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PubMed1986

Effect of the acute phase reaction on blood viscosity after infrainguinal arterial bypass.

A new method of determining apparent blood viscosity at low shear rates using a porous bed viscometer has been validated in an experimental study of canine blood altered by isovolemic hemodilution. The data confirm the ability of the technique to detect the non-Newtonian behavior of blood at higher hematocrit and fibrinogen values. The technique was then employed in a limited clinical study of nine patients undergoing infrainguinal vascular reconstruction to evaluate the effect of operation and the associated increase in serum fibrinogen levels, resulting from the acute phase reaction, on blood viscosity. Although there was a substantial change in serum glycoprotein levels, the concurrent relative decrease in red cell mass after operation resulted in a decrease in whole blood viscosity. These findings support the beneficial effect of moderate hemodilution as a means of compensating for the potentially detrimental effects of the acute phase reaction on blood rheology.

Animals↗
PubMed1996

Blood viscosity in broilers: influence on pulmonary hypertension syndrome.

Elevation in apparent blood viscosity may enhance the pulmonary hypertension that leads to pulmonary hypertension syndrome (PHS) and ascites in fast-growing broilers. We investigated the importance of packed cell volume (PCV) and shear rate in modifying apparent viscosity of the blood from broilers assigned to normal, preascites, and ascites groups. Apparent viscosity of broiler blood increased at all shear rates as PCV increased; the increase in apparent viscosity became greater as the shear rate decreased at PCV above 0.30. At the PCV of normal broilers (0.30 or below), apparent viscosity was nearly shear rate independent, at least down to 11.25 per second, the lowest shear rate studied. Apparent viscosity, at any given PCV and shear rate, was significantly lower in the blood of birds with ascites than in normal birds; however, the relative viscosity was not different between those groups, indicating that lower plasma viscosity in the birds with PHS was responsible for the finding. The results show that the principal factor responsible for increased apparent viscosity of blood in birds with PHS is the increase in PCV. The increased resistance to flow of blood as the result of higher blood viscosity may contribute to the pulmonary hypertension.

Animals↗
PubMed1985

The effects of erythrocythemia on blood viscosity, maximal systemic oxygen transport capacity and maximal rates of oxygen consumption in an amphibian.

Graded erythrocythemia was induced by isovolemic loading of packed red blood cells in the toad, Bufo marinus. Blood viscosity, hematocrit, hemoglobin concentration, maximal aortic blood flow rate and maximal rates of oxygen consumption were determined after each load. Blood viscosity was related to hematocrit in the expected exponential manner; ln eta = 0.43 + 0.035 Hct. Maximal blood flow rates in the dorsal aorta were inversely proportional to blood viscosity and fit predictions of the Poiseuille-Hagen flow formula. The effect of increased blood viscosity was to reduce aortic pulse volume, but not maximal heart rate. Maximal systemic oxygen transport capacity (aortic blood flow rate X hemoglobin concentration X O2 binding capacity of hemoglobin) was linearly correlated with the maximal rate of oxygen consumption. These date indicate that optimal hematocrit theory is applicable for maximal blood flow rates in vivo, and that systemic oxygen transport is the primary limitation to aerial VO2 max in amphibians.

Animals↗
PubMed1982

Blood viscosity during the neonatal period: the role of plasma and red blood cell type.

Adult and newborn infant blood viscosity have been compared, taking into account not only the hematocrit, but also the type of red blood cells (fetal or adult) in the circulation and the plasma viscosity. At all shear rates studied, the viscosity of the adults' blood was higher than that of the newborn infant. At shear rates of 11.5 and 46 second-1, an increase in the hematocrit influences the viscosity of neonatal and adult blood similarly. At 115 and 230 second-1, the rise in hematocrit was associated with a greater increase in viscosity in the presence of fetal red blood cells, probably because of their lesser deformability. Plasma viscosity was 1.18 +/- 0.17 centipoises in the newborn compared to 1.36 +/- 0.10 in the adult group (P less than 0.001). The relative apparent viscosity (apparent viscosity/plasma viscosity) was higher in the neonate at a hematocrit of 65% (P less than 0.05). In normal conditions, blood viscosity is lower in the neonatal period because of a lower plasma viscosity.

Adult↗
PubMed2000

Blood viscosity and aging.

The objective of this study was to evaluate the relationship of whole blood viscosity and its major determinants (plasma fibrinogen level, hematocrit, hemoglobin and blood cell count) to advancing age. A total of 249 subjects (mean age 49.9+/-21.5; range 19-102 years) were included in the study. They were divided into three groups, (A) <30 years of age, n, 58; (B) 30-60 years, n, 107; (C) >60 years, n, 84. Whole blood viscosity at two different rates of shear (450 and 45 s(-1)) was evaluated using a cone-plate digital viscosimeter. The hematological parameters (hematocrit, hemoglobin and blood cell count) were evaluated using an automatic Coulter Counter. Plasma fibrinogen concentration was measured by a clotting method. When both sexes are considered together, whole blood viscosity shows no significant difference among age groups. Plasma fibrinogen concentration significantly increases with age (P<0.001); hemoglobin, red blood cell count and platelet count, on contrary, are significantly lower in aged group. In the male sex, blood viscosity at higher shear rate (450 s(-1)) negatively correlates with advancing age (P<0.005). The age-related decrease of hematocrit value in the male sex accounts for this occurrence.

Journal Article↗
PubMed1991

Effect of hydroxyurea on blood viscosity in chronic myelogenous leukemia with hyperleukocytosis.

The effect of hydroxyurea on blood viscosity was studied in 10 patients with Philadelphia chromosome positive chronic myelogenous leukemia (CML) and hyperleukocytosis (white blood cell counts over 200 x 10(9)/l). All the patients had visible manifestations of leukostasis such as headache, blurred vision, retinal hemorrhage, pulmonary infiltrates, etc. Contraves LS 30 viscometer was used to measure the blood viscosity at 37 degrees C and at different shear rates on paired leukemic blood samples obtained before and after the hydroxyurea treatment. The blood viscosity was significantly higher in CML patients then normal subjects and decreased after treatment with hydroxyurea. In all the cases plasma viscosity was unaffected by the treatment.

Adolescent↗
PubMed2002

Hematological and blood viscosity changes in tail-suspended rats.

BACKGROUND: Fluid shifts during exposure to microgravity result in a decrease in plasma volume which can lead to a transient increase in hematocrit. This transient increase in hematocrit could result in an increased blood viscosity. Yet, hematocrit returns to near normal values within a matter of hours of microgravity exposure as a result of a reduction in red blood cell mass. Rat tail-suspension models mimic the fluid shifts and hematological changes associated with microgravity exposure. METHODS: Tail-suspended rats were monitored for hematological and hemorheological changes over 4, 24, 72, and 168 h of tail suspension. Additionally, hematological and hemorheological changes were followed during recovery periods of 48, 120, and 192 h following 168 h of tail suspension. RESULTS: Although hematocrit increased significantly by 4 h of suspension, blood viscosity did not differ from controls. However, blood viscosity was significantly greater in the 72-, 168-, and 168/48-h suspension groups relative to controls despite no significant differences in hematocrits between groups. Theoretical calculations of blood viscosity at hematocrits of 50 and 60% (values intended to mimic hematocrits that would occur if red blood cell mass did not decrease) show a significant increase relative to the blood viscosities determined for the actual hematocrits in the experimental groups. CONCLUSIONS: The lowering of hematocrit associated with spaceflight may substantially reduce blood viscosity and thereby maintain the hematocrit at an optimal level for oxygen delivery to tissues.

Animals↗
PubMed2003

Changes in blood viscosity with synthetic protease inhibitors.

We examined the effects on whole blood viscosity and coagulation time of various dosages of the synthetic low-molecular protease inhibitors gabexate mesilate and nafamostat mesilate with an oscillation-type viscometer. When either agent was added, blood viscosity decreased dose-dependently along a sigmoid-like curve. Furthermore, coagulation time was shorter with gabexate mesilate than with nafamostat mesilate owing to the differences of half-life in human blood. Thrombin generation, which results from the activation of coagulation factors, is inhibited by synthetic protease inhibitors and subsequently decreases blood viscosity dose-dependently.

Adult↗
PubMed1995

Effect of low-dose oral triphasic contraceptives on blood viscosity, coagulation and lipid metabolism.

The purpose of the study was to determine the relationship between hemorheological profile, i.e. blood viscosity, and other risk factors for cardiovascular and thrombotic diseases in women taking oral contraceptives and if blood viscosity may be considered a marker of cardiovascular risk in OC users. Plasma levels of coagulation parameters, serum lipids, blood viscosity and RBC deformability were determined in a group of 10 women taking OC vs. 10 controls. The blood parameters were evaluated before OC use and thereafter at 3 and 6 months. A significant change in the partial thromboplastin time, fibrinogen, HDL and apolipoprotein A-I was observed, while the other parameters remained unchanged. Plasma viscosity was significantly increased during OC treatment; whole blood viscosity and RBC deformability remained unchanged. However, although some parameters were significantly modified during OC treatment, all alterations remained within the normal range of laboratory values. The data confirm that low-dose triphasic OC therapy does not affect significantly the coagulation system, serum lipid metabolism and blood viscosity. Plasma viscosity measurement may be considered as a marker for monitoring women using OC because it is apparently the most sensitive parameter.

Adolescent↗
PubMed1985

[Blood viscosity indicators in patients with gastric and duodenal diseases].

A total of 102 patients with peptic ulcer of the stomach and duodenum, chronic gastritis, and erosive gastritis were examined. A statistically significant increase in blood viscosity was recorded during the diseases enumerated. In peptic ulcer and chronic gastritis, the fibrinogen and hematocrit levels did not change quantitatively although quantitative changes in the fibrinogen level were likely to influence blood viscosity. Red cell aggregation was found to be increased, being the main factor responsible for blood viscosity deterioration. The authors studied the effect of cimetidine on blood viscosity in patients with peptic ulcer and the effect of peritol in chronic gastritis. These drugs were found to markedly reduce blood viscosity, as a result of which the circulation in the gastric mucosa improved, promoting the cure of patients with peptic ulcer. According to the authors' opinion, cimetidine, that blocks H2 histamine receptors, lessens the effect of histamine on red cell aggregation, thereby improving blood viscosity.

Adolescent↗
PubMed1997

Hemorheologic profiles of plasma fibrinogen and blood viscosity from silent to acute and chronic cerebral infarctions.

Hemorheologic changes from silent to acute and chronic cerebral infarction have seldom been reported. We evaluated hemorheologic profiles of the whole blood viscosity, plasma viscosity and fibrinogen level in stroke at-risk patients with silent cerebral infarction, patients with acute or chronic cerebral lacunar infarction, and subjects at low risk for stroke. Hemorheologic profiles were measured in 88 subjects: (1) 36 patients with silent cerebral infarction (mean 64.7 years), who provided no clinical history of having had definitive stroke but showing > 5 mm lesions of cerebral infarction or periventricular hyperintensity (PVH) observed in magnetic resonance imaging (MRI) T2-weighted images; (2) 12 patients with acute cerebral lacunar infarction (mean 69.1 years), measured within 3 days and repeated 1 month after onset; (3) 25 patients with chronic cerebral lacunar infarction (mean 66.2 years), measured 12.5 months after onset; and (4) 15 subjects at low risk for stroke (mean 65.8 years) without cardiovascular risk factors or lesions on MRI. Patients with silent cerebral infarction were subdivided into two groups of less advanced and more advanced grades, based on the number of infarctions or the grade of PVH. Whole blood viscosity (shear rates: 22.5-225.0 s-1), corrected blood viscosity for 45% standard hematocrit (Hct), plasma viscosity, fibrinogen, serum total protein, albumin, and Hct were measured. Plasma fibrinogen levels were lower in silent cerebral infarctions than in chronic cerebral infarctions (P < 0.01), and patients with more advanced grades of silent cerebral infarction showed higher levels of plasma fibrinogen than those with less advanced grades (P < 0.01 and P < 0.05). Whole blood viscosity, corrected blood viscosity (Hct 45%), plasma viscosity and fibrinogen levels in acute cerebral infarction within 3 days after onset were higher significantly than those in subjects at low risk for stroke. Plasma fibrinogen level persisted to be elevated up to 1 month after onset, which continued as well in patients with chronic cerebral infarction. Advanced grades of silent cerebral infarction in stroke at-risk patients are accompanied by elevations of plasma fibrinogen level, which increases further after onset of cerebral infarction; such abnormalities persist up to the chronic stage. Elevated plasma fibrinogen level might reflect progression of atherogenesis in patients with advanced grades of silent cerebral infarction, resulted in an increased probability as to be a risk factor for cerebral infarction.

Acute Disease↗
PubMed2005

Prognostic impact of low-shear whole blood viscosity in hypertensive men.

BACKGROUND: The role of blood viscosity as a marker for discriminating cardiovascular risk in essential hypertension remains uncertain. The aim of this study was to assess whether whole blood viscosity (WBV) could be useful in assessing cardiovascular risk in men with a first diagnosis of hypertension. DESIGN: A total of 331 middle-aged men with newly diagnosed essential hypertension (age at entry 40-64 years, average blood pressure 151/95 mmHg) underwent low-shear-rate (0.94 s(-1)) and high-shear-rate (94.5 s(-1)) WBV determination and were then followed for a mean of 4.8 +/- 3 years (range 0-12 years). RESULTS: Cardiovascular event rates in the bottom, middle and top tertiles of the distribution of low-shear WBV were 1.10, 2.13 and 4.43 per 100 patient-years, respectively (log-rank test, P < 0.001). After taking into account several established cardiovascular risk factors in a Cox survival analysis, a raised low-shear WBV conferred an increased risk for cardiovascular events (top vs. bottom tertile hazard ratio = 3.42, 95% confidence interval = 1.4-8.4, P = 0.006; middle vs. bottom tertile hazard ratio = 2.25, 95% confidence interval = 0.9-5.6, P = 0.09). The independent association between high-shear-rate WBV and cardiovascular events bordered statistical significance (P = 0.07). Inclusion in the survival model of low-shear-rate resulted in a significantly greater chi(2) improvement (P < 0.05) than inclusion of high-shear-rate WBV. CONCLUSIONS: In hypertensive men, an increased WBV at low shear rate is a predictor of cardiovascular events independently from the effect of several traditional risk factors. Low-shear WBV is a better discriminator of cardiovascular risk than high-shear WBV.

Adult↗
PubMedDate not supplied

[The correction of the increased blood viscosity syndrome in brain ischemia in rats with a combination of dikvertin and ascorbic acid].

In experiments in vitro on a model of the syndrome of increased blood viscosity dikvertin reduced blood viscosity, weakened aggregation of red cells and raised their property of becoming distorted. A mixture of dikvertin and ascorbic acid improved the hemorrheologic parameters better than do dikvertin and tanakan. On a model of chronic ischemia of the brain of rats attended with deterioration of blood rheologic parameters, it was demonstrated that a course of treatment with a dikvertin and ascorbic acid complex decreases the manifestations of the syndrome of increased blood viscosity.

Animals↗
PubMed2005

Influence of contrast media (iopromide, ioxaglate, gadolinium-DOTA) on blood viscosity, erythrocyte morphology and platelet function.

The influence of contrast media on blood viscosity, erythrocyte morphology and platelet function was studied. In vitro blood was incubated with iopromide (Ultravist), ioxaglate (Hexabrix) or gadolinium-DOTA (Dotarem). Plasma viscosity and whole blood viscosity were measured and the mean erythrocyte volume and morphology were assessed. Platelet aggregation was measured with a PFA-100 instrument. In an ex vivo study on patients receiving these contrast media the same measurements as described above were done. All contrast media increased blood viscosity at high shear rate in a dose dependent manner (e.g. with ioxaglate: from 4.9+/-0.2 mPa x s to 8.6+/-0.5 mPa x s at 160 mg I/ml), decreased low shear viscosity (for ioxaglate: from 44.9+/-2.5 to 27.7+/-4.8 mPa x s), increased plasma viscosity (ioxaglate: from 1.2+/-0.1 to 2.8+/-1.3 mPa x s), decreased the mean erythrocytic volume (ioxaglate: from 89.7+/-1.4 to 79.7+/-2.0 fl) and decreased platelet aggregation. Iopromide induced an echinocytic shape transformation of erythrocytes. Ex vivo a decreased hematocrit and a consecutively decreased whole blood viscosity were found with iopromide and ioxaglate. We conclude that contrast media influenced blood rheology, erythrocytes and platelet aggregation in vitro and ex vivo.

Adult↗
PubMed2005

Measurement of whole blood viscosity profiles via an automated viscometer: technical details and clinical relevance.

Recent basic science and large-scale clinical studies involving blood rheological factors have led to a similar conclusion: the mechanics of blood flow play an important role in the development and progression of various cardiovascular diseases (e.g., coronary artery disease, stroke). Several viscometer systems to measure whole blood viscosity have been developed, yet blood viscosity measurements are not routinely employed in clinical practice, primarily due to the complexity of currently available methods. Herein we provide a description of a new, computer-controlled capillary viscometer that offers a convenient approach to the measurement of blood viscosity over a wide range of shear rates. The new viscometer uses a disposable test section, requires small volumes of blood, provides viscosity data that compare well with those from other viscometers, and completes all testing and data analysis within five minutes.

Blood Viscosity↗
PubMed1979

The effect of iron deficiency on whole blood viscosity in polycythaemic patients.

Iron deficiency leads to a significant increase in whole blood viscosity in polycythaemic patients. This can be corrected by simultaneous treatment with iron and venesection. In patients with polycythaemia secondary to hypoxia the haemoglobin concentration may be increased by treating coexisting iron deficiency, without altering the whole blood viscosity, thus increasing oxygen availability to the tissues. Values for whole blood viscosity can be derived from the peripheral blood Hb and MCH, allowing therapeutic decisions to be made on the basis of a simple haematological examination.

Adult↗
PubMed1991

A semi-empirical model of apparent blood viscosity as a function of vessel diameter and discharge hematocrit.

A semi-empirical model is developed to describe the dependence of apparent viscosity of blood on vessel diameter (2.7 to 500 microns) and vessel discharge hematocrit (5% to 60%). The blood flow is modeled as a cell-rich core and a cell-free marginal layer in the larger vessels and an axial-train in the smaller vessels. Laminar (Poiseuille) flow is assumed in all cases. An equation is derived in which apparent viscosity is a function of vessel diameter, core viscosity, and width of marginal layer. This is then complemented by empirical equations in which core viscosity varies exponentially with discharge hematocrit while the width of marginal layer varies linearly with discharge hematocrit. The model correlates well with several sets of experimental data and behaves according to the Fahraeus-Lindqvist effect. Predicted apparent viscosity tends to the expected finite value for large vessel diameters. Dependence of apparent viscosity on vessel diameter is realistically smooth in the whole diameter range.

Blood Vessels↗
PubMed1982

Plasma and blood viscosities, and aggregation of red cells in racehorses.

Nineteen racehorses have been studied for haemorheologic factors as earlier studies showed a definite correlation between physical fitness and these factors in humans. Results included individual values for all viscosity factors, and the arithmetic means, the latter showing 4.70 +/- 0.49 cP for blood viscosity measured at a shear rate of 180 s-1; 1.100 +/- 0.048 cP for plasma viscosity; 1.045 +/- 0.063 for the rigidity of red cells defined by term 'Tk'; 42.2 +/- 4.1% haematocrit; 290 +/- 39 mg per 100 ml for fibrinogen level; and 278 +/- 75 mm h-1 for aggregation of red cells at 37 degrees C (corrected for plasma viscosity and at constant haematocrit of 30%). Data for subgroups have also been obtained. Linear regressions of apparent blood viscosity against log shear rate were found to be specific to individual racehorses, and differed significantly between some racehorses. Data for blood viscosity, plasma viscosity and haematocrit were near the values reported for human athletes, but rigidity of red cells and aggregation of red cells was found to be much higher in horses. No correlation was found between aggregation of red cells and fibrinogen level. In blood samples from some horses, the erythrocyte sedimentation rates increased with decrease of temperature, while in other samples they increased with increase of temperature. It appears that it is possible to characterise individual horses by blood viscosity factors and viscosity functions.

Animals↗