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Mucin and phospholipids determine viscosity of gallbladder bile in patients with gallstones.

AIM: An increased viscosity of gallbladder bile has been considered an important factor in the pathogenesis of gallstone disease. Besides lipids and proteins, mucin has been suggested to affect the viscosity of bile. To further clarify these issues we compared mucin, protein and the lipid componEnts of hepatic and gallbladder bile and its viscosity in patients with gallstones. METHODS: Viscosity of bile (mPa.s) was measured using rotation viscosimetry in regard to the non Newtonian property of bile at low shear rates. RESULTS: Biliary viscosity was markedly higher in gallbladder bile of patients with cholesterol (5.00 +/- 0.60 mPa.s, mean +/- SEM, r= 28) and mixed stones (3.50 +/- 0.68 mPa.s; r= 8) compared to hepatic bile (0.92 +/- 0.06 mPa.s, r= 6). A positive correlation between mucin and viscosity was found in gallbladder biles (r = 0.65; P < 0.001) but not in hepatic biles. The addition of physiologic and supraphysiologic amounts of mucin to gallbladder bile resulted in a dose dependent non linear increase of its viscosity. A positive correlation was determined between phospholipid concentration and viscosity (r = 0.34, P < 0.005) in gallbladder biles. However, no correlation was found between total protein or the other lipid concentrations and viscosity in both gallbladder and hepatic biles. CONCLUSION: The viscosity of gallbladder bile is markedly higher than that of hepatic bile in patients with gallstones. The concentration of mucin is the major determinant of biliary viscosity and may contribute by this mechanism to the role of mucin in the pathogenesis of gallstones.

Adult↗

The kinetics of the sol-gel transformation of deoxyhemoglobin S by continuous monitoring of viscosity.

By continuous monitoring of viscosity during the sol-gel transformation of deoxygenated sickle hemoglobin a time: viscosity profile has been demonstrated that can be subdivided into: (1) initial lag phase, (2) gradual and minor increase in viscosity, (3) rapid and major (180 times initial value) increase in viscosity, (4) moderately rapid decrease in viscosity, and (5) achievement of equilibrium at approximately 50 per cent of maximum viscosity increase. The duration of the lag phase, rate of increase in viscosity, and maximum change are greatly influenced by hemoglobin concentration and markedly altered by temperature. Admixtures of hemoglobins A and F lengthen the lag phase and attenuate the rate of increase and magnitude of viscosity change according to proportions added and capacity to interact with deoxyhemoglobin S, but the general configuration of the curve is maintained. A different time: viscosity profile is obtained for mixtures of S and C hemoglobin that is lacking the phase with decreasing viscosity. Relevance to the pathophysiology of the sickling phenomenon is evidence because the quantitative and qualitative changes induced by variations in concentration of deoxygenated hemoglobin S, temperature, amount and type of admixed hemoglobin (A, C, and F), ionic strength, and 2, 3-DPG are in agreement with their known effects upon the sickling of intact cells and upon the minimum gelling point of deoxyhemoglobin S. No final conclusions can be drawn concerning the extent or form of hemoglobin aggregation present in the various phases of the time: viscosity profile; however, the technique lends itself readily to obtaining samples at various points along the curve for additional studies such as electron microscopy and light scattering.

Blood Viscosity↗

Plasma viscosity as a cardiovascular risk marker in patients with proteinuria.

Plasma viscosity is a major determinant of capillary blood flow. It has been suggested that alteration in plasma viscosity contributes to impaired blood flow and to increased cardiovascular risk. The aim of this study was to investigate the plasma viscosity levels and its possible role in the cardiovascular risk in patients with low grade nephrotic proteinuria. 20 patients with low-grade nephrotic proteinuria (mean age: 35+/-5 years) and 20 healthy controls (mean age: 33+/-4 years) were participated in the study. Plasma viscosity was measured by Harkness capillary viscometer. Biochemical analysis were measured by commercial enzymatic kits. Plasma viscosity, plasma levels of creatinine, fibrinogen and triglyceride were increased in patients with proteinuria than in the healthy controls (p<0.001, p<0.001, p<0.001, and p<0.001, respectively). The plasma levels of total protein and albumin were significantly lower in patients with low grade nephrotic proteinuria than in healthy controls (p<0.001 and p<0.001, respectively). Plasma viscosity was negatively correlated with plasma albumin (r= -0.835, p<0.001) and total protein (r= -0.862, p<0.001) in proteinuric patients. When the correlation analyses were performed a significant positive correlation was found between plasma viscosity and fibrinogen (r=0.636, p<0.001). In the stepwise multiple regression analysis plasma viscosity was found to be related with plasma total protein (t= -6.456, p<0.001) in the patients. When the stepwise multiple regression analysis were performed in healthy controls, the significant relationship was only found between plasma viscosity and fibrinogen (t= +2.202, p<0.01). These results suggested that altered plasma composition associated with low-grade nephrotic proteinuria may be involving the determination of plasma viscosity. Thus, the plasma viscosity in patients with low-grade nephrotic proteinuria may have a prognostic value in assessing cardiovascular risk in this group.

Adult↗

Whole blood viscosity in beta thalassemia minor.

Patients with heterozygous beta-thalassemia minor have a decreased hematocrit (HCT). Since the HCT is a primary determinant of whole blood viscosity, the known reduction in HCT in beta-thalassemia minor should lead to a measurable reduction of whole blood viscosity. The influence of the relatively lower mean corpuscular volume and consequent higher red blood cell count and beta-thalassemia minor on whole blood viscosity using a microporous viscometer has not previously been the subject of investigation. Accordingly, the blood of a group of normal and beta-thalassemia minor subjects was examined with a microporous viscometer to elucidate further the relations between whole blood viscosity, HCT, and red blood cell count. The data show that for normal and beta-thalassemia minor subjects a significant positive correlation (r = 0.65, p less than 0.01) exists between HCT and whole blood viscosity. However, the slope of the regression of whole blood viscosity and HCT of beta-thalassemia minor subjects was significantly higher z = 3.14, p less than 0.001) than that of normals. Thus, for any given HCT their whole blood viscosity was higher than that of normals. Studies of the relation of red blood cell counts to whole blood viscosity indicate the higher whole blood viscosity at a given HCT was related to the increased red blood cell counts in beta-thalassemia minor subjects. Because of the opposing interactions of HCT and red blood cell counts, the mean whole blood viscosity of the group of beta-thalassemia minor subjects examined was not significantly lower than the normal whole blood viscosity.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Viscosity↗

Contributions of red cells and plasma to blood viscosity in preterm and full-term infants and adults.

In preterm infants, plasma and red blood cells display several specific properties (eg, RBC size, plasma composition) that could influence blood flow behavior. Hemorheologic properties of blood from 20 preterm infants (24 to 36 weeks of gestation), ten full-term neonates, and ten adults were studied by means of a cone-plate viscometer adapted with a Couette-type chamber allowing viscometry at a wide range of shear rates (1.15 to 230/s). Blood viscosity (at given hematocrit of 60%), plasma viscosity, and RBC aggregation were very low in the smallest preterm infants, increased with gestational age, and reached the highest values in the adults. Whole blood viscosity increased directly with increasing plasma viscosity, plasma fibrinogen, and total plasma protein concentration, with the strongest correlations at the lowest shear rate of 1.15/s. The viscosity of RBCs suspended in a nonaggregating buffer solution was similar in all groups, thereby indicating that RBC deformability is similar in preterm infants, full-term neonates, and adults. Because mixing of neonatal and adult blood components occurs in most small preterm infants as a result of the transfusion of adult blood products, viscosities of cross suspensions (neonatal RBCs in adult plasma and adult RBCs in neonatal plasma) were measured. The exchange of neonatal plasma for adult plasma increased blood viscosity values in the neonates to adult values. On the other hand, the exchange of neonatal RBCs for adult RBCs did not affect blood viscosity. These results indicate that viscosity of blood with given hematocrit is lower in preterm infants than in term neonates and adults as a result of low plasma viscosity and low RBC aggregation, and that neonatal RBCs do not possess specific properties that influence blood viscosity.

Adult↗

Theoretical correlation between viscosities at dynamic and steady flow states in Aureobasidium pullulans culture fluids.

For the culture fluid and exopolysaccharide solution of the fungus Aureobasidium pullulans in a previous study, the angular frequency dependence of dynamic viscosity is well superimposed on the shear rate dependence of steady flow viscosity. For various polymeric fluids, the superimposition of the dependencies of steady flow viscosity and dynamic viscosity has also been realized. In this study, it is derived that, by assuming the sinusoidal oscillating flow of a viscoelastic fluid, complex viscosity is equivalent to viscosity in a steady flow measurement. A similar relation may also hold for the dynamic viscosity of an ideal viscous fluid. Generally, the measurement of the steady flow viscosity deprives a viscoelastic fluid of its elastic nature due to the disruption of the network structure causing the viscoelasticity. For the culture fluid and exopolysaccharide solution of A. pullulans, the correlation between the dynamic viscosity and the network structure was low. The dynamic viscosity in this case is consistent with the steady flow viscosity in the superimposing correlation.

Journal Article↗

Importance of viscosity in the dissolution rate of cholesterol in monooctanoin solutions.

Several factors affecting the dissolution rate of cholesterol in monooctanoin were investigated. This solvent is used clinically for dissolution of residual cholesterol gallstones in the bile duct after cholecystectomy. The effect of added water on dissolution rate, measured using the static- or rotating-disk methods, was not consistent with the previously measured solubility. The discrepancy was found to be due to the decreasing viscosity of the solvent as water was added. Addition of cholesterol, however, increased the viscosity of monooctanoin. The viscosity effect on dissolution rate was investigated further by addition of polymers (povidone and poloxamer 237) which increased solvent viscosity. Dissolution rate was proportional to viscosity to the -0.4 power with these polymers. An equation was derived which predicts that dissolution rate should be proportional to viscosity to the -2/3 power. The predicted exponent was very close to reported experimental values for benzoic acid, but the dissolution rate/viscosity relationship for cholesterol in aqueous monooctanoin was nonlinear with apparent exponents of -0.65 to -2.3. Although the Arrhenius activation energies for viscosity (3.79 kcal/mol) and dissolution rate constant (3.66 kcal/mol) were almost equal for benzoic acid, a nonlinear relationship was again observed for cholesterol in aqueous monooctanoin with approximate Ea values of 5.6-10 kcal/mol. The strong influence of viscosity on dissolution rate in this system is attributed to the viscosity-increasing effect of cholesterol in the diffusion layer. The increased viscosity at higher cholesterol concentrations reduces the diffusion coefficient of cholesterol and causes the dissolution rate to be slower even though solubility may have been higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Caprylates↗

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↗

Blood viscosity and its relationship to iron deficiency, symptoms, and exercise capacity in adults with cyanotic congenital heart disease.

OBJECTIVES: This study sought to determine the relationship between blood viscosity and iron deficiency and their impact on symptoms and exercise function in adults with cyanotic congenital heart disease. BACKGROUND: Iron deficiency is believed to raise whole blood viscosity in cyanotic congenital heart disease, although available data are inconsistent. METHODS: Thirty-nine cyanotic adults were prospectively assessed for iron deficiency (transferrin saturation < or =5%), hyperviscosity symptoms, and exercise capacity. Same-day measurement of whole blood viscosity and hematocrit (Hct) adjusted viscosity (cells resuspended in autologous plasma to Hct of 45%) was performed at shear rates ranging from 0.277 s(-1) to 128.5 s(-1). RESULTS: Viscosity did not differ between patients with iron deficiency (n = 14) and those without (n = 25). Whole blood viscosity correlated with Hct (r = 0.63, p < 0.001 at low shear and r = 0.84, p < 0.001 at high shear) but not with red blood cell size or iron indices. Hyperviscosity symptoms were independent of iron indices but directly correlated with increased Hct-adjusted viscosity (r = 0.41, p = 0.01). Exercise capacity did not differ in iron-deficient patients. However, peak oxygen consumption was higher in those with Hct > or = 65% (12.6 +/- 3.4 ml/kg/m2 vs. 9.8 +/- 2.6 ml/kg/m2, mean +/- SD, p = 0.036) despite higher whole blood viscosity in these same individuals (p < 0.01 for all shear rates). CONCLUSIONS: Iron deficiency is common in cyanotic adults but does not alter viscosity. Hyperviscosity symptoms are associated with a higher Hct-adjusted viscosity independent of cell size or iron stores. Higher Hct is associated with better exercise capacity. Further work to understand the origin of hyperviscosity symptoms is warranted.

Adult↗

von Willebrand factor, fibrinogen and other plasma proteins as determinants of plasma viscosity.

Plasma viscosity and fibrinogen are risk factors for cardiovascular disease and on rheological grounds, it is widely believed that the latter is a major determinant of the former. However, other plasma constituents may also be important determinants of plasma viscosity. Our aim was to determine whether or not levels of von Willebrand factor contributed to plasma viscosity. We measured plasma viscosity, fibrinogen, von Willebrand factor, immunoglobulins G, A and M, total, HDL- and LDL-cholesterol, triglycerides and albumin in 95 patients with peripheral arterial disease and in 120 healthy controls. A stepwise multivariate analysis was performed to determine the major influences of plasma viscosity. We also measured fibrinogen, von Willebrand factor, immunoglobulins G, A and M, total, HDL- and LDL-cholesterol, triglycerides, albumin and viscosity in 32 smokers as they successfully progressed to being non-smokers. The level of von Willebrand factor was an independent influence on plasma viscosity in the controls (P < 0.05), patients (P < 0.01) and in the combined group (P < 0.001). von Willebrand factor, fibrinogen and plasma viscosity, but not the immunoglobulins, lipoproteins or albumin, fell (P < 0.05) in smokers as they became non-smokers. We find that von Willebrand factor contributes to plasma viscosity, hence a reduction in levels of von Willebrand factor should result in a reduction in viscosity. These data may have implications for the pathogenesis of cardiovascular disease.

Adult↗

Blood viscosity during the neonatal period: the role of plasma and red blood cell type.

Adult and newborn infant blood viscosity have been compared, taking into account not only the hematocrit, but also the type of red blood cells (fetal or adult) in the circulation and the plasma viscosity. At all shear rates studied, the viscosity of the adults' blood was higher than that of the newborn infant. At shear rates of 11.5 and 46 second-1, an increase in the hematocrit influences the viscosity of neonatal and adult blood similarly. At 115 and 230 second-1, the rise in hematocrit was associated with a greater increase in viscosity in the presence of fetal red blood cells, probably because of their lesser deformability. Plasma viscosity was 1.18 +/- 0.17 centipoises in the newborn compared to 1.36 +/- 0.10 in the adult group (P less than 0.001). The relative apparent viscosity (apparent viscosity/plasma viscosity) was higher in the neonate at a hematocrit of 65% (P less than 0.05). In normal conditions, blood viscosity is lower in the neonatal period because of a lower plasma viscosity.

Adult↗

Effects of viscosity and temperature on the kinetics of the electron-transfer reaction between the triplet state of zinc cytochrome c and cupriplastocyanin.

This is a study of the effects of viscosity (in the range of 0.8-790 cP), of temperature (in the range of 260.7-307.7 K), and of ionic strength (in the range of 2.5-20.0 mM) on the kinetics of photoinduced electron-transfer reaction 3Zncyt/pc(II) --> Zncyt+/pc(I) within the electrostatic complex of zinc cytochrome c and cupriplastocyanin at pH 7.0. The unimolecular rate constant is kF. The apparent activation parameters DeltaH*, DeltaS*, and DeltaG* for this reaction were obtained in experiments with aqueous glycerol solutions having a constant composition. The interpolation of kF values obtained at the constant composition into the dependence of kF on temperature at constant viscosity gave the proper activation parameters, which agree with those obtained in experiments with solutions having a constant viscosity. This agreement validates the latter method, which is more efficient than the former, for determining activation parameters of processes that are modulated by viscosity. The smooth change in kF is governed by the change in viscosity, not in other properties of the solvent, and it does not depend on the choice of the viscosigen. Donor/acceptor electronic coupling (HAB) and reorganizational energy (lambda), obtained by fitting of the temperature dependence of kF to the Marcus equation, are consistent with true electron transfer and with electron transfer that is coupled to, or gated by, a preceding structural rearrangement of the diprotein complex 3Zncyt/pc(II). The fact that at very high viscosity kF approaches zero shows that the reaction is probably gated throughout the investigated range of viscosity. Kinetic effects and noneffects of ionic strength, viscosity, and thermodynamic driving force indicate, but do not prove, that the reaction under consideration is gated. The kinetic effect of viscosity is analyzed in terms of two models. Because ln kF is a nonlinear function of ln eta, protein friction has to be considered in the analysis of viscosity effects on kinetics.

Buffers↗

Rheological properties of concentrated skim milk: influence of heat treatment and genetic variants on the changes in viscosity during storage.

Heat treatment during manufacturing of milk powder is one of the most important tools for manipulation of its functional properties, and it is the basis of the classification of these proteins into low-, medium-, and high-heat types. Slight differences in the sequences of the major proteins in milk (genetic variants) seem to have also a significant effect in milk powder processing (U.S. patent). Therefore, the effects of high-temperature storage and heat treatment on skim milk of defined genetic variants of beta-lactoglobulin (beta-LG) were measured. The samples had 45% total solids, the temperature of aging was 50 degrees C, and the heat treatment was 90 degrees C for 10 min prior to evaporation. Measurements on shear rate and on apparent viscosity were determined for each sample. During storage of the concentrated milk, the apparent viscosity and yield values increased markedly, and the age-dependent increase in viscosity in heat-treated concentrated skim milks was much more pronounced than in those prepared from unheated skim milks. The increase in apparent viscosity and yield value with storage time was notably different for milks containing different genetic variants. Unheated concentrated milks containing the B variant of beta-LG showed the most rapid increase in apparent viscosity with storage time, whereas the viscosity increase was slowest in the concentrate containing the A variant. In contrast, heat-treated concentrated milks containing the A variant of beta-LG showed the most rapid increase in viscosity with storage time, whereas the viscosity increase was slowest in the concentrate containing the AB variant. The changes in apparent viscosity of concentrated milk were largely reversible under high shear during the early stages of storage, but samples stored for a long time showed irreversible changes in apparent viscosity. Particle size analysis confirmed irreversible aggregation and fusion of casein particles during storage.

Animals↗

The effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis in humans.

1. Increased blood or plasma viscosity has been observed in almost all conditions associated with accelerated atherosclerosis. Cognizant of the enlarging body of evidence implicating increased viscosity in atherogenesis, we hypothesize that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis. 2. Blood viscometry was performed on samples from 28 healthy, non-fasting adult volunteers using a capillary viscometer. Data were correlated with haematocrit, fibrinogen, serum viscosity, total cholesterol, high-density lipoprotein-cholesterol, triglycerides and calculated low-density lipoprotein-cholesterol. 3. Low-density lipoprotein-cholesterol was more strongly correlated with blood viscosity than was total cholesterol (r = 0.4149, P = 0.0281, compared with r = 0.2790, P = 0.1505). High-density lipoprotein-cholesterol levels were inversely associated with blood viscosity (r = -0.4018, P = 0.0341). 4. To confirm these effects, viscometry was performed on erythrocytes, suspended in saline, which had been incubated in plasma of various low-density lipoprotein/high-density lipoprotein ratios. Viscosity correlated directly with low-density lipoprotein/high-density lipoprotein ratio (n = 23, r = 0.8561, P < 0.01). 5. Low-density lipoprotein receptor occupancy data suggests that these effects on viscosity are mediated by erythrocyte aggregation. 6. These results demonstrate that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity in healthy subjects correlate with their association with risk of atherosclerosis. These effects on viscosity may play a role in atherogenesis by modulating the dwell or residence time of atherogenic particles in the vicinity of the endothelium.

Adult↗

Effect of soluble dietary fibre on the viscosity of gastrointestinal contents and the acute glycaemic response in the rat.

The postprandial glycaemic response following a meal is reduced with the addition of soluble dietary fibre. The reductions in the glycaemia are thought to be due largely to increased viscosity of the gastrointestinal (GI) contents retarding digestion and absorption. The aims of the present study were to determine the effect that the GI tract has on the viscosity of meals containing different soluble fibres and to determine whether the glycaemic response of a meal (containing the soluble fibre) was predicted by the viscosity of the digesta in the small intestine. High carbohydrate diets containing 70 g soluble fibre guar gum, xanthan gum or methylcellulose)/kg or 70 g insoluble fibre (wheat bran)/kg were diluted in water to a final fibre concentration of 18 g/kg. Following dilution the wheat bran diet had no measurable viscosity, while the viscosities of the soluble fibre diets were elevated. When the diets were fed to male Sprague-Dawley rats for 2 weeks the viscosities of the stomach and small intestinal digesta were not predicted by the viscosity of the diets measured before ingestion. The action of the GI tract on the viscosity of the soluble fibres was investigated in vitro by dilution of the diets with acidic and neutralizing solutions, mimicking gastric and duodenal secretions. Dilution of diets with either acidic and neutralizing solutions or saline control significantly lowered the viscosity of all diets, while alterations in the pH of the diets had little impact on the resultant viscosity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Relationships between viscosity of hydroxypropyl methylcellulose and plasma cholesterol in hamsters.

Dietary high viscosity hydroxypropyl methylcellulose (HPMC) lowered plasma and liver cholesterol concentrations in cholesterol-fed hamsters. To determine the level of viscosity needed to effect a significant reduction in total plasma cholesterol, hamsters were fed for 3 wk diets containing 0.12% cholesterol and either 4% cellulose or one of four preparations of HPMC that varied in viscosity between 14 and 1698 centipoise (cP), as estimated in vitro. Blood was collected for plasma cholesterol determination, and intestinal contents were obtained by finger-stripping of the excised small intestine. Contents were centrifuged and the supernatant (ex vivo) viscosity determined. In vitro and ex vivo viscosities were correlated (R2 = 0.96). Plasma cholesterol concentrations declined as in vitro or ex vivo viscosity increased. Maximal plasma cholesterol reduction occurred at an ex vivo viscosity of approximately 150 cP. There was a linear relationship between plasma cholesterol and the logarithm of ex vivo viscosity (R2 = 0.98). Our results suggest that materials that increase the viscosity of intestinal contents can be effective in reducing plasma cholesterol and that only moderate increases in viscosity are necessary to achieve this effect.

Animals↗

Lack of hypercapnic increase in cerebral blood flow at high blood viscosity in conscious blood-exchanged rats.

BACKGROUND: The hypothesis of a compensatory dilation of cerebral vessels to maintain cerebral blood flow at a high blood viscosity was tested during hypercapnia in the study after replacement of blood by hemoglobin solutions of defined viscosities. If compensatory vasodilation exists at normocapnia at a high blood viscosity, vasodilatory mechanisms may be exhausted when hypercapnia is added, resulting in a lack of increase in cerebral blood flow at hypercapnia. METHODS: In conscious rats, blood was replaced by ultrapurified cross-linked hemoglobin solutions that had defined and shear rate-independent low or high viscosities (low- and high-viscosity groups). Blood viscosity differed threefold between both groups (1.2 vs. 3.6 mP x s). Thereafter, rats inhaled either a normal or an increased concentration of carbon dioxide in air. Cerebral blood flow was determined by the iodo[14C]antipyrine method. RESULTS: During normocapnia, global and local cerebral blood flows did not differ between both groups. With increasing degrees of hypercapnia, global and local cerebral blood flows were gradually elevated in the low-viscosity group (2.8 ml x mmHg(-1) CO2 x 100 g(-1) x min(-1)), whereas they remained unchanged in the high-viscosity group. CONCLUSIONS: Changes in blood viscosity do not result in changes of cerebral blood flow as long as cerebral vessels can compensate for these changes by vasodilation or vasoconstriction. However, such vascular compensatory adjustments may be exhausted in their response to further pathophysiologic conditions in blood vessels that have already been dilated or constricted as a result of changes in blood viscosity.

Animals↗

Plasma and whole blood viscosity in treated primary polycythaemia.

Whole blood viscosity at a range of shear rates (230--0.77 s-1) and plasma viscosity have been measured in 39 patients with treated primary polycythaemia (idiopathic erythrocytosis and primary proliferative polycythaemia) and 30 age-matched normal individuals. There was a wider range of plasma viscosity and whole blood viscosity values at the same haematocrit (0.46), particularly at the lower shear rates, in the 'polycythaemic' group than the normal group. Hypochromic microcytic red cell changes present in 14 patients in the 'polycythaemic' group did not have any noticeable influence on whole blood viscosity at a given haematocrit value, since plasma protein factors override any possible effect of these red cell changes. The range of observed whole blood viscosity results in the 'polycythaemic' patients at the same haematocrit (0.46) was equivalent to the effect on whole blood viscosity of a rise in haematocrit from 0.41 to 0.51. Since there is such a range of whole blood viscosity at the same haematocrit, the haematocrit alone does not necessarily give a precise assessment of the viscosity of a whole blood sample. Since there is evidence from other publications that blood flow in vitro may be critically influenced by whole blood viscosity, this lack of precision should be considered when treating patients at risk of vascular occlusive episodes.

Adult↗