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PubMed1992

Effects of thyroidectomy on the hematocrit and blood viscosity in ovariectomized rats.

The hematocrit and blood viscosity were measured in ovariectomized (Ovx) rats following thyroidectomy or sham operation. Rats were thyroidectomized (Tx) or sham Tx immediately after ovariectomy. Three months later, Ovx, Ovx+Tx, and intact rats at proestrus stage were bled. Blood was collected by heart puncture in rats under ether anesthesia and heparinized. One month after the first bleeding, Ovx and Ovx+Tx rats were bled once again. the viscosity of whole blood and plasma was measured at various shear rates at 37 degrees C by means of a Mooney-Ewart viscometer. The hematocrit was determined by a microhematocrit centrifuge. The plasma osmolality was measured by a computerized micro-osmometer. Concentrations of plasma sodium and potassium were measured by a flame photometer. The concentration of plasma thyroid stimulating hormone (TSH) was measured by a radioimmunoassay. In Ovx+Tx rats, the plasma TSH concentration was higher, but the hematocrit and blood viscosity were lower than those in Ovx and proestrus rats. The levels of plasma sodium, osmolality and viscosity were not altered by ovariectomy and thyroidectomy. These results suggest that the lower blood viscosity in thyroidectomized rats is due to a reduction of hematocrit.

Animals↗

PubMed1998

Comparison of blood viscosity in red-eared sliders (Trachemys scripta) adapted to cold and room temperature.

Red-eared sliders (Trachemys scripta) in their northern range undergo hibernation at temperatures of about 5 degrees C, which may result in a profound bradycardia and a drop in blood pressure leading to very slow blood flows. Blood viscosity increases with decreasing temperature and at low shear rates associated with slow blood flows. To investigate the effects of temperature on the blood viscosity of these animals, 20 red-eared sliders were randomly assigned to each of two groups, cold environment (5 degrees C) or room-temperature environment (25 degrees C). At the end of 5 months treatment, hematocrit values, plasma protein concentration, and whole-blood viscosity values were determined for each turtle. Blood viscosity measurements were determined at five shear rates (3.75, 15, 30, 75, and 150 s-1) at 5 degrees C and 25 degrees C for all animals. No significant differences were found in hematocrit or plasma protein values between cold-adapted and room temperature-adapted animals. Whole-blood viscosity between groups at any shear rate at a temperature of 5 degrees C was also nonsignificant. The only significant difference in blood viscosity between turtles adapted to cold and room temperature occurred at a shear rate of 3.75 s-1 at 25 degrees C. The whole-blood viscosity of red-eared sliders, whether adapted to cold or to room temperature, tended to be lower as compared to other vertebrates under similar conditions of temperature, shear rate, and hematocrit. This innate lower blood viscosity may compensate for the potential detrimental effects on blood viscosity brought about by the low temperatures and decreased shear rates that occur in these animals during hibernation.

Adaptation, Physiological↗

PubMed1991

Umbilical artery flow velocity waveforms and cord blood viscosity.

The role of cord blood viscosity in determining the umbilical artery Doppler flow velocity waveform (FVW) was investigated in 22 normal pregnancies and 29 complicated pregnancies. FVWs were quantified by calculating the pulsatility index (PI). There was a significant correlation between an abnormal PI (more than 2 SD from the mean) and fetal growth retardation (less than 5th birthweight centile), cesarean section for fetal distress, and raised cord blood hematocrit. However, there was no relationship between whole blood or plasma viscosity measurements and the umbilical artery PI.

Birth Weight↗

PubMed2002

[Studies on blood viscosity and external thrombus in patients with silicosis and silicosis complicated with tuberculosis].

OBJECTIVE: To explore the changes of blood viscosity and external thrombus in patients with silicosis and silicosis complicated with tuberculosis (TB). METHOD: Blood viscosity and external thrombus were measured in 288 patients with silicosis, 178 patients with silicosis complicated by TB and 150 healthy subjects. RESULTS: Blood viscosity and external thrombus value were significantly higher in the patients of silicosis and silicosis complicated with TB than in the healthy controls, except for patients of phase I of silicosis. Blood viscosity in the silicotics increased significantly with the advance of the disease, but no significant difference in external thrombus between patients in different phases. Apparent viscosity of whole blood significantly increased in the high-shear rate (200 s(-1)) and middle-shear rate (30 s(-1)) in patients of silicosis complicated with TB than in those without complication of TB at the same phases, but not seen in the low-shear rate (5 s(-1)) and in plasma viscosity, and the length and dried weight of external thrombus increased significantly too. There was no significant difference in blood viscosity and external thrombus between patients of silicosis at phase III and those of silicosis complicated with TB at the same phase. CONCLUSION: Blood in patients with silicosis appeared highly viscous and highly coagulant status. Blood viscosity and external thrombus value significantly increased with the advance of the disease, especially in the patients complicated with TB.

Adult↗

PubMed2001

Effects of blood viscosity on proximal flow convergence calculations of regurgitant flow rate and jet dimensions as evaluated by color Doppler flow mapping: an in vitro study.

There are limited data on the potential influence of blood viscosity on the quantification of valvular regurgitation by color Doppler in the clinical setting. This study was designed to evaluate the effects of blood viscosity on jet dimensions and the proximal flow convergence (proximal isovelocity surface area, PISA) method of estimating valvular insufficiency severity. We used an in vitro flow model filled with human blood at varying hematocrits (15%, 35%, and 55%) and blood viscosity (blood/water viscosity: 2.6, 4.8, 9.1) in which jets were driven through a known orifice (16 mm(2)) into a 110-mL compliant receiving chamber (compliance: 2.2 mL/mm Hg) by a power injection pump. Blood injections (2 and 4 mL) at flow rates of 4, 6, 8, 10, and 12 mL/s were performed. Proximal flow convergence and spatial distribution of jets were imaged by a 3.5-MHz transducer. Pressure and volume in the flow model were kept constant before each injection. Ultrasound settings were the same for all experiments. Jet area decreased significantly with increasing blood viscosity, but the difference in jet dimensions was much larger for lower than for higher flow rates and for highest blood viscosity. Estimation of flow rate by the PISA method was not significantly influenced by blood viscosity. Blood viscosity has a major influence in jet area, especially for lower flow rates, but did not change significantly the grading of regurgitation by the PISA method. Thus this factor should be considered for determining the method of choice when quantification of valvular regurgitation is performed in patients with anemia or polycythemia.

Blood Viscosity↗

PubMed1983

Blood viscosity and haemostasis in the nephrotic syndrome.

Blood viscosity and its major determinants (haematocrit, plasma viscosity and fibrinogen) as well as several haemostatic variables were measured in 21 patients with the nephrotic syndrome, and 21 controls matched for age, sex, smoking habit and serum creatinine. Blood viscosity was significantly increased in the nephrotic group, measured at a low shear rate (mean increase 41%, p less than 0.01) and at a high shear rate (mean increase 25%, p less than 0.01). Haematocrit was not significantly increased, but plasma viscosity was significantly higher (p less than 0.01), associated with increased plasma macroglobulins especially fibrinogen, which was increased to double the plasma concentration of the control group (p less than 0.01). Nephrotic subjects also had increased plasma levels of alpha 2-macroglobulin, factor VIII activity, factor VIII antigen and beta-thromboglobulin; differences in antithrombin III, fibrin degradation products, plasminogen, and platelet count were not significant. We suggest that increased blood and plasma viscosity may play a role in the vascular complications of the nephrotic syndrome.

Adult↗

PubMed1990

Blood viscosity as a chronic contributing factor of vasodilatation in humans.

Since resistance to flow is theoretically determined by arteriolar geometry and blood viscosity, we studied these two factors in 44 normal and 106 hypertensive subjects. Brachial bed vascular resistance was calculated as the ratio between mean pressure and brachial artery flow. Systemic blood viscosity in vitro was determined at 96 per s, while microvessel blood viscosity in vivo was estimated from the haematocrit-viscosity relationship at 240 per s. A resistive radius index was calculated which was only related to the microvessel viscosity: resistance ratio. Compared to normal subjects, hypertensive subjects had higher systemic in vitro blood viscosity (4.75 +/- 0.47 versus 4.50 +/- 0.43 mPa.s; P less than 0.005) and microvessel blood viscosity (2.60 +/- 0.21 versus 2.43 +/- 0.16 mPa.s; P less than 0.001). Hypertensive subjects also had a higher brachial vascular resistance (161 +/- 89 versus 124 +/- 58 mmHg/ml per s; P less than 0.01), but showed a similar resistive radius index (2.47 +/- 0.36 versus 2.57 +/- 0.35) compared to normal subjects. There was a positive correlation between systemic viscosity and brachial artery diameter and a negative correlation between microvessel viscosity and vascular resistance in the normotensive (P less than 0.05 and P less than 0.001, respectively) and hypertensive groups (P less than 0.001 and P less than 0.005, respectively). The resistive radius index was positively related to viscosity in normal and in hypertensive groups (P less than 0.001) but these relationships were significantly different (P less than 0.001), showing that, at the highest viscosities, arterial radius increased less in hypertensive than in normal subjects. Thus, the level of blood viscosity might influence arterial diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Diltiazem reduces whole blood viscosity following trauma-hemorrhagic shock and resuscitation.

Although diltiazem improves function in several organs following trauma-hemorrhagic shock, the mechanism remains unknown. It is hypothesized that diltiazem maintains red blood cell calcium-to-magnesium ratio, resulting in better deformability of red blood cells. This should reduce blood viscosity, allowing red blood cells to traverse the microcirculation more efficiently and improve tissue oxygenation. To study this, rats (n = 23) underwent cannulation of various blood vessels and were divided into five groups: Group 1, control rats which had surgery only; Group 2, sham-operated rats which were not hemorrhaged but were infused with a volume of lactated Ringer's solution (LRS) equivalent to that given to the hemorrhaged animals (Groups 4 and 5); Group 3, hemodilution animals which were maintained at normal blood pressure but with the hematocrit lowered to values equivalent to hemorrhaged rats (Groups 4 and 5); Groups 4 and 5, animals which underwent fixed pressure (40 mm Hg) hemorrhage, followed by resuscitation with LRS, 5x the shed blood volume, and were given IV saline (Group 4) or 400 micrograms diltiazem/kg (Group 5) with the resuscitation. Blood viscosity was measured at the end of resuscitation with a Brookfield DV-III viscometer. Results showed that blood viscosity was markedly reduced in the diltiazem treatment group, but was unchanged in any of the other groups versus the control. Thus, the beneficial effects of diltiazem after trauma-hemorrhage and resuscitation may be due in part to the marked decrease in blood viscosity allowing for improved oxygen delivery and removal of metabolites.

Animals↗

PubMed1993

Blood viscosity during thrombolytic therapy with anistreplase in acute myocardial infarction.

It has been postulated that a reduction in blood viscosity due to degradation of plasma fibrinogen may be of benefit to patients with acute myocardial infarction (AMI), who are treated with thrombolytic agents. The aims of this study were to investigate the time course of rheologic parameters, to identify the principal factors determining blood viscosity, and to find possible correlations between viscosity and cardiac function during thrombolytic therapy with anistreplase. Therefore, the viscosity of whole blood and plasma and the hematocrit were measured before and at 10 time points after thrombolysis in 10 patients with AMI. In addition, plasma fibrinogen and fibrin(ogen) degradation products were determined. Immediately after the start of thrombolysis, the viscosity of blood (both at high and low shear rate) and plasma decreased significantly and continued to do so for 24 hours. The mean hematocrit also decreased markedly, and even after correction for these hematocrit changes, the reduction in blood viscosity remained significant: it decreased to 72% of pretreatment (measured at low shear rate), whereas the high-shear viscosity decreased to 95% of baseline. The viscosity of plasma significantly decreased from 1.39 +/- 0.13 mPa.s (mean +/- SD) before thrombolysis to 1.22 +/- 0.08 mPa.s after 2 hours. There was a rapid, nearly complete depletion in fibrinogen, followed by a striking rebound after the second day. The decrease in blood viscosity lasted for 2 days after anistreplase and was mainly accounted for by the reduction in hematocrit. The contribution of fibrinogen to blood viscosity appeared less prominent. Despite these rheologic changes, no improvement in cardiac output was noticed in the patients.

Aged↗

PubMed1997

Effects of Whole Blood Viscosity on Atherogenesis.

There is a high correlation between high whole blood viscosity and the well known risk factors for arterial occlusive disease: hypertension, hyperlipidemia, diabetes, male sex, age, smoking, and obesity. These risk factors increase whole blood viscosity, whereas the preventive factors of arterial occlusive disease such as fish oil, aspirin, alcohol, and exercise probably tend to reduce whole blood viscosity. The protective adaptation theory recently presented by Kensey and Cho1 proposed high whole blood viscosity as one of the major factors that make up the mechanical injury possibly inducing arterial occlusive disease. New diagnostic and prophylactic treatments for arterial occlusive disease are suggested. An accurate, convenient, and cost-effective blood viscometer that can be used in a clinical environment might become a useful diagnostic screening device for patients at risk for arterial occlusive disease, and it would help discover new prophylactic treatments.

Journal Article↗

PubMed1976

Correlations between radioiodine uptake and blood viscosity factors in hypothyroid and hyperthyroid states.

A study of blood viscosity factors was undertaken in six hypothyroid and eleven thyrotoxic patients (females) whose thyroid function was defined by means of radioiodine uptake and protein bound (PB) 131I tests. Results indicate that: (i) significant differences exist between hypothyroid and hyperthyroid groups in correlations between radioiodine tests and blood viscosity factors (and fibrinogen levels); (ii) blood viscosity in thyrotoxic patients decreases as the degree of thyrotoxicity increases, while an opposite phenomenon is observed in hypothyroid patients, and (iii) degree of rigidity of the red cells is associated with the radioiodine uptake and PB 131I tests, the correlations being significant and negative.

Blood Viscosity↗

PubMed1987

The effect of donor age on the flow properties of blood. Part I: Plasma and whole blood viscosity in adult males.

The relationship between blood viscosity and age was studied using heparinized blood samples obtained from 50 normal male blood donors between the ages of 20 and 65 years. There was a slight but significant decline in packed cell volume (hematocrit) with age. Plasma viscosity showed no significant variation with donor age, but the viscosity of blood samples standardized to a packed cell volume of 45 ml/dl showed an increase as the age of the donor rose. The age-related trend to a higher viscosity was present at shear rates below 46 s-1, but not at higher shear rates. This shows that with age there is a rising trend in the red cell contribution to blood viscosity, which is not dependent on the packed red cell volume; this component increases across a wide age range in early and middle adult life, and is not a characteristic appearing exclusively in later age periods. The tendency for the viscosity trend to be greater at lower shear rates indicates increased shear thinning in blood obtained from older subjects, the cause of which may be either diminished red cell deformability in these subjects, or an increased tendency to form aggregates at low shear rates.

Adult↗

PubMed1975

Observations on blood viscosity changes after acute myocardial infarction.

Serial blood rheologic measurements were made in 25 patients with acute myocardial infarction; measurements included blood and plasma viscosities, hematological data and plasma protein concentrations. The blood viscosity was elevated on admission and for more than 21 days after acute myocardial infarction. However, the cause of the elevated viscosity was changed as a function of time after acute myocardial infarction. During the first three days after admission, the high blood viscosity was mainly attributable to high hematocrit values. Thereafter, the hematocrit fell, but blood viscosity remained high. High blood viscosity after the first three days of acute myocardial infarction can be correlated with increases in plasma viscosity and red cell aggregation, which in turn are explained by elevations of alpha 2 globulin and fibrinogen concentrations. Patients with higher blood viscosity on admission had a significantly higher incidence of complications, i.e., shock, thromboembolism and left ventricular failure.

Alpha-Globulins↗

PubMed1999

Low high density lipoprotein levels are associated with an elevated blood viscosity.

Low levels of high density lipoprotein (HDL) have been inversely correlated with blood viscosity and plasma viscosity; however, the contribution of concomitant hypertriglyceridemia may confound this association. This study evaluated the relationship between blood viscosity and HDL cholesterol in 70 subjects with fasting levels of total cholesterol <5.2 mmol/l (200 mg/dl) and triglycerides <2.3 mmol/l (200 mg/dl). Viscosity (mPa x s) was measured at 37 degrees C with a coaxial cylinder microviscometer. HDL cholesterol was inversely associated with corrected blood viscosity at 100 s(-1) (beta = -0.49, P<0.00005) and 20 s(-1) (beta = -0.38, P = 0.001) but not at 1 s(-1) (beta = -0.05, P = 0.69) using stepwise multivariate analyses. Low HDL levels are associated with an elevated blood viscosity, and this rheological abnormality may contribute to cardiovascular risk in subjects with isolated low HDL levels.

Adult↗

PubMed1997

Blood viscosity and risk of cardiovascular events: the Edinburgh Artery Study.

We examined the relationships of whole blood viscosity and its major determinants to incident cardiovascular events (ischaemic heart disease and stroke) in a prospective study of a random population sample of 1592 men and women aged 55-74 years (the Edinburgh Artery Study). 272 fatal and non-fatal cardiovascular events occurred during 5 years of follow-up (cumulative incidence 17.1%). Age and sex adjusted mean levels of blood viscosity (3.70 v 3.55 mPa.s), haematocrit (46.2 v 45.7%), haematocrit-corrected blood viscosity (3.57 v 3.48 mPa.s), plasma viscosity (1.35 v 1.33 mPa.s) and fibrinogen (2.88 v 2.67 g/l) were significantly higher in subjects who experienced events than in subjects who did not. The relationships of these rheological variables to cardiovascular events were at least as strong as those of conventional risk factors (smoking habit, diastolic blood pressure, and low-density lipoprotein cholesterol). After adjustment for these conventional risk factors, the associations of blood viscosity and haematocrit remained significant for stroke, but not for total events; whereas the associations of plasma viscosity and fibrinogen remained significant for total events and for stroke. These findings suggest that increased blood viscosity may be one plausible biological mechanism through which increases in haematocrit and fibrinogen may promote ischaemic heart disease and stroke. Randomized controlled trials of viscosity reduction in the prevention of cardiovascular events (e.g. by lowering high levels of haematocrit or plasma fibrinogen) are suggested.

Aged↗

PubMed1990

Blood viscosity and optimal hematocrit in narrow tubes.

Blood viscosity in normal adults was measured in glass tubes with diameters of 50, 100 and 500 microns for a wide range of adjusted feed hematocrits (15-70%). Blood viscosity decreased at each of the adjusted feed hematocrits when going from a 500-micron tube to a 50-micron tube. The viscosity reduction increased with increasing hematocrit. The steepness in the hematocrit-viscosity curves decreased with decreasing tube diameter. Erythrocyte transport efficiency (hematocrit/blood viscosity) was calculated to estimate the optimal hematocrit for oxygen transport. Optimal hematocrit averaged 38% in 500-micron tubes, 44% in 100-micron tubes and 51% in 50-micron tubes. Our results suggest that the strong Fåhraeus-Lindqvist effect at high hematocrits may help to maintain oxygen transport in polycythemic patients as long as the driving pressure is sufficient.

Adult↗

PubMed2002

The role of whole blood viscosity in premature coronary artery disease in women.

BACKGROUND: Impaired hemorheology has been demonstrated in atherosclerotic disease and has shown a relationship with classical risk factors. Blood viscosity (eta), being the ratio of shear stress over shear rate, is an important parameter of hemorheology. In women with premature coronary artery disease (CAD), the underlying risk factors are a matter of debate and the role of whole blood viscosity in its pathogenesis has not been documented. AIM: To investigate the association of whole blood viscosity with premature CAD in women, with complaints suggestive of angina pectoris. METHODS: Eighty-eight women (mean age 53 years) were divided into two groups, those with a high likelihood of CAD (LIKELI+) and those with a low likelihood of CAD (LIKELI-), based on medical history and technical investigations. Assessment of risk factors comprised smoking, diabetes mellitus, arterial hypertension, left ventricular hypertrophy (LVH), systolic and diastolic blood pressures, total low-density lipoprotein (LDL)- and high-density lipoprotein (HDL)-cholesterol, triglycerides, body mass index, menopause, hormone replacement therapy, uric acid and creatinine, and predicted 10-year cardiovascular risk according to the Framingham study was calculated. Whole blood viscosity was determined at 37 degrees C using a rotational cone-and-plate viscosimeter. RESULTS: Baseline characteristics did not differ significantly between the groups except for antiplatelet therapy (P=0.001), prevalence of diabetes mellitus (P=0.002), predicted 10-year cardiovascular risk (P=0.007), essential hypertension (P=0.02), LVH (P=0.03) and smoking habits (P=0.04). LIKELI+ women had a significantly higher whole blood viscosity at all shear rates compared with LIKELI- women (P<0.05). All blood viscosities measured from 25 to 125 s(-1) were highly significantly (P<0.0001) correlated with eta(250s(-1)). Univariate correlates with eta(250s(-1)) comprised triglycerides (P=0.006) and haematocrit (P=0.026). Binary logistic multivariate regression analysis for high likelihood of CAD revealed that only presence of arterial hypertension (P<0.0001) was predictive. Multiple regression analysis demonstrated that haematocrit (P=0.001) and likelihood of CAD (P=0.01) were the only significant determinants of eta(250s(-1)). CONCLUSION: In this study, blood viscosity did not appear as an independent risk factor for the prediction of premature CAD in women. Viscosity may act as a marker of CAD or of classical risk factors.

Adult↗

PubMed1983

Echinocytes in the blood of hyperproteinaemic mice with proteinuria. Is the effect of such cells on blood viscosity the cause of the proteinuria?

Early studies in this series failed to obtain evidence for the cause of hyperproteinaemic proteinuria although it was speculated that blood viscosity, increased because of high plasma protein levels, might play a significant role. As we had no means of measuring blood viscosity it was decided to investigate the effects of reducing blood viscosity in a small number of mice made anaemic before subjecting them to albumin overload. All but one of the mice given injections i.p. of 250 mg HSA on 2 successive days developed proteinuria within 24 h of the first injection. This result seemed to show that altered blood viscosity was not a factor in the mechanism of the hyperproteinaemic proteinuria. However, it has been shown that changes in the red cell environment can lead to red cell deformation resulting in an increase in blood viscosity. To check on this possibility another small group of mice were injected with HSA as previously. On the morning after their second injection the mice were bled by percutaneous heart puncture and the blood was examined by scanning electron microscopy. This showed that a vast preponderance of red cells, probably more than 95%, were echinocytes. Although no measurements of blood viscosity were made, it can be speculated that hyperproteinaemic proteinuria is caused by the intraglomerular effects of blood with increased viscosity (because of the red cell transformation) being made more viscous by glomerular filtration. Enhanced protein filtration would occur because of the increase in glomerular pressure needed to restore flow of viscous blood at the efferent arteriole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗