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PubMedDate not supplied

[Blood viscosity analyzer].

An analyzer that determines blood viscosity at different shift speed has been designed. Its operation principle is based on the use of rotation viscosity measurement using a rotor freely floating in the sample. A blood sample is placed between the stationary thermostabilized measuring cylinder and a free floating rotor. The system creates a rotating magnetic field which makes the rotor rotate with a preset speed, determines shift stress, calculates the magnitude of viscosity and indicates it on the display. The magnitude of viscosity is proportional to the square of the current drawn in the windings of a stator, which divided by the rotational speed of a rotor. The analyzer provides viscosity measurements in the range of 0.7-14 mPa.sec at shift rate of 20-200 sec-1, the sample volume is less than 1 cm3. The device can be used for the diagnosis of the diseases whose pathogenesis microcirculatory and coagulative disorders play an important role in.

Blood Viscosity↗
PubMed1998

Evaluation of erythrocyte morphology as deformability index in patients suffering from vascular diseases, with or without diabetes mellitus: correlation with blood viscosity and intra-erythrocytic calcium.

The aim of our study was to evaluate the erythrocytic morphology in vascular patients, with or without diabetes, showing cell alterations correlated to blood viscosity and intra-erythrocytic calcium. We studied 108 subjects: 20 normal subjects, 58 vascular patients (25 suffering from CHD, 19 from CVD, 14 from POAD) and 30 non-insulin-dependent diabetes patients with vascular disease in metabolic compensation (13 CHD, 9 CVD, 8 POAD). Erythrocytic morphology, blood viscosity and intra-erythrocytic calcium were evaluated. Our results show that bowls, the most deformable red cells, decreased significantly in vascular patients and in POAD diabetics, while the discocytes, having a stiffer form, greatly increased in subjects suffering from ischemic disease and in POAD diabetics. The altered red cells (echinocytes and knizocytes) reached a statistical significance in CVD and POAD diabetics. Comparing the percentage of discocytes to intraerythrocytic calcium content in vasculopathic subjects, we obtained a significant correlation. No evidence of a relationship between discocytes and blood viscosity was found, even if blood viscosity significantly increased in patients affected by ischemic disease. These results suggest that ischemia decreases the deformability of red cells which is supported by the study of red cells morphology, by the erythrocytic morphology index (EMI), which becomes < 1, and by the evaluation of cytosolic calcium content.

Adult↗
PubMed1982

A hypothesis proposing increased blood viscosity as a cause of proteinuria and increased vascular permeability.

Currently accepted concepts of renal and vascular physiology are inadequate to explain the reversible increases in vascular permeability which occur during episodes of increased blood viscosity. On the basis that all basement membranes exhibit biological thixotropy, it has been suggested that basement membranes are pressure dependent. The physiological significance of increased blood viscosity lies in the associated increase in peripheral vascular resistance which develops because of altered blood rheology. In order to overcome the peripheral resistance, intravascular pressure rises, and if adequate pressures develop, plasma proteins may deform and pass through the vascular basement membrane. This is considered to be the mechanism of proteinuria. In the treatment of high blood viscosity disorders it is suggested that the immunosuppressant drug, Thiamphenicol, may be useful because of its ability to induce a reversible dose-related depression of erythropoiesis, and thereby reduce blood viscosity.

Blood Viscosity↗
PubMed1987

Effects of plasma hyperviscosity on skeletal muscle blood flow and blood viscosity in vivo.

The effect of plasma hyperviscosity on skeletal muscle blood flow and blood viscosity in vivo was studied. Blood flow and viscosity in vivo were determined in the isolated and vasodilated calf muscle of one hind limb in dogs. Plasma hyperviscosity was induced by suspending red blood cells in concentrated and isotonic solutions of low molecular weight dextran in saline. Viscosity in vivo was determined by comparing pressure-flow relationships for blood and a reference solution. Blood viscosity in vitro was determined in a Wells-Brookfield cone-plate viscometer. Determinations were made for plasma viscosities of 1.3, 2.2 and 4 cP. It was found that blood flow and viscosity in vivo were strongly dependent on plasma viscosity and that the effects in vivo could be predicted from values obtained in vitro.

Animals↗
PubMed1983

Blood viscosity in proliferative diabetic retinopathy and complicated retinal vein thrombosis.

Forty-two patients with longstanding retinal vein thrombosis and 36 patients with diabetes had their blood viscosity levels measured. In both conditions blood viscosity, plasma viscosity, and plasma fibrinogen levels were significantly higher in those patients with capillary non-perfusion and/or new vessels on fluorescein angiography, compared to those patients without these complications. The possible role of abnormal blood viscosity in producing capillary non-perfusion and its sequelae in both conditions is discussed.

Aged↗
PubMed1981

Clinical relevance of blood viscosity and red cell deformability including newer therapeutic aspects.

Peripheral ischemia is mostly due to narrowing of the vessels, although blood supply is also influenced by the hemorheologic properties of the blood. Recent research has revealed that abnormally high blood viscosity can be a contributing cause in ischemia. Therapeutically decreasing the blood viscosity improves the ischemia by increasing flow through the narrowed vessels and may as such offer a valuable alternative to surgery. Different possible therapeutic approaches for decreasing blood viscosity and the related clinical evidence are discussed.

Adenosine Triphosphate↗
PubMedDate not supplied

Air pollution by gasoline exhaust fumes: effect on platelet function and blood viscosity.

Air pollution induced by automobile exhaust fumes seems to be involved in increased cardiovascular and respiratory morbidity. The effects of inhalation of such pollutant gases on platelet function and blood viscosity have not been sufficiently investigated, even if these parameters seem to be in strict correlation with cardiovascular function. Twelve healthy non-smoking volunteers were exposed for 30 minutes in a closed room to air polluted by automobile fumes. Platelet aggregation, blood viscosity, HbCO levels and P50 STD were determined before and after exposure. Cardiovascular parameters (blood pressure, heart rate and ECG) were also measured. At the end of the test, HbCO levels were significantly increased, but P50 STD was significantly reduced; an impairment of both platelet function and blood viscosity was observed. No significant changes in cardiovascular parameters were recorded. The decreases in platelet aggregation and blood viscosity were not directly correlated with either the increase in carbon monoxide levels or with the reduced P50 STD levels. It can be reasonably concluded that gasoline exhaust fumes could have been responsible for the observed alterations.

Adult↗
PubMed2006

Effects of a new perfluorocarbon emulsion on human plasma and whole-blood viscosity in the presence of albumin, hydroxyethyl starch, or modified fluid gelatin: an in vitro rheologic approach.

BACKGROUND: Artificial oxygen carriers such as perfluorocarbon (PFC) emulsions have reached Phase III clinical trials as alternatives to homologous blood, but their rheologic effects have not been characterized. In this study, the rheologic effects of PFC emulsion in the presence of clinically used volume expanders were investigated. STUDY DESIGN AND METHODS: The effects of a new PFC emulsion (small droplet size with narrow size distribution) at two PFC concentrations (4 and 8 g/dL) on plasma and whole-blood viscosity in the presence of human albumin solution (HAS), hydroxyethyl starch (HES), or modified fluid gelatin (MFG) were investigated. Three hematocrit (Hct) levels were investigated: 30, 20, and 13 percent. Plasma, PFC emulsions, and whole-blood viscosity, with a Couette viscometer, and RBC elongation, with an ektacytometer, were measured for shear rates of 0.2 to 128 per second. RESULTS: The two PFC concentrations increased plasma and whole-blood viscosities. Viscosity values similar to physiologic ones (Hct level, 40%) were observed at: 1) Hct level of 13 percent, with 4 or 8 g per dL MFG-PFC; 2) Hct level of 20 percent, with 4 g per dL MFG-PFC; and 3) Hct level of 30 percent, with 4 g per dL HES-PFC and 4 and 8 g per dL HAS-PFC. RBC deformability was unchanged. CONCLUSION: It is concluded that this new PFC emulsion increases plasma and blood viscosity and that among the three studied volume expanders, the interaction with MFG can result in viscosity values above the physiologic one even at low Hct values. The possible consequences of the increased viscosity at low Hct values are discussed.

Albumins↗
PubMed1977

[Experimental investigations on the effect of various doses of streptokinase on blood viscosity (author's transl)].

The decrease in blood viscosity induced by streptokinase (SK) in the present investigation in proportional to the streptokinase concentration up to a concentration of 2000 IE/ml blood. A maximum decrease in viscosity is attained with a dosage of between 200 and 300 IE/ml blood. The decrease in viscosity is already clearly detectable at 10 minutes at all investigated doses and is completed after 20 to 30 minutes. An increase in SK resistance delays the decrease in viscosity. Prevention of the decrease, however, only seems to occur with a very high SK resistance and a very low SK dosage (50 IE/ml blood). The optimum dosage of SK to achieve a maximum decrease in viscosity is 200 IE/ml blood.

Blood Viscosity↗
PubMed1983

Studies of blood viscosity with a newly constructed rotational viscometer which operates via a desk top computer.

Increasing interest is being shown in blood viscosity and the whole field of haemorheology. This study presents a newly constructed rotational Couette type viscometer which operates via a commercially available desk top computer and a digital plotter. The influence of haematocrit on blood viscosity is shown and the study also presents blood viscosity values of six to eight healthy men at 24 degrees C and 37 degrees C. At 37 degrees C values are shown both at natural haematocrit and at haematocrit 45%.

Blood Viscosity↗
PubMed2003

Correction of the high blood viscosity syndrome by a mixture of Diquertin and Ascorbic Acid in vitro and in vivo.

Diquertin was shown to diminish blood viscosity, to decrease the aggregation of erythrocytes, and to increase their deformability using a model of the high blood viscosity syndrome in vitro. A mixture of Diquertin with Ascorbic Acid was more effective in improving rheological indicators of blood, then either Diquertin or Tanakan. On a model of chronic brain ischemia, which is accompanied by significant deterioration of the rheological properties of blood, it was shown that a therapy with a mixture of Diquertin and Ascorbic Acid decreases the expression of the high blood viscosity syndrome.

Animals↗
PubMed1977

Effects of pentoxifylline on red blood cell deformability and blood viscosity under hyperosmolar conditions.

Using a hyperosmolar erythrocyte model, the authors studied the effect of changes in red cell deformability on whole blood viscosity and investigated the possibility of using pentoxifylline to modify red cell deformability and whole blood viscosity. In vitro studies reveal a significant correlation between the two parameters in as much as they are inversely proportionate, i.e. viscosity increases as red cell deformability decreases and vice versa. Addition of pentoxyfylline improves impaired red cell deformability under hyperosmolar conditions and simultaneously produces a reduction in whole blood viscosity.

Blood Viscosity↗
PubMed1991

Gender differences in left ventricular anatomy, blood viscosity and volume regulatory hormones in normal adults.

Gender differences in left ventricular (LV) anatomy, whole blood and plasma viscosity, and blood volume regulatory hormones were studied in 110 normotensive employed adults (28 black and 34 white men [mean age 51 +/- 12 years], 20 black and 28 white women [mean age 53 +/- 12 years]). LV mass and wall thicknesses were positively related to whole blood viscosity, primarily because of higher values of both variables in men. LV chamber size was inversely related to hematocrit and to blood viscosity (p less than 0.002) in women but not in men. Whole blood viscosity increased with age in men (p less than 0.01), but tended to decrease in women; older women also had better LV function, larger LV chambers, and a trend toward increasing LV mass. Atrial natriuretic factor increased with age in women but not in men (r = 0.60, p less than 0.001), and plasma renin activity decreased (r = -0.35, p less than 0.02). Thus, in women, increase in LV chamber size with age and associated changes in LV systolic function, atrial natriuretic factor levels and plasma renin activity suggest plasma volume expansion related to the aging process. These findings also suggest that an increase in LV volume load with age may contribute to previously reported increases in LV mass in older women.

Adolescent↗
PubMed2004

Changes in blood viscosity with heavy and light exercise.

To clarify the relationship of the intensity of acute exercise to sudden cardiac death, we examined the effects of short-term heavy and light exercise on whole blood viscosity. Nine healthy sedentary male volunteers performed ten minutes of heavy (more than 95% of maximum oxygen consumption) or light (60% to 65% of maximum oxygen consumption) exercise. Blood samples were obtained before, immediately after, and one hour after exercise. The whole blood viscosity was immediately examined with an oscillation-type viscometer and was found to increase significantly after exercise and subsequently return to baseline levels within one hour after exercise. The whole blood viscosity increased by a similar degree after heavy or light exercise. Therefore, our results suggest that there is a similar risk of sudden cardiac death, due to increased whole blood viscosity, after short-term heavy or light exercise.

Adult↗
PubMed1989

The influence of buflomedil on blood viscosity parameters in insulin-dependent diabetic patients: a preliminary study.

We have evaluated the effect of buflomedil on blood viscosity in insulin-dependent diabetic patients. At the start several rheological parameters were disturbed in these patients. After 3 months of treatment with buflomedil, blood viscosity was significantly decreased at low (P less than 0.05) and high (P less than 0.05) shear rates. The decrease in whole blood viscosity was due to a significant decrease (P less than 0.05) in plasma viscosity, which could be attributed to a significant (P less than 0.01) fall in plasma fibrinogen. There was no effect on erythrocyte deformability as assessed by erythrocyte viscosity measurements. We conclude that treatment with buflomedil improved but did not normalize some rheological parameters in insulin-dependent diabetic patients.

Adolescent↗