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PubMed2004

Increased incidence of adverse perinatal outcome with low maternal blood viscosity in preeclampsia.

Hyperviscosity of the maternal blood has been reported to be associated with an increased incidence of adverse perinatal outcome in preeclampsia. We related the changes in maternal blood viscosity to perinatal outcome in 47 preeclamptic, nulliparous, black Jamaican women. A group of 49 non-preeclamptic, nulliparous, gestation-matched women acted as controls. Perinatal outcome was also compared between the women with high blood viscosity (> or = 5 mPa.s) and those with low blood viscosity (< 5 mPa.s) in both the preeclamptic and non-preeclamptic groups. Data was analysed by the comparison of two proportions, the chi-squared test, the Fisher's exact test and the Pearson's correlation method. The level of statistical significance was taken at p < 0.05. The incidence of adverse perinatal outcome was significantly (p < 0.001) higher in the preeclamptic women as compared with that of the non-preeclamptic controls. However, of interest, was the fact that within the preeclamptic group, the incidence of adverse perinatal outcome was significantly (p = 0.001, Fisher's exact test) higher in those with low blood viscosity as compared with those with high blood viscosity. These results suggest that low maternal blood viscosity may be related to increased incidence of adverse perinatal outcome in Jamaican women with preeclampsia.

Adolescent↗
PubMed1982

Whole blood viscosity in preeclampsia.

Whole blood viscosity was measured in 41 patients with preeclampsia and in 51 normotensive control subjects. The mean viscosity in the preeclamptic group had a highly significant elevation (t = 9.752, p less than 0.001, at a shear rate of 0.1 sec-1 and t = 4.223, p less than 0.001, at a shear rate of 100 sec-1). The slower shear rate gave the better discrimination between the two groups as only four patients with preeclampsia had a value within 1 SD of the mean of the control group. It is suggested that the measurement of whole blood viscosity may be clinically useful in the management of patients with preeclampsia.

Blood Pressure↗
PubMed1996

Distribution of blood viscosity values and biochemical correlates in healthy adults.

Increases in the viscosity of blood and plasma predict clinical manifestations of atherothrombotic vascular disease. The clinical utility of viscosity measurements in cardiovascular risk factor analysis requires reference values established from a healthy disease-free population. A cohort of 126 (71 men, 55 women) healthy nonsmoking adults had fasting blood analysis after a 12-14-h fast. Viscosity measurements were made on samples of whole blood, plasma, and serum at 37 degrees C with a coaxial cylinder microviscometer. The mean blood viscosity at shear rates of 100, 50, and 1 s-1 were 3.26 +/- 0.43, 4.37 +/- 0.60, and 5.46 +/- 0.84 mPa.s, respectively. Men had significantly higher blood viscosity values than women at each shear rate. The differences in blood viscosity did not remain significant after blood viscosity values were normalized to a hematocrit of 45%, except at 100 s-1. For the entire group, normalized blood viscosity values at each measured rate correlated inversely with HDL cholesterol and positively with fibrinogen. The mean plasma viscosity was 1.39 +/- 0.08 mPa.s and the mean serum viscosity was 1.27 +/- 0.06 mPa.s. Plasma viscosity correlated with fibrinogen (r = 0.51, P < 0.0001), total serum protein (r = 0.33, P < 0.0001), and triglyceride concentrations (r = 0.33, P < 0.0015). Serum viscosity correlated with total serum protein (r = 0.50, P < 0.0001) and LDL cholesterol (r = 0.24, P = 0.0065). This study provides reference values for the viscosity of blood, plasma, and serum that may assist in evaluating hemorheological profiles.

Adult↗
PubMed1976

Effect of low-dose subcutaneous heparin on whole-blood viscosity.

The change in blood-viscosity at low shear-rates (0.77 s-1 and 2-62 s-1 was measured in eighteen normal subjects and postoperatively in sixteen patients after administration of 5000 I.U. of subcutaneous heparin. In both groups there was a significant decrease in the mean blood-viscosity 4 to 6 hours after the injection of heparin. This fall in blood-viscosity may be involved in the prophylactic effect of low-dose subcutaneous heparin in preventing venous thrombosis.

Blood Viscosity↗
PubMed2005

Microvascular blood viscosity in vivo and the endothelial surface layer.

The apparent viscosity of blood in glass tubes declines with decreasing diameter (Fåhraeus-Lindqvist effect) and exhibits a distinctive minimum at 6-7 microm. However, flow resistance in vivo in small vessels is substantially higher than predicted by in vitro viscosity data. The presence of a thick endothelial surface layer (ESL) has been proposed as the primary cause for this discrepancy. Here, a physical model is proposed for microvascular flow resistance as a function of vessel diameter and hematocrit in vivo; it combines in vitro blood viscosity with effects of a diameter-dependent ESL. The model was developed on the basis of flow distributions observed in three microvascular networks in the rat mesentery with 392, 546, and 383 vessel segments, for which vessel diameters, network architecture, flow velocity, and hematocrit were determined by intravital microscopy. A previously described hemodynamic simulation was used to predict the distributions of flow and hematocrit from the assumed model for effective blood viscosity. The dependence of ESL thickness on vessel diameter was estimated by minimizing deviations of predicted values for velocities, flow directions, and hematocrits from measured data. Optimal results were obtained with a layer thickness of approximately 0.8-1 microm for 10- to 40-microm-diameter vessels and declined strongly for smaller diameters, with an additional hematocrit-dependent impact on flow resistance exhibiting a maximum for approximately 10-microm-diameter vessels. These results show that flow resistance in vivo can be explained by in vitro blood viscosity and the presence of an ESL and indicate the rheologically effective thickness of the ESL in microvessels.

Animals↗
PubMed1982

Heparin effect on blood viscosity.

The effect of heparin on blood viscosity was investigated in a group of patients with acute myocardial infarction (AMI) and preinfarction angina (PA), whose blood viscosity was elevated. Viscosity was measured with Cannon, Fenske, and Routine viscometers. Kinematic viscosity, bath and whole blood, plasma, and serum viscosity were determined as well as dependent parameters (fibrinogen, serum proteins, number of platelets, and hematocrit). All of them were found to increase, and it was significantly proved that intravenous heparin immediately decreased plasma viscosity, but has a lesser effect on serum and whole blood viscosity. A dose of 1 cc = 50 mg = 5000 IU intravenous heparin, will maintain this decrease for a month. In our four-week-study, 1 cc i.v. heparin was administered at 6-hour intervals for the first 2 weeks, and 2 cc heparin subcutaneous injections were administered at 12-hour intervals for the next 2 weeks. We found that heparin also decreased fibrinogen, hematocrit, serum alpha 2 globulin, and number of platelets. Hyperviscosity, hypercoagulability, and the increase of platelet adhesiveness arae some of the most important physiopathological alterations of AMI and PA. The decrease of blood viscosity due to heparin is one of the most important and beneficial effects of it in this pathology.

Adult↗
PubMed1983

[Effect of anticoagulants on blood viscosity].

In 21 cases the blood viscosity of native blood was determined in comparison to heparin blood at a shear rate of 218.7 and 1312 sec-1 by using the rotational viscosimeter Rheotest 2. As a result, a low viscosity of the heparin blood could be found. In addition, the impact of phenprocoumon treatment on several rheologic parameters was examined in 20 healthy test persons. With the haematocrit and fibrinogen level remaining constant, a reduction of blood viscosity could be observed when the Quick value decreased. This was detected with Rheotest 2 at 7 different shear rate between 218.7 and 1312 sec-1. The influence of anticoagulants on the erythrocyte deformability is discussed as a possible cause underlying the obtained decreases of viscosity. This would have to be proved by investigations using erythrocyte filters.

4-Hydroxycoumarins↗
PubMed1991

Effects of endurance training and long distance running on blood viscosity.

The effect of endurance training on blood viscosity was studied by comparing blood rheological properties in control subjects (untrained) and endurance trained subjects. The effect of running on blood viscosity was studied in the 33 endurance trained subjects before and after a 48-km mountain race (Sandia Wilderness Crossing Research Run). Runners started at an altitude of 1700 m, ran 26 km to 3300 m, then descended 22 km to finish at 1900 m. Venous blood viscosity (eta b) and plasma viscosity (eta p) were measured at 37 degrees C at shear rates of 11.25, 22.5, 45, 90, and 225.s-1, using a cone-plate viscometer. Endurance trained subjects had significantly higher pre-race blood viscosity at 11.25 and 22.5.s-1 than control subjects but similar plasma viscosity and hematocrits. Following the race, there was no significant change in mean hematocrit, but eta b increased significantly at all shear rates except 225.s-1. Plasma viscosity at 225.s-1 increased significantly from 1.44 to 1.53 cP following the run. Since eta b did not increase, an increase in red cell deformability is inferred. The mechanism of the increase in eta b at lower shear rates in runners is due in part to the higher plasma viscosity. An additional mechanism at lower shear rates is in an increase in red cell aggregation. Increased plasma fibrinogen was measured in six of six resting subjects taken from 1600 m to 3300 m and is speculated to be the mechanism of enhanced aggregation and deformability in the runners.

Adult↗
PubMed2005

Alpha-tocopherol supplementation favorable effects on blood pressure, blood viscosity and cardiac remodeling of spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) were separated into two groups (n = 6 per group) and, since 5 months old, received alpha-tocopherol (alpha-tocopherol acetate120 IU) or vehicle by daily gavage for 2 weeks. Blood viscosity, blood pressure (BP) and myocardial remodeling were analyzed. The SHRs treated with alpha-tocopherol showed a significant reduction of BP and a major reduction of blood viscosity in comparison with the control SHRs. The cardiac hypertrophy indices showed some differences when the two SHR groups were compared, the LV mass index was not different between the groups; however, the cardiomyocyte size was more than 20% smaller in SHRs treated with alpha-tocopherol than in control SHRs (P < .05). The intramyocardial vessels distribution was more than 45% greater in alpha-tocopherol-treated SHRs than in control rats, significantly improving the vessels-to-myocytes ratio in treated SHRs than in control SHRs (P < .05). In conclusion, present findings strongly suggest a beneficial effect of alpha-tocopherol supplementation to genetically hypertensive rats. This was observed by a reduction of both blood viscosity and BP, and a consequent cardiomyocyte hypertrophy in treated SHRs; an improvement of vessels-to-myocytes ratio in these rats was also observed.

Animals↗
PubMed1977

Changes in blood viscosity and plasma proteins in carcinoma.

Blood viscosity and plasma protein concentrations were measured in 31 patients with a variety of visceral carcinomas. The mean whole blood viscosity was not elevated over normal controls because of a significantly lowered mean hematocrit. However, when hematocrit was eliminated as a variable by adjusting the hematocrit to 45%, the mean whole blood viscosity was significantly elevated in the group with carcinoma. Both the plasma viscosity and the tendency for red cell aggregation were significantly elevated. Since blood is a non-Newtonian fluid, and its viscosity increases markedly at low shear rates, these rheological abnormalities would be most important at the low shear rates characteristic of the venous circulation. It is suggested that these abnormalities in blood viscosity and red cell aggregation may be contributing to the high incidence of venous thromboembolism seen in patients with neoplastic.

Alpha-Globulins↗
PubMed2000

[Study of an in-vivo and real-time method to measure blood viscosity].

The traditional methods to measure blood viscosity are out-line. They have the disadvantages of long measurement time, many disturbance factors during measurement, the damage to blood sample, and etc. So rapidity, accuracy and repeatability are not satisfactory. A new method to measure blood viscosity is proposed in this paper, which uses needle instead of capillary and can measure blood viscosity during collecting blood. Owing to the advantages of small amount of blood sample, rapidity and repeatability, the new method is of value for clinical application.

Animals↗
PubMed1998

Opposite effects of low-density and high-density lipoprotein on blood viscosity in fasting subjects.

Given the enlarging body of evidence implicating increased blood viscosity in atherogenesis, the authors hypothesize that lipoproteins modulate the atherogenic process by affecting blood viscosity. In order to define the magnitude of the effect of lipoproteins on blood viscosity, capillary viscometry was performed on blood from 16 healthy, fasting subjects, and results were correlated with lipoprotein-cholesterol levels. Low-density lipoprotein-cholesterol was positively associated with blood viscosity (r = 0.610, p = 0.01). High-density lipoprotein-cholesterol was negatively associated with blood viscosity (r = -0.479, p = 0.06). A multiple regression model was developed with these data, revealing that 54% of variation in blood viscosity was attributable to these lipoproteins. This model was validated on a second dataset, in which these lipoproteins accounted for 28% of variation in blood viscosity. A second model, including hematocrit, serum viscosity, and high-density lipoprotein-cholesterol levels, explained 73% of variation in blood viscosity. By modulating blood viscosity and flow, lipoproteins may affect the residence time of atherogenic particles and atherogenesis.

Adult↗
PubMed2001

Elevated blood viscosity in systemic lupus erythematosus.

OBJECTIVES: It has been proposed that elevated blood viscosity contributes to atherothrombotic and thromboembolic processes. We evaluated whether there is increased blood viscosity in systemic lupus erythematosus (SLE) that might contribute to cardiovascular complications and reduced tissue perfusion. METHODS: Blood viscosity profiles were evaluated in SLE patients to determine whether rheologic disturbances contribute to the cardiovascular risk profile. Blood viscosity profiles were evaluated in 27 patients with SLE and 46 age- and gender-matched controls. Blood viscosity was measured at 37 degrees C and shear rates of 1 s(-1) and 100 s(-1), then corrected to the average hematocrit of the SLE patients. RESULTS: Corrected blood viscosity values were higher in SLE patients than in controls at 100 s(-1) (P =.002). Positive correlations were found between the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index for SLE, which quantifies damage to 12 organ systems and fibrinogen (rho =.39; P =.042) and plasma viscosity (rho =.38; P =.049). CONCLUSIONS: Our data indicate that blood viscosity values at a standard hematocrit are elevated in SLE patients. Further investigations are needed to evaluate whether the increased blood viscosity values in SLE patients contribute to cardiovascular complications and tissue ischemia. CLINICAL RELEVANCE: Because blood viscosity values correlate with the clinical severity of SLE, blood viscosity may contribute to the cardiovascular complications and reduced tissue perfusion in SLE patients. Semin Arthritis Rheum 31:52-57.

Adult↗
PubMed1992

[Factors that determine the high blood viscosity syndrome in rheumatoid arthritis patients].

High blood viscosity is a syndrome that may be attributed to a group of the most important disorders of microcirculation under different pathological conditions of the body. The given syndrome manifests itself by disorders of red blood cell deformability (RBCD), high plasma and whole blood viscosity. 32 patients with a verified diagnosis of rheumatoid arthritis (RA) were examined, showing varying activity and systemic manifestations. There was a significant decrease of RBCD from 82.0 + 4.5% in patients with grade I activity to 33.0 + 15.0% in patients with grade III activity (p < 0.01). At the same time plasma viscosity remained practically unchanged. Whole blood viscosity rose with RA activity enhancement: in grade I, it was 1.87 + 0.60 relative units, in grade II, it was 2.80 + 0.80 relative units, in grade III, it constituted 5.30 + 3.70 relative units (p < 0.02). It is assumed that RBCD disturbance is one of the most leading signs in the development of high blood viscosity in RA patients.

Adult↗
PubMed1977

Blood viscosity in Waldenström macroglobulinemia.

Patients with Waldenström macroglobulinemia were studied for the presence or absence of the hyperviscosity syndrome, the relative serum viscosity value, and the calculated whole blood viscosity to identify a level at which symptoms occurred. The majority of symptomatic patients had whole blood viscosity values above 8.0 centipoises. There was a direct correlation between whole blood viscosity and relative serum viscosity, r = 0.75. One patient with central nervous system abnormalities was identified as having a high whole blood viscosity but a low serum viscosity. It was concluded that the vast majority of patients with the hyperviscosity syndrome will be identified by measuring the relative serum viscosity. In patients with central nervous system findings and a low serum viscosity, the whole blood viscosity should be determined either by direct measurement or by calculation.

Blood Viscosity↗
PubMed1981

Direct relationship between blood pressure and blood viscosity in normal and hypertensive subjects. Role of fibrinogen and concentration.

Blood pressure and components of blood viscosity were measured in 49 normal subjects and in 49 untreated patients with essential hypertension. Blood viscosity values measured at six different shear rates were significantly correlated with blood pressure (r = 0.432 to 0.505, p less than 0.001). Blood viscosity was higher in hypertensive patients. This was due to both higher plasma viscosity (1.29 +/- 0.08 standard deviation versus 1.24 +/- 0.05 centipoise (cPs), p less than 0.001) and increased hematocrit values (44.4 +/- 4 percent versus 41.5 +/- 3 percent, p less than 0.005). When blood viscosity was evaluated in subgroups of normal and hypertensive subjects with matched hematocrit values, it remained higher in the hypertensive patients, and the relationship between blood pressure and viscosity was still significant. Regardless of the hematocrit value, fibrinogen levels were elevated in hypertensive patients (p less than 0.006) and, in association with the increased globulin concentration, fibrinogen was largely responsible for the increased plasma viscosity in hypertensive patients. Since the viscosity of defibrinated blood was similar in normal and hypertensive subjects with matched hematocrit values, the elevated fibrinogen level also affected whole blood viscosity. Defibrinated blood viscosity and arterial pressures were not correlated. These studies demonstrate a direct correlation between blood pressure and blood viscosity among normotensive and hypertensive subjects. This relationship is, in part, due to the rheologic effects of an elevated fibrinogen level and to an increased hematocrit value. The basis for hyperfibrinogenemia in hypertensive patients is unclear.

Adult↗
PubMed1982

The influence of iron-deficient indices on whole blood viscosity in polycythaemia.

The relationship of the red-cell indices, packed-cell volume (PCV) and plasma viscosity to whole-blood viscosity was examined in 18 patients with polycythaemia. Sixteen were examined again following a course of venesection. The results were analysed by multiple regression analysis which allowed the effects of individual variables to be independently assessed. A reduction of the MCH or MCV was associated with increased whole-blood viscosity especially at low-shear rates. It is concluded that the reduced size of iron-deficient cells results in increased cell-cell interaction causing an increase in whole-blood viscosity.

Adult↗