce
-
rebral area, blood flow is more affected by plasma vis
-
cosity rather than whole blood viscosity.
1,4
High whole
blood viscosity with high hemoglobin concentration
might increase the risk of poor pregnancy outcome,
5
or
the potential for increased thrombosis.
6
Many factors
can affect blood viscosity, such as red blood cell count,
hematocrit, immunoglobulins and fibrinogen. The aim
of the present study focused on the blood cells which
Chao-Hung Ho Journal of the Chinese Medical Association Vol. 67, No. 8
396
Fig. 2. The relationship between log-WBC, log-platelet and whole blood viscosity.
Table 2. Mean of various variables in 3 subgroups with different levels of whole blood viscosity
Group A (£ 3, 58)
a
Group B (3.01-4, 39)
a
Group C (> 4, 16)
a
p value
Mean ± SD
Age (year) 66.1 ± 15.6 66.7 ± 18.5 67.8 ± 12.4 0.868
Hemoglobin (g/dL) 8.2 ± 2.1 11.1 ± 2.6 13.6 ± 4.3 < 0.005
Hematocrit (%) 25.6 ± 5.9 34.0 ± 7.1 42.3 ± 13.9 < 0.005
Red cell count (´ 10
12
/L) 3.07 ± 0.84 4.17 ± 0.93 4.89 ± 1.72 < 0.005
MCV (fL) 85.4 ± 15.1 82.4 ± 12.7 87.5 ± 7.6 0.734
White cell count (´ 10
9
/L) 10.5 ± 43.4 6.2 ± 3.7 12.8 ± 12.0 0.005
Platelet count (´ 10
9
/L) 170 ± 164 303 ± 376 323 ± 246 0.016
Fibrinogen (mg/dL) 373 ± 101 366 ± 101 341 ± 151 0.896
Cholesterol (mg/dL) 159 ± 49 176 ± 40 159 ± 58 0.190
Triglyceride (mg/dL) 123 ± 127 114 ± 56 128 ± 57 0.270
a
Whole blood viscosity & number of cases.
would affect blood viscosity.
In our study, the levels of hemoglobin, hematocrit,
RBC, WBC and platelet counts were in a rather great
range as the patients were from the hematology clinic.
Thus, we had a chance to check the influence of high
platelet and high white blood cell counts on viscosity.
In our study, we used 2 methods of classification to
detect the differences among variables. One was to di
-
vide the patients according to their levels of viscosity to
see the differences of every variable, and the other was to
show the relationship between the viscosity and different
variables. Both methods showed that no variables could
affect the plasma viscosity, including fibrinogen, choles
-
terol, triglyceride, HDL and LDL as well as all the blood
cell components. On the other hand, hemoglobin, hemat
-
ocrit, RBC and WBC counts were found to affect the
whole blood viscosity, whichever method was used.
RBC and their related indexes are well known to af
-
fect viscosity. We further proved this fact. Though their
influence found in the present in vitro study was mainly
on whole blood viscosity rather than on plasma viscosity,
in microcirculation, increased hemoglobin would de-
crease the deformability and thus increase plasma vis-
cosity.
4
This should be kept in mind when the blood flow
occurs in vivo.
Since high leukocytosis and high platelet count can-
not be easily found in medical settings other than hema-
tology, their influences on viscosity have seldom been
investigated. Our study gave us a chance to know their
influence on viscosity and, thus, that they might also be a
possible risk factor of thromboembolic disease. Further
study should be performed to make more solid conclu
-
sions.
In conclusion, not only the RBC but also the WBC
and platelet count can affect whole blood viscosity. Fur
-
ther studies should be performed to identify their clinical
significance.
ACKNOWLEDGEMENTS
This research was supported by a grant (VGH 91-53)
from Veterans General Hospital, Taipei, Taiwan, R.O.C.
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397
August 2004 WBC, Platelet Count and Viscosity
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Impaired blood flow due to abnormal rheologic characteristics results in a multiplicity of clinical manifestations, collectively termed the hyperviscosity syndrome. A basic knowledge of the principles of rheology is important in the understanding of its pathophysiology, especially the relationship between viscosity and flow conditions. The flow characteristics in different types of blood vessels are also determinants in the location of the clinical manifestation. The syndrome can occur in a wide variety of diseases and is best grouped according to the causative element or elements in blood. Abnormalities in the cellular components of blood can occur in the quantity and the quality of erythrocytes, leukocytes, and platelets. Abnormal plasma components can also be in both the quantity and quality of the plasma proteins. Clinical manifestations are the result of vascular occlusion, especially in the microcirculation. The altered rheologic characteristics of either the cellular or the protein component may be temperature dependent, being abnormal only at temperatures below 37 degrees C, so that only the cooler parts of the body are affected. The management of these conditions should be primarily directed at the removal of the abnormal component. At the same time, it should be accompanied by measures that can control the production of the causative element.
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Full correction of anemia with recombinant human erythropoietin (rhEPO) has been reported to reduce the risk of cardiovascular morbidity and mortality and improve the quality of life in hemodialysis (HD) patients. Effects of normalization of hematocrit on cerebral blood flow and oxygen metabolism were investigated by positron emission tomography. Regional cerebral blood flow (rCBF), cerebral blood volume (rCBV), oxygen extraction ratio (rOER), and metabolic rate for oxygen (rCMRO2) were measured in seven HD patients before and after correction of anemia and compared with those in six healthy control subjects. In addition, blood rheology before and on rhEPO therapy was measured in HD patients, which included blood viscosity, plasma viscosity, erythrocyte fluidity, and erythrocyte aggregability. The results showed that plasma viscosity was high (1.51+/-0.19 mPa x s) and erythrocyte fluidity was low (85.8+/-4.8 Pa(-1) x s(-1)), while whole blood viscosity was within the normal range (3.72+/-0.38 mPa x s) before rhEPO therapy. After treatment, the hematocrit rose significantly from 29.3+/-3.3 to 42.4+/-2.2% (P<0.001), accompanied by a significant increase in the whole blood viscosity to 4.57+/-0.16 mPa x s, nonsignificant decrease in erythrocyte fluidity to 79.9+/-7.4 mPa(-1) x s(-1) and nonsignificant change in plasma viscosity (1.46+/-1.3 mPa x s). Positron emission tomography measurements revealed that by normalization of hematocrit, rCBF significantly decreased from 65+/-11 to 48+/-12 ml/min per 100 cm3 (P<0.05). However, arterial oxygen content (caO2) significantly increased from 5.7+/-0.7 to 8.0+/-0.4 mmol/L (P<0.0001), rOER of the hemispheres significantly increased from 44+/-3 to 51+/-6% (P<0.05) and became significantly higher than healthy control subjects (P<0.05). In addition, rCBV significantly increased from 3.5+/-0.5 to 4.6+/-0.6 ml/100 cc brain tissue. The results showed that oxygen supply to the brain tissue increased with normalization of hematocrit, but it was accompanied by increased oxygen extraction in the brain tissue. This may be assumed to be related to the decrease of erythrocyte velocity in the cerebral capillaries as a result of the decreased blood deformability and the increased plasma viscosity.
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An association between moderate anemia and poor perinatal outcomes has been found through epidemiologic studies, although available evidence cannot establish this relation as causal. Anemia may not be a direct cause of poor pregnancy outcomes, except in the case of maternal mortality resulting directly from severe anemia due to hypoxia and heart failure. Preventing or treating anemia, whether moderate or severe, is desirable. Because iron deficiency is a common cause of maternal anemia, iron supplementation is a common practice to reduce the incidence of maternal anemia. Nevertheless, the effectiveness of large-scale supplementation programs needs to be improved operationally and, where multiple micronutrient deficiencies are common, supplementation beyond iron and folate can be considered. High hemoglobin concentrations are often mistaken as adequate iron status; however, high hemoglobin is independent of iron status and is often associated with poor health outcomes. Very high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxygen delivery to tissues and cerebrovascular complications. Epidemiologic studies have also found an association between high maternal hemoglobin concentrations and an increased risk of poor pregnancy outcomes. Evidence does not suggest that this association is causal; it could be better attributed to hypertensive disorders of pregnancy and to preeclampsia. The pathophysiologic mechanism of these conditions during pregnancy can produce higher hemoglobin concentrations because of reduced normal plasma expansion and cause fetal stress because of reduced placental-fetal perfusion. Accordingly, higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications, not necessarily as a sign of adequate iron nutrition, because iron supplementation does not increase hemoglobin higher than the optimal concentration needed for oxygen delivery.
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We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on "baseline" CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H(2) clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 +/- 10.2 ml. 100 g(-1). min(-1) (+/-SD). In control animals, changing plasma viscosity to 1. 0 or 3.0 cP resulted in CBF of 55.9 +/- 8.6 and 42.5 +/- 12.7 ml. 100 g(-1). min(-1), respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1. 0 cP, CBF varied from 98 to 115 ml. 100 g(-1). min(-1). When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml. 100 g(-1). min(-1) and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.
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The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen‐carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non‐haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non‐haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin–oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3‐diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia‐induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end‐diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non‐catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia‐stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia‐related LVH develops in an otherwise ‘healthy’ humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (haemoglobin concentration <4–5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end‐stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alternations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima–media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.