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At least 19 recordsLinked to original sources
PubMed1997

Whole blood viscosity, blood pressure and cardiovascular risk factors in healthy blood donors.

Whole blood viscosity contributes to the total peripheral resistance and has been suggested to be a risk factor for cardiovascular disease. Whole blood viscosity was measured using a direct technique in 105 healthy blood donors and in addition to establishing our reference values, the relationship to blood pressure and other cardiovascular risk factors was assessed. Whole blood viscosity correlated with systolic blood pressure (r = 0.29, p = 0.003), cholesterol (r = 0.21, p = 0.034), cholesterol/HDL cholesterol ratio (r = 0.33, p = 0.01), triglycerides (r = 0.37, p < 0.0005), body mass index (r = 0.29, p = 0.003) and waist-hip ratio (r = 0.30, p = 0.002). Subjects with systolic blood pressure > 130 mmHg (n = 16) had higher whole blood viscosity (p = 0.017) than those with lower blood pressure. Whole blood viscosity was significantly lower in women (n = 52) than in men at all shear rates (0.045 > p > 0.001). These results suggest that even in a population of healthy normotensive blood donors of a wide age range and either gender, there are positive correlations between directly assessed whole blood viscosity and a number of the components of the metabolic cardiovascular syndrome including systolic blood pressure, weight and blood lipids.

Adult↗
PubMed1990

Changes in the functional state of the erythrocyte membrane: significance for red cell filterability and blood viscosity.

Blood samples from nine healthy men were studied to determine the effect of ouabain and elevated serum calcium concentration on blood viscosity, measured by a rotational viscometer, and on red cell filterability by the St George's Filtrometer, giving values for clogging particles (CP) and red cell transit time (RCTT). Blood viscosity at a standardized haematocrit of 45% and red cell filterability was investigated in blood samples incubated for 1 h with Ringer's solution only (control), with ouabain (0.70 mmol/l) in plasma, or with serum calcium concentration increased by 3.0 mmol/l by addition of CaCl2. Incubation with ouabain significantly reduced erythrocyte K+ concentration and increased that of Na+. Ouabain caused a decrease in blood viscosity (p less than 0.05-0.005) compared to controls, although there was no decrease in red cell filterability parameters. When incubating with calcium, CP and RCTT increased significantly indicating 'stiffer' red cells, but there was no increase in blood viscosity. It is concluded that blood viscosity may be influenced by red cell factors not detected by CP or RCTT, which in turn appear to reflect red cell deformability with greater sensitivity and specificity than blood viscosity. It is concluded also that the functional state of the cell membrane may be of significance for the rheological properties of erythrocytes.

Adult↗
PubMed1989

Viscous resistance to blood flow in solid tumors: effect of hematocrit on intratumor blood viscosity.

Blood flow rate in a vascular network is proportional to the arteriovenous pressure difference and inversely proportional to the geometric and viscous resistances. We have recently shown that the geometric resistance to blood flow increases with increasing tumor size and/or decreasing arterial pressure. In this study, the viscous resistance to blood flow within tumor microvasculature was determined by alternately perfusing mammary adenocarcinoma [R3230AC; N = 12; tumor weight, 2.2 +/- 1.6 (SD) g] ex vivo with Krebs-Henseleit solution and with RBC suspensions at hematocrits between 1 and 60%. Our results demonstrate that: (a) intratumor blood viscosity increases with increasing hematocrit; and (b) for fixed hematocrits between 10 and 60%, the intratumor blood viscosity is significantly reduced (P less than 0.0001) compared to bulk viscosity measured at shear rates of 460 s-1 using a cone/plate viscometer. However, this reduction of intratumor blood viscosity is not as pronounced as in a previous study of skeletal muscle. Further comparison shows that as arterial pressure is lowered, intratumor blood viscosity increases at a greater rate and at lower hematocrits than in normal tissues. We attribute the increased viscous resistance in tumor microvasculature to (a) a less pronounced Fahraeus effect (i.e., reduction in hematocrit in small vessels) and a less pronounced Fahraeus-Lindqvist effect (i.e., reduction in blood viscosity in small vessels) in dilated tumor microvessels compared to normal microvessels; (b) low shear rates (i.e., velocity gradients) associated with tumor vessels which may facilitate rouleaux formation at moderate pressures and even at low hematocrits; and (c) vascular fluid losses of 5-14% which may also increase microvessel hematocrit. We also propose that intratumor blood viscosity may be even higher in vivo than ex vivo due to the presence of WBC and cancer cells in vivo; considerably more rigid than RBC, these cells may cause increased viscous resistance and transient vascular stasis in tumors. The implications of these results in tumor blood flow modulation using chemical and physical agents are discussed.

Adenocarcinoma↗
PubMed1980

Relation between extent of coronary artery disease and blood viscosity.

Blood viscosity (shear rate 100/s) and its major determinants (packed cell volume, plasma fibrinogen concentration, and plasma viscosity) were measured before coronary angiography in 50 men aged 30-55 and related to the extent of coronary artery disease. Twenty-six men had extensive disease (stenosis of two or three major coronary vessels), and 24 had either stenosis of one vessel or no stenosis. The 26 men with extensive disease had significantly higher mean blood viscosity than those with mild or no disease and 25 healthy controls (p less than 0.001). The increased viscosity was due partly to a higher packed cell volume and partly to a higher fibrinogen concentration; plasma viscosity was not significantly increased. These differences could not be explained by smoking history. These results suggest an association between increased blood viscosity and extensive coronary artery disease in men, which merits further investigation.

Adult↗
PubMed1994

Effect of hemodialysis and recombinant human erythropoietin on determinants of blood viscosity.

Blood viscosity (hemorheology) is a major determinant of the rate of blood flow, and increases in viscosity are known to be involved in the etiology of vascular diseases. This placebo-controlled study investigated the independent and combined effects of hemodialysis and recombinant human erythropoietin (rHuEpo) on determinants of blood viscosity in patients with chronic renal failure and related any changes to the normal physiological range. Hemodialysis patients were shown to have a high incidence of rheological abnormalities although the degree of anemia associated with chronic renal failure compensated for these changes. The main effect of both hemodialysis and rHuEPO treatment was an increase in hematocrit associated with a rise in blood viscosity and inconsistent changes in red blood cell (RBC) deformability. The rise in viscosity was significant only following rHuEPO treatment. Hemodialysis-induced increases in blood and plasma viscosity correlated strongly with the degree of hemoconcentration. Although hemodialysis patients have inherent hemorheological abnormalities, correction of renal anemia with rHuEPO to a hematocrit level of < 0.35 in conjunction with dialysis-induced hemoconcentration did not result in adversely high blood viscosity levels in any patient.

Anemia↗
PubMed1993

The relationship between blood viscosity and blood pressure in a random sample of the population aged 55 to 74 years.

Blood viscosity is elevated in hypertensive subjects, but the association of viscosity with arterial blood pressure in the general population, and the influence of social, lifestyle and disease characteristics on this association, are not established. In the Edinburgh Artery Study, 1592 men and women aged 55-74 years selected randomly from the general population attended a university clinic. A fasting blood sample was taken for the measurement of blood viscosity and its major determinants (haematocrit, plasma viscosity and fibrinogen). Systolic pressure was related univariately to blood viscosity (P < 0.001), plasma viscosity (P < 0.001) and plasma fibrinogen (P < 0.01), but the association with fibrinogen did not persist after adjusting for body mass index. Diastolic pressure was related univariately to blood viscosity (P < 0.001) and plasma viscosity (P < 0.001) and haematocrit (P < 0.001) but not to fibrinogen. The only difference between the sexes was that the association between blood viscosity and systolic pressure was confined to males. Blood viscosity was associated equally with systolic and diastolic pressures in males, and remained independently related on multivariate analysis adjusting for age, sex, body mass index, social class, smoking, alcohol intake, exercise, angina, HDL and non-HDL cholesterol, diabetes mellitus, plasma viscosity, fibrinogen, and haematocrit.

Aged↗
PubMed1975

[Clinical and statistical considerations on the relation between hematocrit value and blood viscosity].

Blood viscosity at various speed gradients was determined in 186 patients, a range of 245 haematocrit readings varying between 12 and 72 being examined. Statistical analysis of the results revealed a direct proportionality relationship between the two parameters, with viscosity expressed in logarithms. The regression lines accentuate their slope as the speed gradient falls. When determined at high speed gradients, blood viscosity can quintuplicate its value by varying the haematocrit from 10 to 70, while it can increase fully ten times at low speed gradients with the same haematocrit reading variations. Using blood from the same subject, resuspended at different haematocrits, viscosity values were obtained along the lines of regression up to haematocrits of about 70; for higher readings, viscosity data lie above these lines to a greater extent the higher is the speed gradient. Emphasis is laid on the great importance of the haematocrit reading from the rheological viewpoint and the significant clinical deductions that can be made.

Adult↗
PubMed2000

Influence of blood viscosity on blood flow in the forebrain but not hindbrain after carotid occlusion in rats.

That cerebral blood flow remains unchanged at an increased blood viscosity, as long as the vascular supply is not compromised, was tested. To induce a reduced blood supply of some parts of the brain and to keep the supply unchanged in others both carotid arteries were occluded in anesthetized, ventilated rats. By this procedure, blood supply to the rostral brain, but not to the brainstem and cerebellum, was compromised. Blood viscosity was increased by intravenous infusion of 20% polyvinylpyrrolidone (high viscosity group) or decreased by infusion of 5% albumin (low viscosity group). Cerebral blood flow was measured by the [14C]iodoantipyrine method in 50 complete coronal sections of the rostral brain and 22 complete coronal sections of the brainstem and cerebellum in each rat. In the high viscosity group, mean cerebral blood flow of the rostral brain was significantly lower (46 +/- 7 mL/100 g(-1) x min(-1)) than in the low viscosity group (82 +/- 18 mL/100 g(-1) x min(-1)). No differences could be observed in brainstem and cerebellum between both groups (162 +/- 29 mL/100 g(-1) x min(-1) vs. 156 +/- 18 mL/100 g(-1) x min(-1)). Local analysis of cerebral blood flow in different brain structures of the coronal sections showed the same identical results; i.e., in 29 of the 31 brain structures analyzed in rostral brain, local cerebral blood flow was lower in the high viscosity group, whereas no differences could be observed in the 11 brain structures analyzed in the brainstem and cerebellum. It is concluded that under normal conditions cerebral blood flow can be maintained at an increased blood viscosity by a compensatory vasodilation. When the capacity for vasodilation is exhausted by occlusion of supplying arteries, an increased blood viscosity results in a decrease of cerebral blood flow.

Animals↗
PubMed1971

Influence of blood viscosity on blood flow and the effect of low molecular weight dextran.

Changes in whole blood viscosity are related to changes in the leg blood flow during infusions of low-molecular-weight dextran and Hartmann's solution. A close inverse correlation exists between changes in viscosity and blood flow, the change in blood flow being about three times greater than the change in blood viscosity. The dextran and Hartmann's solution had a similar effect on blood viscosity and blood flow if corrections are made for the difference in haemodilution.

Blood Flow Velocity↗
PubMed1990

[Blood viscosity and blood factors in non-embolic cerebral infarction].

We compared blood viscosity at a high and a low shear rate, hematocrit, as well as levels of fibrinogen, cholesterol, triglyceride and high density lipoprotein-cholesterol between 42 patients with nonembolic cerebral infarction and 39 normal subjects. Blood viscosity, levels of fibrinogen, cholesterol and triglyceride were significantly higher, and high density lipoprotein-cholesterol levels were significantly lower, in patients than in normal persons. Blood viscosity had a positive correlation with hematocrit and fibrinogen, and a negative correlation with high density lipoprotein-cholesterol, but no correlation with cholesterol and triglyceride.

Adult↗
PubMed1995

[Effect of acute hypoxia on blood viscosity, red blood cell deformability and the left ventricular function in rats].

Experiments were performed on SD rats anaesthetized with urethane and chloralose. The left ventricular function and the parameters of hemorrheology during acute hypoxia were investigated. It was found that during acute hypoxia of 15 min, arterial blood gas value PaO2 decreased markedly. The parameters of the left ventricular function such as +/- dP/dtmax, Peak, HR, Vce40, Vmp, Vmax, L0 (CFU), decreased markedly either. At the same time, hyperviscosity was induced and red blood cell filtration (IF) increased. All these parameters recovered to normal control level after reoxygenation of 15 min. By intravenous injection of propranolol (0.5 mg/kg) and then hypoxia, the left ventricular function were suppressed markedly; and so were to the elevation of blood viscosity and IF. Preinjection of regitine (3 mg/kg) prior hypoxia has the same effect on the blood viscosity and IF. Acute hypoxia induced hyperviscosity and elevation of IF could be suppressed by destruction of carotid sinus region with phenol, but the left ventricular function decreased markedly. These results suggest that acute hypoxia induces hyperviscosity and decreases of red blood cell deformability and left ventricular function, which is probably mediated via the sympathetic nervous system and carotid sinus region.

Animals↗
PubMed1994

Lack of dependence of cerebral blood flow on blood viscosity after blood exchange with a Newtonian O2 carrier.

Whether the increase in cerebral blood flow measured after hemodilution is mediated by a decrease in blood viscosity or in oxygen delivery to the brain is debated. In the present study, blood was replaced by an oxygen-carrying blood substitute, ultrapurified, polymerized, bovine hemoglobin (UPBHB). In contrast to normal blood, UPBHB yields a constant and defined viscosity in the brain circulation, since its viscosity is not dependent on the shear rate. CBF was determined after blood exchange with UPBHB in one group of conscious rats (UPBHB group) and in another group of blood-exchanged conscious rats in which viscosity was increased fourfold by the addition of 2% polyvinylpyrrolidone (PVP), mw 750,000 (UPBHB-PVP group). Local CBF (LCBF) was measured in 34 brain structures by means of the quantitative iodo(14C)antipyrine method. After blood replacement, systemic parameters such as cardiac index, arterial blood pressure, blood gases, and acid-base status were not different between the UPBHB and the UPBHB-PVP groups. In particular, arterial oxygen content was similar in both groups. Compared with a control group without blood exchange, LCBF was increased after blood exchange in the different brain structures by 60-102% (UPBHB group) and by 33-101% (UPBHB-PVP group). Mean CBF was increased by 77% in the UPBHB group and by 69% in the UPBHB-PVP group. No significant differences were observed in the values of LCBF or mean CBF between the UPBHB group and the UPBHB-PVP group. The results show that a fourfold variation in the viscosity of a Newtonian blood substitute does not result in differences in CBF values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Intra- and postoperative changes in blood viscosity].

Blood and plasma viscosity has been controlled in a group of patients undergone to aorto-iliac reconstruction and in a group of control after thyroidectomy, cholecystectomy, and hernioplasty. The hemodilution induced by intraoperative infusion in the vascular reconstruction produced an important decrease of hematic and plasmatic viscosity which lasted for several days after the operation. Removing the hemodilution effect by a mathematical correction of the viscosity measured values to a standard haematocrit, it has demonstrated as surgical operation, apart from its entity, promoted an increase of the viscosity which persisted long in the postoperative course. For what it concerns the risk of postoperative thrombosis from one side protective effect of hemodilution is confirmed, from the other, in absence of the hemodilution, it would be useful to continue the antithrombotic prophylaxis longer the perioperative time as usual.

Aged↗
PubMed1993

[Blood viscosity and cerebral blood flow in aged].

It is well known that there is a close correlation between blood viscosity and blood flow. To clarify any relationship between blood viscosity and regional cerebral blood flow (rCBF) in the elderly, we simultaneously studied both CBF with PET (positron emission tomography) and blood viscosity with viscosimeter before and after phlebotomy in the elderly with various kinds of polycythemia. These subjects consisted of five male cases of secondary polycythemia due to pulmonary fibrosis, one male case of essential erythrocytosis (average age 66.6 +/- 4.6 years old) and one female case of stress polycythemia (47 years old). Before phlebotomy an increase in blood viscosity, decrease in rCBF and regional cerebral metabolic rate of oxygen (rCMRO2) were observed in all cases. After phlebotomy (total amount of 800 to 1,000 ml) blood viscosity rapidly decreased, and both rCBF and rCMRO2 tended to increase. There was a significant negative or positive correlation between CBF and blood viscosity or rCMRO2, respectively. However, no increase in cerebral oxygen transport was observed in any subject after phlebotomy. It was noted that cerebral infarction is not infrequent among elderly visitors to Kusatsu spa, which is characterized by high temperature hot spring water. From the authors' observation of 23 cases of cerebral infarction encountered during the last five years, it is noteworthy that the disease tended to occur more frequently during midnight to morning, specially 3:00 to 6:00. Thus, to clarify the pathogenetic mechanism of the cerebral infarction occurring after bathing in hot spring water, we studied the changes in blood viscosity, blood pressure and coagulation-fibrinolytic system after bathing in hot spring water.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗