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PubMed2006

Dietary fibers affect viscosity of solutions and simulated human gastric and small intestinal digesta.

Two experiments were conducted to determine the viscosities of both soluble and insoluble dietary fibers. In Expt. 1, corn bran, defatted rice bran, guar gum, gum xanthan, oat bran, psyllium, soy hulls, stabilized rice bran, wheat bran, wood cellulose, and 2 methylcellulose controls (Ticacel 42, Ticacel 43) were hydrated in water overnight at 0.5, 1, 1.5, or 2% concentrations. In Expt. 2, guar gum, oat bran, psyllium, rice bran, wheat bran, and wood cellulose were subjected to a 2-stage in vitro gastric and small intestinal digestion simulation model. Viscosity was measured every 2 and 3 h during gastric and small intestinal simulation, respectively. Viscosities in both experiments were measured at multiple shear rates. Viscosities of all fiber solutions were concentration- and shear rate-dependent. Rice brans, soy hulls, and wood cellulose had the lowest viscosities, whereas guar gum, psyllium, and xanthan gum had the highest viscosities, regardless of concentration. During gastric simulation, viscosity was higher (P < 0.05) at 4 h than at 0 h for guar gum, psyllium, rice bran, and wheat bran. During small intestinal simulation, viscosities were higher (P < 0.05) between 3 and 9 h compared with 18 h for guar gum, oat bran, and rice bran. Guar gum, psyllium, and oat bran exhibited viscous characteristics throughout small intestinal simulation, indicating potential for these fibers to elicit blood glucose and lipid attenuation. Wheat and rice brans and wood cellulose did not exhibit viscous characteristics throughout small intestinal digestion; thus, they may be beneficial for laxation.

Avena↗

PubMed2005

The influence of flow, vessel diameter, and non-newtonian blood viscosity on the wall shear stress in a carotid bifurcation model for unsteady flow.

OBJECTIVES: The atherosclerotic process in arteries is correlated with the local wall shear stress (WSS). Plaque development particularly occurs in regions with recirculation (ie, where the WSS oscillates). We investigated the effects of non-Newtonian blood viscosity, variations in flow rate, and vessel diameter on wall phenomena in a carotid bifurcation model. MATERIALS AND METHODS: The flow through a model of a carotid artery bifurcation was simulated by means of the finite element method. The whole-blood viscosity is a function of shear rate, and was modeled by the Carreau-Yasuda (CY) model. Flow rate and vessel morphology were assessed with magnetic resonance imaging. Flow rate, blood viscosity, and hematocrit levels (Hct) were measured in 49 healthy volunteers. We propose an adaptation of the CY model so that differences in Hct can be incorporated; furthermore, plasma viscosity was varied in the CY model. RESULTS: The data from our model indicate that flow increases have a larger effect on the WSS than predicted with a simple paraboloid model. Hct had more influence on the WSS when the plasma viscosity was low. Low plasma viscosity was associated with a low WSS, which implies a contradiction, because both high WSS and low plasma viscosity are thought to be indicators for a healthy system. Maximum WSS oscillations were found at the edges of the recirculation region. CONCLUSIONS: Flow and diameter changes have significant influence on wall shear stress values; the same is true for the viscosity, but to a lesser extent.

Adult↗

PubMed1985

Reversal of increased whole blood and plasma viscosity after treatment of hypothyroidism in man.

Blood and plasma viscosity was measured in 13 patients with hypothyroidism before and during replacement therapy with l-thyroxine. Blood viscosity was measured at natural hematocrit and after adjustment to 40%. The values were compared to those of 12 healthy subjects. Both blood viscosity at hematocrit 40% and plasma viscosity were increased in the hypothyroid state and decreased to the levels of the reference group after treatment. The therapy-induced changes in blood and plasma viscosity were intercorrelated at low but not at high shear rates. The changes in viscosity were not correlated to the reductions in lipoprotein concentrations resulting from therapy. The institution of l-thyroxine replacement therapy was also followed by reductions in erythrocyte sedimentation rate and diastolic blood pressure, both with significant correlations to the decrease in blood viscosity. It is concluded that in hypothyroidism there are changes in both plasma and erythrocytes that increase blood viscosity, with normalization upon treatment with l-thyroxine to euthyroidism.

Adult↗

PubMed1978

Viscosity, haematocrit, fibrinogen and plasma proteins in maternal and cord blood.

The viscosity at low shear rate of whole blood, plasma and serum, the haematocrit, plasma fibrinogen, plasma proteins, and IgM were measured in maternal and cord blood immediately following delivery. The whole blood viscosity in maternal blood (mean 19.96 +/- 3.74 centipoise or c/p) was similar to cord blood viscosity (mean 19.44 +/- 4.28 c/p). The mean haematocrit in maternal blood (0.385 +/- 0.026) was significantly lower than the cord haematocrit (0.488 +/- 0.39). Mean plasma viscosity (1.86 +/- 0.47 c/p) and plasma fibrinogen (4.25 +/- 0.75 g/litre) in maternal blood were significantly higher than cord plasma viscosity (1.12 +/- 0.19 c/p) and cord plasma fibrinogen (1.81 +/- 0.61 g/l). Mean serum viscosity (1.22 +/- 0.28 c/p) and mean IgM levels (2.38 +/- 0.36 g/l) in maternal blood were significantly higher than cord serum viscosity (0.90 +/- 0.15 c/p) and cord IgM (0.48 +/- 0.06 g/l). The low low levels of IgM and fibrinogen may protect the fetus from the increased viscosity that could be expected in association with a high haematocrit.

Blood Proteins↗

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↗

PubMed1980

Viscosity, cerebral blood flow and haematocrit in patients with paraproteinaemia.

It has been suggested that blood viscosity is involved in the control of cerebral blood flow (CBF) (Thomas et al. 1977a, b, Humphrey et al. 1979). CBF, using the intravenous Xenon133 technique, blood viscosity and haematocrit were measured in 21 patients with elevated viscosity due to paraproteinaemia and found to be the same as in normal subjects. However, the paraproteinaemic patients were anaemic with a mean haematocrit of 0.342. This degree of anaemia would normally be associated with a high CBF. The paraproteinaemic patients were then compared with a group of 10 anaemic patients with matched haematocrits but without paraprotein bands. The whole blood and plasma viscosities were significantly higher in the paraproteinaemic patients and the CBF was significantly lower. The haematocrit, and therefore oxygen carriage, was similar in the two groups. It is likely that in the anaemia of paraproteinaemia the expected increase in CBF did not occur because of the limiting factor of increased viscosity. This suggests that in this instance viscosity rather than oxygen carriage is a major determinant in the control of CBF. This is further emphasized by the better correlation between CBF and blood viscosity than between CBF and haematocrit. It seems likely that viscosity and oxygen carriage are independent variables in the control of CBF.

Aged↗

PubMed1982

Effects of biological stimuli on the viscosity of the vitreous.

Changes in the physical properties of the vitreous induced by various biological stimuli were investigated with Cannon-Fenske kinematic and cone-plate rotary viscometers. Heating greatly decreased the viscosity of the human vitreous, the critical temperature being between 50 degrees C and 60 degrees C. Freezing also affected the viscosity, but less so than heating. Viscosity of hyaluronic acid was also decreased by heating to approximately 60 degrees C. Preliminary incubation with hyaluronidase made the viscosity of both the vitreous and hyaluronic acid heat-stable. Lens extraction decreased vitreous viscosity markedly, suggesting a decrease of hyaluronic acid concentration and/or a lowering of hyaluronic acid molecular weight. Vitreous haemorrhage resulted in decreased vitreous viscosity. Cryoretinopexy at the level employed in this study induced little change in vitreous viscosity, while retinal diathermy caused a moderate decrease. In the course of vitreous haemorrhage and retinal diathermy, a return towards normal of the viscosity was observed, suggesting the presence of local hyaluronic acid production.

Aged↗

PubMed1982

Effect of viscosity of test meals on gastric emptying in dogs.

In five dogs gastric emptying of low, medium and high viscosity meals was measured via a duodenal cannula. The rate of emptying depended on the viscosity of the test meals: the time for half emptying was 4.5 +/- 2.2 min with the low viscosity liquid meal (1 centipoise), 28.9 +/- 9.5 min with the test meal of medium viscosity (10(5) centipoise), and 43 +/- 11.8 min with the test meal of high viscosity (10(6) centipoise). The emptying curves of the medium and high viscosity meals were sigmoid, whereas the curve representing the emptying of the low viscosity liquid meal followed an exponential pattern. Results indicate that the viscosity of the meal is an important factor for the rate of gastric emptying.

Animal Feed↗

PubMed1991

Increased plasma viscosity and erythrocyte aggregation: indicators of an unfavourable clinical outcome in patients with unstable angina pectoris.

OBJECTIVE: To determine the prognostic significance of altered plasma viscosity and erythrocyte aggregation in unstable angina. DESIGN: A prospective study of 96 consecutive patients with unstable angina allocated to one of two groups according to predefined threshold values for plasma viscosity and erythrocyte aggregation at study entry. The patients received a standardised treatment and were followed up for six months or until angioplasty or bypass surgery. MAIN OUTCOME MEASURE: Frequency of myocardial infarction. RESULTS: Myocardial infarctions occurred in 7/26 patients with a plasma viscosity greater than or equal to 1.38 mPa s and in 8/35 with a rate constant of erythrocyte aggregate formation greater than or equal to 0.5 mPa (corrected for plasma viscosity) but in only 4/70 with a plasma viscosity less than 1.38 mPa s and in 3/61 with an erythrocyte aggregation less than 0.5 mPa (odds ratios: 6.1 (95% confidence interval 1.3 to 31), p = 0.008, and 5.7 (95% CI 1.2 to 35), p = 0.016). Plasma viscosity and erythrocyte aggregation were more predictive of myocardial infarction than age, male gender, fibrinogen concentration, ST segment abnormalities, or coronary score. Furthermore, Holter monitoring with ST segment analysis showed that ischaemic episodes were more common in patients in whom the rate constant of erythrocyte aggregate formation was greater than 0.5 mPa (15/27 v 17/50, p = 0.029). Cardiac troponin T release was increased in patients with a plasma viscosity of greater than 1.38 mPa s (10/26 v 9/70, p = 0.010). CONCLUSIONS: In patients with unstable angina a considerable increase in plasma viscosity and erythrocyte aggregation identified a subgroup of patients at a high risk of acute myocardial infarction in whom medical treatment was likely to be unsuccessful.

Aged↗

PubMed1992

Plasma viscosity in inflammatory bowel disease.

AIMS: To assess the relation of plasma viscosity to disease activity in patients with inflammatory bowel disease. METHODS: Crohn's disease (n = 60) and ulcerative colitis (n = 71) were diagnosed on the basis of typical histological or radiological features. Active Crohn's disease was defined as a Crohn's disease activity index of 150 or over. Active ulcerative colitis was defined as a liquid stool passed three times a day or more with blood. Blood samples were assessed for haemoglobin concentration, total white cell count, platelets, plasma viscosity, erythrocyte sedimentation rate, serum albumin, and C-reactive protein. RESULTS: Plasma viscosity was higher in those with active Crohn's disease compared with those with inactive Crohn's disease or active ulcerative colitis. Plasma viscosity correlated significantly with erythrocyte sedimentation rate, C-reactive protein, and platelet count in patients with Crohn's disease. In ulcerative colitis plasma viscosity correlated only with serum C-reactive protein. Plasma viscosity showed a low sensitivity for detecting active Crohn's disease, with 48% of those with active disease having a plasma viscosity within the laboratory reference range. CONCLUSIONS: Plasma viscosity is related to disease activity in Crohn's disease, but is insufficiently sensitive for it to replace erythrocyte sedimentation rate as a measure of the acute phase response in Crohn's disease.

Blood Sedimentation↗

PubMed1985

Regulation of plasma lipid levels by plasma viscosity in nephrotic rats.

The viscosity of the extracellular medium of cultured hepatocytes has been shown to be a regulator of the secretion and synthesis of very low-density lipoproteins (Yedgar et al., J. Biol. Chem. 257: 2188-2192, 1982). At present, the role of plasma viscosity in regulation of plasma lipoprotein levels was examined in vivo using nephrotic hyperlipidemic rats. Plasma viscosity was increased by injection of macromolecules: simultaneously with induction of nephrosis by aminonucleoside; and after the lipid level had reached its maximum. In experiment 1 the elevation of plasma viscosity (which persisted for at least 2 days) delayed the development of the hyperlipidemia by at least 2 days. In experiment 2 increasing the plasma viscosity reduced plasma triglyceride and cholesterol levels by 70 and 40%, respectively, within 2 days. The hyperlipidemia was accompanied by increased plasma viscosity. The contribution of lipoproteins to plasma viscosity was 27% in the nephrotic-hyperlipidemic rats, compared with 4% in normal rats. It is suggested that plasma viscosity regulates lipoprotein levels in vivo concordant with the observation in cultured hepatocytes.

Animals↗

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↗

PubMed1990

Relation of blood viscosity to demographic and physiologic variables and to cardiovascular risk factors in apparently normal adults.

Although increased blood viscosity occurs in several cardiovascular diseases, little is known of factors influencing blood rheology in normal adults. Accordingly, we examined the relations of whole blood viscosity (WBV) to its rheologic determinants (hematocrit level, plasma viscosity, protein concentration, and red cell aggregability and rigidity), to demographic and laboratory variables, and to cardiovascular risk factors in 128 normotensive employed adults. Hematocrit levels accounted for 67-84% of variability of WBV at shear rates from 208 to 0.1 sec-1 with lesser contributions from plasma viscosity, red cell aggregability, and rigidity (multiple r = 0.95-0.97); WBV was predicted accurately from standard measurements of hematocrit and total plasma protein levels (multiple r = 0.78-0.92 in "learning" and "test" analysis). Male sex, obesity, dietary Na+ intake, and increasing age had additive effects on WBV (multiple r greater than or equal to 0.59, p less than 0.00001); the last three of these factors and black race independently predicted plasma viscosity (multiple r = 0.36, p less than 0.001). Among regulators of plasma volume, plasma renin activity and urinary Na+ excretion bore independent positive relations to WBV. Diastolic and mean blood pressures were independent predictors of WBV and hematocrit levels (all p less than 0.05). Conventional risk factors (e.g., triglycerides, obesity, and cholesterol levels) were positively related to WBV or plasma viscosity. Thus, in apparently normal adults, 1) WBV or plasma viscosity are increased by male sex, obesity, high sodium intake, aging, and black race, 2) WBV is positively related to plasma renin activity, 3) WBV or plasma viscosity are related to diastolic and mean blood pressures, triglycerides and cholesterol concentrations, and 4) WBV can be predicted from simple measurements of hematocrit and total plasma protein levels.

Adult↗

PubMed1997

Leisure-time physical activity but not work-related physical activity is associated with decreased plasma viscosity. Results from a large population sample.

BACKGROUND: Regular leisure-time physical activity (LTPA) is inversely associated with coronary heart disease (CHD). This has been mainly explained by its impact on traditional CHD risk factors, but more recently it was also shown to lower fibrinogen, which largely determines plasma viscosity. No data on the effect of work activity (WA) on plasma viscosity have been published. METHODS AND RESULTS: We studied the relationship between self-reported LTPA or WA and plasma viscosity as well as other CHD risk factors in 3522 men and women age 25 to 64 years. Physical activity was assessed by questionnaire. LTPA was inversely associated with plasma viscosity in both sexes. The unadjusted mean differences in plasma viscosity in men between no activity and the highest activity were 0.024 mPa.s (95% confidence interval [CI], 0.016 to 0.032 mPa.s, P < .001) during winter and 0.024 mPa.s (95% CI, 0.016 to 0.031 mPa.s, P < .001) during summer. After adjustment for age, cholesterol, smoking, blood pressure, body mass index, and years of education, mean differences decreased but still remained substantial and statistically significant (0.010 mPa.s; 95% CI, 0.003 to 0.018 mPa.s [P = .009] for winter activity; and 0.010 mPa.s; 95% CI, 0.002 to 0.017 mPa.s [P = .011] for summer activity). Similar results were found in women. WA showed no appreciable association with plasma viscosity after controlling for the covariates. CONCLUSIONS: LTPA is inversely associated with plasma viscosity, independent of other risk factors, whereas WA shows no material effect in men and women. Decreased plasma viscosity may represent one mechanism through which LTPA confers a decrease of CHD risk.

Adult↗

PubMedDate not supplied

Elevated blood viscosity in patients with borderline essential hypertension.

In patients with borderline hypertension, total peripheral resistance (TPR) is either elevated or abnormally related to cardiac output. Since blood viscosity is one determinant of TPR, we compared various components of blood viscosity in 25 patients with borderline hypertension and 25 normal subjects. Under all experimental blood flow conditions examined, blood viscosity directly correlated with systolic and diastolic blood pressure (p less than 0.05 or better) and was greater in the hypertensive than in normal subjects. Venous hematocrit and plasma viscosity were higher in the hypertensive patients. These latter rheologic abnormalities accounted for the increased blood viscosity at higher shear rates. At lower shear rates, increased red cell aggregation, primarily mediated by elevated fibrinogen concentration, accounted for the higher blood viscosity in the hypertensive subjects. We conclude that even relatively small elevations in arterial pressure are associated with increased viscous resistance of blood to flow, and that the increased blood viscosity is a consequence of increased hematocrit, plasma viscosity, and red cell aggregation.

Adult↗

PubMedDate not supplied

Failure of pentoxifylline or cilostazol to improve blood and plasma viscosity, fibrinogen, and erythrocyte deformability in claudication.

Peripheral artery disease is associated with altered blood rheologic properties, including increased viscosity and decreased red blood cell (RBC) deformability. Pentoxifylline and cilostazol are available therapies for intermittent claudication. Improvement of blood viscosity and erythrocyte deformability have been cited as potential mechanisms of action for pentoxifylline. Cilostazol is a new drug with antiplatelet and vasodilating activity, but the mechanism by which it promotes an improvement in walking is not known. This study was performed to evaluate and compare the hemorheologic effects of pentoxifylline and cilostazol on viscosity, fibrinogen levels, and erythrocyte deformability when administered to adults with moderate to severe claudication. A double-blind, controlled study was conducted and included 59 patients (46 male, 13 female; mean age 65 yr) randomized to pentoxifylline 400 mg orally thrice daily (n=20), cilostazol 100 mg orally twice daily (n=19), or placebo (n=20); all subjects were observed for 24 weeks. Walking ability was assessed before, during, and at the conclusion of treatment by standard constant speed, variable grade treadmill testing. Erythrocyte deformability was measured by passage of washed RBCs, 10% hematocrit in phosphate buffered saline (PBS), through a polycarbonate membrane with 4.7 to 5.0 microm pores. Whole blood and plasma viscosity were measured using a cone/plate viscometer at variable shear rates (from 4.5 to 450 sec(-1)). Erythrocyte sedimentation rate was measured by a modified Westergren technique. Fibrinogen was assayed by a commercial reference laboratory. Plasma viscosities did not change significantly in any treatment group. Within-group comparisons demonstrated a significant (p<0.01) drop in whole blood viscosity (week 24 compared with week 0) for cilostazol-treated subjects (at shear rates of 45, 90, 225, and 450 sec(-1)), but these changes were not significantly different from those in the placebo group. There were no significant changes in whole blood viscosity for subjects treated with pentoxifylline or placebo. There were no significant changes in erythrocyte deformability, fibrinogen, or erythrocyte sedimentation rate. A trend toward improved walking distances was noted for both pentoxifylline and cilostazol in comparison with placebo. This trend was not correlated with changes in any underlying rheologic parameter. Ex vivo rheologic characteristics of blood from patients with intermittent claudication are not significantly affected by long-term administration of pentoxifylline or cilostazol. Pentoxifylline did not modulate viscosity or red cell deformability, a finding at variance with its putative mechanism of action. Pentoxifylline cannot be differentiated from cilostazol based on specific hemorheologic effects evaluated in this study. Different mechanisms of action for these medications should be considered.

Adult↗

PubMed1977

Blood viscosity factors in evaluation of submaximal work output and cardiac activity in men.

Sixty-two male subjects, including patients with postmyocardial infarction, angina, other disorders, and normals, were studied by exercise testing on the bicycle ergometer, including exercise ECG, and by in vitro determination of blood viscosity, plasma viscosity, aggregation of red cells, and other factors. Significant correlations were found between the blood viscosity factors on the one hand, and different terms describing physical fitness and cardiac functions on the other. In all correlations an elevation of blood viscosity factors led to lower fitness or lower cardiac efficiency; and a decrease of blood viscosity (or plasma viscosity, or compound viscosity product) was associated with better fitness and higher cardiac efficiency. Similarly, ECG ST-segment depression was proportional to increase of blood viscosity factors. All these highly significant correlations were found within a very narrow range of hematocrits, while the hematocrit value itself was not significant in this study.

Adult↗

PubMed1989

Viscosity reduction of red blood cells from preterm and full-term neonates and adults in narrow tubes (Fahraeus-Lindqvist effect).

In artificial tubes as well as in blood vessels with diameters less than 500 microns, blood viscosity decreases with decreasing diameter (Fahraeus-Lindqvist effect). Our study measured viscosity of red blood cells (RBC) from 10 preterm infants, 10 term neonates, and 10 adults by means of a capillary viscometer. RBC were suspended in buffer at hematocrits of 0.20, 0.40, and 0.60 1/1 (1.00 1/1 = 100%). Tubes with diameters of 50, 100, and 500 microns were perfused with these suspensions. Viscosity in the 500-microns tubes was not significantly different, at any hematocrit, among the three groups. Viscosity decreased at each of the adjusted hematocrits in the three groups when going from a 500-microns tube to a 50-microns tube. At a hematocrit of 0.60 1/1, viscosity reduction averaged 48 +/- 7% in the preterm infants, 42 +/- 8% in the full-term neonates, and 35 +/- 5% in the adults, whereas the reductions at a hematocrit of 0.20 1/1 were only 32 +/- 6, 27 +/- 4, and 24 +/- 6%, respectively. For the combined data from the neonates and adults, there was a significant inverse relationship of the viscosity in 50-microns tubes at a hematocrit of 0.60 1/1 to the mean corpuscular volume (r = 0.69). To evaluate whether increased membrane elasticity of neonatal RBC contributes to the stronger viscosity reduction of neonatal RBC in narrow tubes, heated neonatal and adult RBC were also studied. The resulting loss of membrane elasticity caused a marked decrease in the viscosity reduction in 50-microns tubes, particularly in the neonates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗