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PubMed1975

[Clinical significance of changes in blood viscosity in cerebrovascular insufficiency (author's transl)].

In 50 patients with encephalomalacia and 50 patients with a transient cerebral ischemic attack (TIA) the risk factors and viscosity of the whole blood as well as the hematocrit were determined before the start of treatment. Compared to a control group, the blood viscosity in patients with encephalomalacia was significantly increased (p less than 0.001) in all ranges of shearing velocity tested, in patients with TIA only at that shearing velocity which may be assumed for the area of microcirculation. This increase was related to the presence of arterial hypertension, hyperlipemia, heart failure, diabetes mellitus, hyperfibrinogenemia and increased tendency of thrombocytes and erythrocytes to aggregate. From the results obtained it was concluded that increased blood viscosity in the cerebral area of microcirculation with insufficient cerebral collateral circulation may decisively favor the development of encephalomalacia.

Acute Disease↗
PubMedDate not supplied

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 +/- 6 ml/100g/min, in the left 38 +/- 6 (p less than 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p less than 0.01 and p less than 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right (p less than 0.001 and p less than 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism.

Animals↗
PubMed1990

Neonatal polycythaemia: effect of partial dilutional exchange transfusion with human albumin on whole blood viscosity.

Haematocrit (HCT) and viscosity of whole blood were measured in ten polycythaemic hyperviscous newborn infants both before and after dilutional partial exchange transfusion with 5% albumin. This was performed in order to evaluate the effect on the lowering of HCT and whole blood viscosity. Mean umbilical HCT values decreased from 68.7% before, to 54.4% post transfusion. This decrease in HCT and viscosity was highly significant (P less than 0.001). Safety and lack of complications make human albumin solution superior to human plasma for exchange transfusion in neonatal polycythaemia.

Blood Proteins↗
PubMed1989

Changes in blood viscosity following nifedipine administration and its relation to the contents of adenosine triphosphate and 2,3-diphosphoglyceric acid in red blood cells in patients with angina pectoris.

The effect of oral administration of nifedipine (Adalat) on whole blood viscosity in patients with angina pectoris was investigated. Whole blood viscosity at a low shear rate of 37.5 s-1 was significantly reduced from 7.90 +/- 0.18 cP to 7.30 +/- 0.27 cP (1 cP = 1 mPa x s) after nifedipine administration (p less than 0.01), though the value at the high shear rate of 375 s-1, Casson yield stress value and Casson viscosity hardly decreased. Content of adenosine triphosphate (ATP) and 2,3-diphosphoglyceric acid (2,3-DPG) in the erythrocytes affecting blood viscosity, especially low shear rate viscosity, showed little change, and the hematocrit value was little varied either. Nifedipine, a Ca antagonist, has been known to inhibit Ca entry into the cells. These findings suggest that nifedipine reduces whole blood viscosity, especially low shear rate value, due to inhibition of Ca entry into the red blood cells, without increasing metabolic changes of ATP or 2,3-DPG in the erythrocytes, though measurement of Ca content in erythrocyte was unsolved.

2,3-Diphosphoglycerate↗
PubMedDate not supplied

On whole blood viscosity measurements in healthy individuals and in rheumatoid arthritis patients.

Different methods of measuring whole blood viscosity using a couette rotational viscometer were compared to establish its use in clinical rheumatological practice. The relationship between blood viscosity and hematocrit was approximately exponential and no significant differences in the slopes were found between healthy controls and rheumatoid arthritis patients. Correction of native blood viscosity to a standard hematocrit of 40% by extrapolation from a standard regression curve, established by concentration/dilution of samples from healthy persons to correct for hematocrit differences and at shear rate 92s-1, was the best method for differentiating between viscosities of patients and controls. It was also the least laborious method, requiring the smallest amounts of blood and having the lowest method error. Native blood viscosity, corrected blood viscosity, plasma viscosity and red cell aggregation were all significantly higher and hematocrit significantly lower in rheumatoid arthritis patients than in controls.

Adolescent↗
PubMed1987

Relationship between blood viscosity and cerebral ischemia after surgical treatment of ruptured intracranial aneurysms.

To determine the role of blood viscosity after surgical treatment of ruptured intracranial aneurysms, the relationship between blood viscosity and clinical condition was examined in 17 patients. A total of 213 blood samples were analyzed. An inverse correlation was found between blood viscosity and level of consciousness; in addition, blood viscosity was higher when focal neurologic deficit was observed. Hematocrit was similarly related to clinical condition, although the correlations observed were less strong. Postoperative plasma viscosity was higher in patients with focal neurologic deficit. Regular blood viscosity measurements are of value in patients at risk for developing cerebral ischemia.

Blood Viscosity↗
PubMed1986

Effects of blood viscosity on plasma renin activity and renal hemodynamics.

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

Animals↗
PubMed1989

Studies on blood viscosity during the menstrual cycle and in the postmenopausal period in healthy women.

Blood viscosity was measured in 14 healthy, menstruating women, aged 17-51 years and in 10 healthy, postmenopausal women, aged 55-64 years. The fertile women were studied once a week during a normal menstrual cycle and the postmenopausal women twice with an interval of 2 weeks. Blood viscosity was measured at natural hematocrit as well as at hematocrit 45%. In the postmenopausal women no changes in blood viscosity were found. In the fertile women, blood viscosity at hematocrit 45% was lowest at the start of the menstrual bleeding and increased to a peak at day 7 (p less than 0.01), with a similar pattern when measured at natural hematocrit. Plasma viscosity also had its lowest value at the onset of menstrual bleeding, increasing to a maximum at day 21. Changes in plasma triglycerides, but not in fibrinogen or cholesterol, seemed to contribute to this increase. Plasma factors only partly explained the variations in blood viscosity, and changes in red cell properties were also found to be of importance. The clinical significance of these rheological changes remains to be established, but at least theoretically there may be an increased risk for thromboembolism, e.g. at surgery, during days 5-15 of the cycle. In studies on blood flow and rheological conditions in fertile women, it seems advisable to standardize for time in the menstrual cycle.

Adult↗
PubMed1976

Microrheology of erythrocytes, blood viscosity, and the distribution of blood flow in the microcirculation.

The normal rheological behavior of the red blood cells is prerequisite for the survival of the red cells and also for the functioning of microcirculation. Severe alterations of red cell deformability are incompatible with life. When compensated by anemia, even relatively severe rheological incompetence of individual red cells is tolerable. Functional loss of red cell deformability is widely known to occur under conditions of sustained hypoperfusion, and disseminated stagnation of blood in the paracapillary bed occurs. The resulting capillary occlusion does not necessarily reveal itself in grossly reduced flow rates or increased "total peripheral resistance," since it is compensated by shunting through microscopic anastomoses. The biological significance of the phenomenon of red cell aggregation (collateral loss of blood fluidity, "collateral blood viscidation") is related to hemodynamics only on the level of individual capillaries. Since the compensatory potentials of vasomotor factors at this level are also very high, the collateral viscidation is not only facilitated but by the same token partially compensated. Therefore, unless complicated by a defect in the macrocirculation, the biological significance of blood rheology seen under the aspects of entire organs is not primarily related to hemodynamics, but to diffusive transcapillary exchange. As a consequence of collateral blood viscidation, diffusion takes place under sub-optimal conditions. The available surface area for exchange is reduced, the diffusion distances are increased. In themselves, these changes are no acute threat to the survival of the entire individual. In combination with other defects, they are capable of sustaining prolonged states of flow arrest. Since the rheological properties of blood can be easily manipulated, sustained circulatory deficiencies can be avoided or treated by improving blood fluidity.

Animals↗
PubMed1979

Dynamic study of the blood viscosity of insulin-dependent diabetics by means of an artificial pancreas.

The blood viscosity of 15 insulin-dependent, poorly controlled, diabetic subjects was determined by using a microviscosimeter at low shear rates, with cylindrical cuvettes of the Couette type. It was found that the blood viscosity of these diabetics was more elevated than that of control patients (p less than 0.001). In ten diabetics, the return to a strict metabolic control over a period of more than 24 h by means of an artificial pancreas resulted in a significant systematic lowering of blood viscosity. These results suggest that the metabolic control of diabetes influences blood viscosity, and they underline the importance of an artificial pancreas for the dynamic study of the factors affecting blood viscosity during the course of diabetes.

Adolescent↗
PubMed1977

[Blood viscosity in ischemic heart disease with different types of hyperlipoproteinemia].

Fifty patients with chronic forms of ischaemic heart disease were examined, their blood viscosity being determined with the aid of a rotational viscosimeter, and their hematocrit and fibrinogen levels being measured. Some increase in blood viscosity was found in patients with ischaemic heart disease with a tension shift of 0.7 and 0.5 dyn/cm2. In analysing the interrelationship between the blood viscosity figures and the risk factors inherent in ischaemic heart disease it was found that smoking results in an increasing blood viscosity with low tension shifts. The highest blood viscosity with low tension shifts. The highest blood viscosity values were found in patients with IIb and IV types of hyperlipoproteinemia. A direct correlation was established between the level of triglycerides and blood viscosity with a tension shift of 0.7 dyn/cm2.

Adult↗
PubMed2000

Influence of parathyroid hormone, calcitonin, 1,25(OH)2 cholecalciferol, calcium, and the calcium ionophore A23187 on erythrocyte morphology and blood viscosity.

Parathyroid hormone and calcitonin, both endocrine modulators of calcium homeostasis, may influence blood rheology. Parathyroid hormone is known to reduce erythrocyte survival, leading to anemia. Calcitonin has been found to have some vascular effects. We have analyzed the Influence of parathyroid hormone (10(-7) to 10(-10) mol/L), calcitonin (10(-6) to 10(-12) mol/L), 1,25(OH)2 cholecalciferol (10(-7) to 10(-10) mol/L), additional calcium in plasma (+1 and 2 mmol/L), and the calcium lonophore A23187 (50 micromol/L) on erythrocyte morphology and blood viscosity at high shear rate (94 s(-1)) and low shear rate (0.1 s(-1)) in vitro. The loading of erythrocytes with calcium by the ionophore A23187 produced a marked echinocytic shape transformation, an increased blood viscosity at high shear rate caused by decreased deformability of these cells, and a decreased viscosity at low shear rate caused by decreased aggregation of echinocytes. In contrast, increasing plasma calcium concentrations, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3 had no effect on erythrocyte morphology and blood viscosity. We conclude that an increase in intraerythrocytic calcium leads to severe echinocytosis and altered blood viscosity. The endocrine modulators of calcium homeostasis--namely, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3--apparently do not influence intraerythrocytic calcium to a significant degree and have, therefore, no influence on cell morphology and blood viscosity.

Blood Viscosity↗
PubMed1998

Venous dysfunction and the change of blood viscosity during head-up tilt.

The precise stimulus that induces vasovagal syncope is still unclear. We have previously demonstrated that the peripheral distribution of blood volume (venous pooling) is a strong predictor of tilt induced vasovagal reaction. We hypothesized that an increase in venous pooling during tilt accentuates the measured increase in blood viscosity. This hypothesis is based on the previously demonstrated increase in venous pressure and subsequent increase in transcapillary fluid transudation during tilt. The increased blood viscosity, in turn, increases vascular shear rate, which may alter the vasoconstrictive and other cardiovascular responses to decreased preload. We measured blood viscosity (supine and tilt) in 56 patients with a history of orthostatic intolerance (37 with venous pooling [VP] and 19 without venous pooling [non-VP]). VP and non-VP were separated into subgroups based on blood pressure and heart rate response to tilt. There was a positive correlation between blood viscosity and plasma aldosterone in the supine. In the group as a whole, neither supine blood viscosity nor its increase during tilt differed between VP and non-VP. However, the tilt induced increase of blood viscosity was significant only in patients with tilt provoked tachycardia plus normal blood pressure response in VP group. We suggest that the increase of blood viscosity in this group led to the normal blood pressure response. The positive correlation between supine blood viscosity and supine plasma aldosterone indicates that the normal blood pressure response in this group possibly was via stimulation of the renin-angiotensin-aldosterone system.

Adult↗
PubMed1989

Blood viscosity parameters in coronary heart disease: effect of fish oil supplementation.

We have evaluated blood viscosity parameters in 20 men suffering from coronary heart disease (CHD) and in 15 control subjects. Whole blood viscosity at a standardized haematocrit of 45% was significantly increased in the CHD-patients, both at low (p less than 0.001) and high (p less than 0.05) shear rate. The increased whole blood viscosity in these patients was explained by an increased plasma viscosity (p less than 0.01), while the erythrocyte suspension viscosity values at a standardized haematocrit of 70%, reflecting erythrocyte deformability, were within the normal range. We have studied the effects of a daily supplementation of 1.5 g omega-3 polyunsaturated fatty acids on blood viscosity in the CHD patients. After 6 weeks of treatment whole blood viscosity, at low and high shear rate, and plasma viscosity were significantly improved (all p less than 0.05), although not normalized. There was no effect of the fish oil on erythrocyte deformability.

Aged↗
PubMed2001

[Coping with stress and blood viscosity in stroke prevention patients].

INTRODUCTION: Hematocrit, fibrinogen and blood viscosity influence blood fluidity and are well known stroke risk factors. Studies have shown relationships between these factors and psychological stress. AIM: The aim of this study was to investigate how stroke risk patients with increased hematocrit, increased fibrinogen, or increased plasma viscosity differ from patients free of these risk factors in their ways of stress coping. METHOD: 6503 persons participated in the following stroke risk investigations: biographical and risk factor orientated anamnesis, neurological status investigation, laboratory investigation, sonographic investigation and psychological investigation. After assessment of several risk factors, differences in stress coping between risk factor and non-risk factor groups were investigated by means of the t-test and the Wilcoxon-test. RESULTS: Men with pathological hematocrit showed significantly higher scores in the coping strategy resignation and a tendency to less positive self instruction and response control attempts. Women with higher values of hematocrit demonstrated higher values in resignation and drug intake. Men with higher fibrinogen showed significantly higher scores in distraction, vicarious satisfaction, minimising by comparison and tendency to flee as well as a tendency towards drug intake. Women with increased fibrinogen showed no differences. Men with normal plasma viscosity had significantly higher values in tendency to flee and tendencially in desire for social support and lower values in minimising by comparison. Women with increased plasma viscosity demonstrated higher scores in resignation and aggression. CONCLUSIONS: The presence of elevated values in parameters of blood viscosity coincides with increased passive and defensive coping mechanisms, whereas non-risk factor persons show raised values in active coping styles.

Adaptation, Psychological↗
PubMed1991

Relation between blood viscosity and hematocrit in rabbits subjected to repeated treatment with endotoxin.

Blood rheology was studied in rabbits repeatedly treated with endotoxin at a dose of 0.1 mg administered 3 times, at intervals of 3 days. On the 7th day after the last endotoxin injection, blood was sampled 3 times from the femoral artery under anesthesia using pentobarbital sodium. Blood viscosity was determined at a shear rate of 150 s-1 at 37 degrees C using a cone-plate viscometer. Plasma fluidity was determined using the filtration method. Hematocrit and whole blood viscosity showed no significant differences between the untreated rabbits (Group A) and rabbits treated with endotoxin (Group B). Plasma fluidity was significantly lowered in Group B. Whole blood viscosity correlated well with hematocrit in Group A, but there was no correlation in Group B. The ratio of hematocrit to whole blood viscosity, which is considered to be the index of oxygen delivery from the blood rheological point of view, indicated no significant difference between the two groups. The optimal hematocrit to oxygen delivery, however, was higher in Group B than in Group A. These data suggest that the high hematocrit rather becomes an advantage to oxygen delivery in endotoxicosis because the hematocrit-viscosity relation is disturbed.

Animals↗
PubMed2001

Commercial taxane formulations induce stomatocytosis and increase blood viscosity.

1. Taxanes are antineoplastic drugs which have cardiovascular side effects of unknown mechanism. We investigated their influence on blood viscosity and erythrocyte morphology. 2. Whole blood was incubated in vitro with increasing concentrations of Taxol, Taxotere, paclitaxel (0-100 microM) and the vehicles Cremophor-EL and Tween 80 (0-5% vol) for 1 h at 37 degrees C. Plasma and whole blood viscosity (Haematocrit 45%) were measured and erythrocyte morphology was assessed on glutaraldehyde-fixed cells. The same investigations were performed in seven patients before and after a Taxol-infusion. 3. Taxol and Taxotere induced a dose- and time-dependent stomatocytic shape transformation of erythrocytes. Paclitaxel alone had no effect, but the vehicles cremophor-EL and Tween 80, used in Taxol and Taxotere, respectively, induced a comparable degree of stomatocytosis. This suggests a preferential intercalation of these substances into the inner hemileaflet of the membrane lipid bilayer. Associated with this shape change a dose-dependent increase in plasma and whole blood viscosity was observed. Neither shape nor viscosity changes were reversible upon removal of the agents. After the infusion of 130-300 mg Taxol in patients a slight shift towards stomatocytosis and an increase in whole blood viscosity at high shear rate from 5.09+/-0.30 to 5.44+/-0.38 mPa.s (P<0.05) were confirmed. 4. Commercial taxane drug formulations induce stomatocytosis and increase blood viscosity, which is due to their formulation vehicles. These findings may contribute to the understanding of the cardiovascular side effects of these drugs.

Aged↗