[Interrelation of viscosity resistance, viscosity respiratory function and alveolar aeration in chronic obstructive pulmonary emphysema].
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Airway Obstruction↗
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Results for “VISCOSITY”
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Blood viscosity, erythrocyte sedimentation rate, packed cell volume, osmolality, and plasma viscosity of the Wistar rat.
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Animals↗
Microrheology of human blood in health and disease. Effect of blood subphases (I.A., the internal viscosity and aggregation of the blood cells) on blood viscosity and microcapillary flow, occlusion and infarction.
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Blood Circulation↗
[The effect of dextran on the blood viscosity variation of the whole blood and plasma viscosity after operation (author's transl)].
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Animals↗
Exogenous dietary xylanase ameliorates viscosity-induced anti-nutritional effects in wheat-based diets for White Pekin ducks (Anas platyrinchos domesticus).
Nutrient utilisation and growth performance responses of White Pekin ducks (Anas platyrinchos domesticus) offered diets containing low- or high-viscosity wheat supplemented with xylanase were investigated in two studies. In Expt 1, six diets consisting of low-viscosity wheat or high-viscosity wheat supplemented with 0.0, 1.5 or 3.0 g xylanase (2590 units/g)/kg diet were used in a true metabolisable energy (TME) bioassay with eight 8-week-old ducks per diet group. In Expt 2, eight pens of ten 3-d-old ducks per pen for each of six wheat-based diets arranged in a 2 x 3 factorial of low-viscosity or high-viscosity wheat and 0.0, 1.5 or 3.0 g xylanase/kg were used in a 42 d growth study. High-viscosity wheat depressed (P<0.001) TME and xylanase supplementation improved (P<0.001) TME, more so for high-viscosity than low-viscosity wheat. Xylanase supplementation of the high-viscosity wheat-based diet improved (P<0.05) weight gain and gain:feed ratio by 13 and 12 % respectively. There was no weight gain or gain:feed ratio response to xylanase supplementation of the low-viscosity wheat-based diet. Xylanase supplementation reduced (P<0.001) the viscosity of duodenal and ileal digesta for high-viscosity but not low-viscosity wheat-based diets. Ileal digestibilities of nutrients and energy were higher (P<0.001) for low-viscosity than high-viscosity wheat-based diets; xylanase supplementation improved (P<0.05) energy, fat, N and starch digestibilities. Given that xylanase supplementation of high-viscosity wheat assuaged its anti-nutritional effect, it is surmised that digesta viscosity plays a role in anti-nutritional effects in wheat-based diets for ducks.
Animal Feed↗
Role of plasma viscosity in platelet adhesion.
Platelet adhesion to the vessel wall is initiated by transport of blood platelets from the bulk flow to the wall. The process of diffusion and convection of the platelets is affected by rheological conditions such as well shear rate, red blood cell (RBC) deformability, and viscosity of the medium. To study the effect of plasma viscosity on platelet adhesion, perfusion experiments with a rectangular perfusion chamber were performed. Reconstituted blood, consisting of washed platelets and washed RBCs, was circulated through this chamber for 5 minutes at a wall shear rate of 300 s-1. Different albumin concentrations were made, to obtain different medium viscosities (0.89 to 1.85 mPa.s). Platelet adhesion decreased with increasing medium viscosity up to viscosities of 0.95 mPa.s, but increased with medium viscosity above this value. Instead of human albumin solution, different plasma viscosities were obtained by dilution of Waldenström plasma with buffer. Plasma was depleted of fibronectin, which gave a final plasma viscosity of 2.0 mPa.s, and was dialyzed against HEPES buffer and subsequently diluted with the dialysis buffer in different fractions (0.89 to 2.00 mPa.s). Perfusions were performed over a purified von Willebrand factor coating on glass, or over an endothelial cell matrix, preincubated with von Willebrand factor. With both surfaces, platelet adhesion was dependent on the plasma viscosity in a similar way: at low plasma viscosities, adhesion was decreased with increasing plasma viscosity, while at higher plasma viscosities, adhesion increased with plasma viscosity. Adhesion values at higher plasma viscosity or at higher human albumin concentrations could be explained by effects of the medium on the rigidity of the RBCs, since platelet adhesion is known to be increased by enhanced RBC rigidity. Effects of the medium on the deformability of the RBCs were measured separately with the laser diffraction method. These experiments confirmed that presence of human albumin or plasma in the measuring suspension increased the rigidity of RBCs. To prevent influence of the medium on the RBCs in perfusion experiments, the RBCs were fixated with glutaraldehyde. Perfusion experiments with fixated RBCs in plasma over a von Willebrand factor preincubated endothelial cell matrix, showed a consequent decrease in adhesion with increasing plasma viscosity, according to the diffusion theories, whereas the increase of adhesion at high plasma viscosities was lacking. This suggests that the latter effect was entirely due to increased transport of platelets by more rigid RBCs.
Blood Viscosity↗
Gastric response to increased meal viscosity assessed by echo-planar magnetic resonance imaging in humans.
Normal meals are highly viscous, and viscosity is a key factor in influencing gastric emptying of food. However, the process of meal dilution and mixing is difficult to assess with the use of conventional methods. The aim of this study was to validate an in vivo, novel, noninvasive, echo-planar magnetic resonance imaging (EPI) technique, capable of monitoring the viscosity of a model meal, and to use this to investigate the effects of viscosity on gastric emptying, meal dilution and satiety. Healthy volunteers (n = 8) ingested 500 mL of locust bean gum (0.25, 0.5, 1.0 or 1.5 g/100 g), nonnutrient, liquid meals of varying viscosities, and labeled with a nonabsorbable marker, phenol red. Meal viscosity was calibrated against the water proton transverse relaxation rate (T(2)(-1)) in vitro before ingestion, thus viscosity was measured in vivo via EPI measurements of T(2)(-1). Viscosity and dilution were also measured directly using nasogastric aspirates. Gastric volumes as measured by EPI, fullness, appetite and hunger were also assessed serially. Before ingestion, the log of initial meal viscosity was linearly related to T(2)(-1) (n = 8, r(2) = 0.95). Similarly, T(2)(-1) measured in vivo was also linearly related to the viscosity of the aspirates (r(2) = 0.88). All meals underwent rapid dilution, leading to a reduction in viscosity, which was greatest for the most viscous meal (P < 0.01). Surprisingly, despite the fact that the initial meal viscosity varied 1000-fold, there was only a small delay in gastric emptying (P for trend < 0.05). The area under the curve for satiety increased with initial meal viscosity, whereas that for hunger decreased (P < 0.05). In conclusion, the viscosity of a meal in vivo can be measured noninvasively using EPI. The stomach responds to meal ingestion by rapid intragastric dilution, causing a reduction of meal viscosity, and gastric emptying is minimally delayed. However, increased viscosity is associated with more prolonged satiety.
Adult↗
Impact of pancreas and kidney transplantation on determinants of blood and plasma viscosity.
Simultaneous pancreas and kidney transplantation (PKT) is associated with a deterioration of hemorheology. We investigated the determinants of plasma and blood viscosity (hct. 35%) after PKT (n = 49), in type 1 diabetes (n = 26) and in healthy controls (n = 24). Patients after PKT were subdivided due to their graft function (intact pancreas and kidney graft, n = 26; pancreas rejected, intact kidney graft, n = 23). We examined the correlations of total serum protein, albumin, fibrinogen, alpha 2-macroglobulin, total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides with plasma and blood viscosity (hct. 35%) measured at a continuous shear range of 600-0.2 s-1 with a rotational viscometer (Haake, Germany). Total protein was strongly associated with plasma viscosity in all examined groups (r > 0.5, p < 0.03), it determined blood viscosity over the whole shear range in type 1 diabetic patients, but only at high shear rates after PKT (> or = 100 s-1). The strong association of albumin and blood viscosity in type 1 diabetes and in healthy controls (shear rates > or = 10 s-1) was not found after PKT. Fibrinogen correlated with plasma and blood viscosity (> or = 25 s-1) after PKT (p < 0.03) but no in type 1 diabetic patients or healthy controls. Alpha 2-macroglobulin correlated with plasma and high shear blood viscosity after PKT only after pancreas rejection, no correlation was found after successful PKT. It also correlated with plasma and blood viscosity at low and high shear rates in type 1 diabetes. Total cholesterol and low shear blood viscosity correlated positively in successfully transplanted patients (r > 0.44), but negatively after pancreas rejection (r > -0.44). No correlation was found in type 1 diabetic patients, a positive association was found in healthy controls for plasma and low shear blood viscosity. LDL cholesterol correlated negatively (after pancreas rejection) or positively (healthy controls) with low shear blood viscosity (p < 0.03) and positively with plasma viscosity. HDL cholesterol was negatively associated with high shear blood viscosity in all groups (p < 0.05), except after successful PKT, where no association was found. It did not correlate with plasma viscosity in any group. Triglycerides did not contribute significantly to blood viscosity in the examined groups. The metabolic alterations after PKT influence plasma proteins, lipids and corpuscular elements of blood with regard to their effect on rheology.
Adult↗
Detection of red cell aggregation by low shear rate viscometry in whole blood with elevated plasma viscosity.
The viscosity of whole blood measured at low shear rates is determined partly by shear resistance of the red cell aggregates present, stronger aggregation increasing the viscosity in the absence of other changes. Effects of cell deformability can confound interpretation and comparison in terms of aggregation, however, particularly when the plasma viscosity is high. We illustrate the problem with a comparison of hematocrit-adjusted blood from type 1 diabetes patients and controls in which it is found the apparent and relative viscosities at a true shear rate of 0.20 s-1 are lower in the patient samples than age matched controls, in spite of reports that aggregation is increased in such populations. Because the plasma viscosities of the patients were higher on average than controls, we performed a series of experiments to examine the effect of plasma protein concentration and viscosity on normal blood viscosity. Dilution or concentration by ultrafiltration of autologous plasma and viscosity measurements at low shear on constant hematocrit red cell suspensions showed (a) suspension viscosity at 0.25 and 3 s-1 increased monotonically with plasma protein concentration and viscosity but (b) the relative viscosity increased, in concert with the microscopic aggregation grade, up to a viscosity of approximately 1.25 mPa-s but above this the value the relative viscosity no longer increased as the degree of aggregation increased in concentrated plasmas. It is suggested that in order to reduce cell deformation effects in hyperviscous pathological plasmas, patient and control plasmas should be systematically diluted before hematocrit is adjusted and rheological measurements are made. True shear rates should be calculated. Comparison of relative viscosities at low true shear rates appears to allow the effects of red cell aggregation to be distinguished by variable shear rate viscometry in clinical blood samples.
Adult↗
[Effect of temperature on rheologic properties of blood and internal viscosity of erythrocytes].
BACKGROUND: The blood viscosity is one of the factors affecting tissue blood flow. Aim of the study was to establish how the blood viscosity and internal viscosity of the red cell (Tk) may be influenced by change of the temperature. METHODS AND RESULTS: We have measured plasma and blood viscosity in 20 samples of human plasma and 17 samples of human blood. Viscosity was established with rotational viscometer under the temperature ranging from 25 degrees C to 45 degrees C. Concomitantly the internal viscosity of the red cell (Tk) was estimated. Plasma and blood viscosities are decreasing with the temperature elevation but the change is not linear through temperature range used for testing. The most pronounced change was found in relatively lower temperatures. Relative viscosity of the blood did not change significantly with the temperature except of measurements under low shear conditions performed in low temperature. Relative blood viscosity increased with temperature fall in such a situation. The internal viscosity of the red cell (Tk) increased significantly with temperature elevation. CONCLUSIONS: The average values of the blood and plasma viscosity fell with temperature elevation but the change was not linear. The plasma viscosity change was the highest in the low temperature range. These findings together with significant differences between relative and dynamic blood viscosity in low shear conditions and in 25 degrees C showed that blood viscosity was influenced by qualitative changes of the plasma followed by higher aggregation of the red cells.
Blood Viscosity↗
Red blood cell deformation in shear flow. Effects of internal and external phase viscosity and of in vivo aging.
Shear deformation of young and old human red blood cells was examined over a range of shear stresses and suspending phase viscosities (eta o) using a cone-plate Rheoscope. The internal viscosities (eta i) of these cell types differ, and further changes in internal viscosity were induced by alteration of suspension osmolality and hence cell volume. For low suspending viscosities (0.0555 or 0.111 P) old cells tended to tumble in shear flow, whereas young cells achieved stable orientation and deformed. Changes in osmolality, at these external viscosities, altered the percentage of cells deforming, and for each cell type threshold osmolalities (Osm-50) were determined where 50% of cells deformed. The threshold osmolalities were higher for younger cells than for older cells, but the internal viscosities of the two cell types were similar at their respective Osm-50. Threshold osmolalities were also higher for the higher external viscosity, but the ratio of internal to external viscosities (i.e., eta i/eta o) was nearly constant for both external viscosities. Deformation of stably oriented cells increased with increasing shear stress and approached a value limited by cell surface area and volume. For isotonic media, over a wide range of external viscosities and shear stresses, deformation was greater for younger cells than for older cells. However, deformation vs. shear stress data for the two cell types became nearly coincident if young cells were osmotically shrunk to have their internal viscosity close to that for old cells. Increases in external viscosity, at constant shear stress, caused greater deformation for all cells. This effect of external viscosity was not equal for young and old cells; the ratio of old/young cell deformation increased with increasing eta o. However, if deformation was plotted as a function of the ratio lambda = eta i/eta o, at constant shear stress, young and old cell data followed similar paths. Thus the ratio lambda is a major determinant of cell deformation as well as a critical factor affecting stable orientation in shear flow.
Erythrocyte Aging↗
Distribution of blood viscosity values and biochemical correlates in healthy adults.
Increases in the viscosity of blood and plasma predict clinical manifestations of atherothrombotic vascular disease. The clinical utility of viscosity measurements in cardiovascular risk factor analysis requires reference values established from a healthy disease-free population. A cohort of 126 (71 men, 55 women) healthy nonsmoking adults had fasting blood analysis after a 12-14-h fast. Viscosity measurements were made on samples of whole blood, plasma, and serum at 37 degrees C with a coaxial cylinder microviscometer. The mean blood viscosity at shear rates of 100, 50, and 1 s-1 were 3.26 +/- 0.43, 4.37 +/- 0.60, and 5.46 +/- 0.84 mPa.s, respectively. Men had significantly higher blood viscosity values than women at each shear rate. The differences in blood viscosity did not remain significant after blood viscosity values were normalized to a hematocrit of 45%, except at 100 s-1. For the entire group, normalized blood viscosity values at each measured rate correlated inversely with HDL cholesterol and positively with fibrinogen. The mean plasma viscosity was 1.39 +/- 0.08 mPa.s and the mean serum viscosity was 1.27 +/- 0.06 mPa.s. Plasma viscosity correlated with fibrinogen (r = 0.51, P < 0.0001), total serum protein (r = 0.33, P < 0.0001), and triglyceride concentrations (r = 0.33, P < 0.0015). Serum viscosity correlated with total serum protein (r = 0.50, P < 0.0001) and LDL cholesterol (r = 0.24, P = 0.0065). This study provides reference values for the viscosity of blood, plasma, and serum that may assist in evaluating hemorheological profiles.
Adult↗
A perceptual analysis of viscosity.
The perception of viscosity was studied using the contralateral limb-matching procedure in which subjects adjusted the viscosity of a motor connected to the wrist of one (matching) arm until it was perceived to be the same as that of the motor attached to the other (reference) arm. Two servo-controlled electromagnetic linear motors with computer-controlled viscosity were used to present viscosities ranging in amplitude from 2 to 1024 N.s/m to 11 subjects. Ten different viscosities were matched by subjects, and there were ten repetitions of each stimulus amplitude. The psychophysical function relating the reference to matching viscosity was linear (99% variance accounted for), and the accuracy with which the viscosities were matched (slope of 0.88) paralleled that reported previously for force, limb position and stiffness. The Weber fraction for viscosity was 0.34, which is 50% larger than that measured for stiffness and over twice that reported for force. An analysis of the movements and forces generated to perceive the reference viscosity revealed that subjects did not vary the amplitude of the movements and typically made very small excursions of the forearm, but that both the velocity of the movements and force changed significantly as a function of the reference viscosity. These findings were interpreted as indicating that the human proprioceptive system is capable of integrating information regarding force and movement velocity so as to perceive the viscosity of a mechanical system connected to the limbs, but that its sensitivity to changes in viscosity is much less than would be predicted from its capacity to detect variations in muscle force and limb movement.
Adult↗
Concentration-dependent, temperature-dependent non-Newtonian viscosity of lung surfactant dispersions.
The bulk shear viscosities of aqueous dispersions of lavaged calf lung surfactant (LS) and its chloroform:methanol extract (CLSE) were measured as a function of concentration, shear rate and temperature. At 10-mg phospholipid per milliliter, dispersions of LS and vortexed CLSE in 0.15 M NaCl (saline) had low viscosities near 1 cp over a range of shear rates from 225 to 1125 s(-1). Lung surfactant viscosity increased with phospholipid concentration and became strongly non-Newtonian with higher values at low shear rates. At 37 degrees C and 40 mg/ml, LS and vortexed CLSE in saline had viscosities of 38 and 34 cp (77 s(-1)) and 12 and 7 cp (770 s(-1)), respectively. Viscosity values for LS and CLSE were dependent on temperature and, at fixed shear, were lower at 23 degrees C than at 37 or 10 degrees C. Hysteresis was also present in viscosity measurements depending on whether shear rate was successively increased or decreased during study. Addition of 5 mM Ca(2+) at 37 degrees C markedly reduced CLSE viscosity at all shear rates and decreased LS viscosity at low shear rates. Dispersion by sonication rather than vortexing increased the viscosity of CLSE at fixed shear, while synthetic phospholipids dispersed by either method had low, relatively Newtonian viscosities. The complex viscous behavior of dispersions of LS and CLSE in saline results from their heterogeneous aggregated microstructure of phospholipids and apoproteins. Viscosity is influenced not only by the aggregate surface area under shear, but also by phospholipid-apoprotein interactions and aggregate structure/deformability. Similar complexities likely affect the viscosities of biologically-derived exogenous surfactant preparations administered to patients in clinical surfactant therapy.
1,2-Dipalmitoylphosphatidylcholine↗
Postprandial changes in plasma and serum viscosity and plasma lipids and lipoproteins after an acute test meal.
The influence of a fat-rich test meal on postprandial changes in plasma viscosity and serum viscosity was assessed in 12 normolipidemic adults. After a 12-14-h fast, volunteers (five men and seven women aged 23-50 y) were challenged with a test milk shake containing 50 g fat/m2 body surface area (BSA). Plasma viscosity, serum viscosity, and plasma lipids and lipoproteins were assessed at 0, 2, 3, 4, and 6 h. Viscosity values were determined by using a Mettler Contraves LS-40 rotational microviscometer. Postprandial changes in the study variables were assessed by area under the curve and included triacylglycerols (2.02 mmol/L), plasma viscosity (-0.10 mPa.s), and serum viscosity (-0.01 mPa.s). Peak plasma triacylglycerol concentrations were significantly greater than those observed at baseline (P = 0.0022). There were no significant changes in any other variable when fasting and peak values were compared. Peak plasma viscosity increased in three and decreased in two subjects with no changes in the remaining seven subjects. Changes in peak plasma viscosity ranged from -7% to 7% with similar changes for serum viscosity, from -8% to 10%, and a slightly greater range for plasma fibrinogen, -16% to 10%. In this cohort of normotriacylglycerolemic subjects, there were no significant postprandial changes in plasma viscosity or serum viscosity.
Adult↗
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↗
Plasma viscosity increase with progression of peripheral arterial atherosclerotic disease.
Increased blood and plasma viscosity has been described in patients with coronary and peripheral arterial disease. However, the relation of viscosity to the extent of arterial wall deterioration--the most important determinant of clinical manifestation and prognosis of the disease--is not well known. Therefore, the authors studied plasma viscosity as one of the major determinants of blood viscosity in patients with different stages of arterial disease of lower limbs (according to Fontaine) and its relation to the presence of some risk factors of atherosclerosis. The study encompassed four groups of subjects: 19 healthy volunteers (group A), 18 patients with intermittent claudication up to 200 m (stage II; group B), 15 patients with critical ischemia of lower limbs (stage III and IV; group C), and 16 patients with recanalization procedures on peripheral arteries. Venous blood samples were collected from an antecubital vein without stasis for the determination of plasma viscosity (with a rotational capillary microviscometer, PAAR), fibrinogen, total cholesterol, alpha-2-macroglobulin, and glucose concentrations. In patients with recanalization procedure local plasma viscosity was also determined from blood samples taken from a vein on the dorsum of the foot. Plasma viscosity was most significantly elevated in the patients with critical ischemia (1.78 mPa.sec) and was significantly higher than in the claudicants (1.68 mPa.sec), and the claudicants also had significantly higher viscosity than the controls (1.58 mPa.sec). In patients in whom a recanalization procedure was performed, no differences in systemic and local plasma viscosity were detected, neither before nor after recanalization of the diseased artery. In all groups plasma viscosity was correlated with fibrinogen concentration (r=0.70, P < 0.01) and total cholesterol concentration (r=0.24, P < 0.05), but in group C (critical ischemia) plasma viscosity was most closely linked to the concentration of alpha-2-macroglobulin (r=0.78, P < 0.01). These results indicate that in patients with peripheral arterial disease plasma viscosity increases with the progression of the atherosclerotic process and is correlated with the clinical stages of the disease.
Aged↗
Apparent viscosity of chicken muscle homogenates. Influence of pH and muscle type.
The effect of pH and type of muscle on apparent viscosity of chicken breast, thigh and combined B/T muscles was investigated. The apparent viscosity of thigh muscle homogenate at pH from 5.8 to 6.6, and combined B/T muscle homogenate at pH from 5.8 to 6.3 was increasing. The apparent viscosity of breast muscle homogenate increased with pH increase, reaching a maximum at pH 6.3 and then decreased. When pH raised from 5.8 to 6.3, breast muscle homogenate apparent viscosity increased 3.5-6.0 times more than apparent viscosity of thigh muscle homogenate. An increase of combined B/T muscle homogenate apparent viscosity under shear rate 0.3333-48.6 (s-1) was approximately an average of increases for its individual muscles. At pH 5.8 and 6.0, apparent viscosity of thigh muscle homogenate was approximately two times higher than that of breast muscle homogenate, and reversibly, at pH 6.3, breast muscle homogenate apparent viscosity was about 20% higher than that of thigh muscle homogenate. The apparent viscosity of combined B/T muscle homogenate at pH 5.8 and 6.0, was greater than apparent viscosity of breast muscle homogenate, and at pH 6.3, was greater than apparent viscosity of thigh muscle homogenate. The present data extend the results reported by other researches that there are remarkable differences not only in functional and rheological properties of myofibrillar proteins (SSP, myosin) but also in those of homogenates from chicken white and red muscles.
Animals↗