Internal viscosity of the red cell: problems associated with definition of plasma viscosity and effective volume of red cells in the blood viscosity equation.
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The effect of the ionic contrast media diatrizoate, iocarmate and metrizoate and the non-ionic metrizamide on whole blood viscosity, plasma viscosity and hematocrit was investigated. All the contrast media increased whole blood and plasma viscosity and reduced the hematocrit. The whole blood viscosity increased with increasing osmolality of the contrast medium solutions, whereas the plasma viscosity increased with increasing viscosity of the contrast medium solutions. The higher the osmolality of the contrast media, the lower the hematocrit became. The normal shear-thinning (decreasing viscosity with increasing shear rate) property of blood was reduced when contrast medium was added to the blood. At 50% volume ratio (contrast medium to blood), the ionic contrast media converted the blood into a shear-thickening (increasing viscosity with increasing shear rate) suspension, indicating a marked rigidification of the single red cell, while the non-ionic contrast medium still produced shear-thinning, indicating less rigidification of the red cell (p less than 0.01).
A systematic study of the spectral characteristics of the viscosity artifact in Fura-2 based [Ca2+] measurements reveals that, by selecting excitation wavelengths approximately 10 nm longer than those routinely employed and modestly reducing excitation bandpasses, the magnitude of the artifact can be reduced to experimentally undetectable levels without greatly impairing [Ca2+] measurements. The feasibility of this approach was confirmed on a ratio imaging microscope; the magnitude of the artifact observed in dextran-conjugated Fura-2 solutions prepared in water or in 50% sucrose was not statistically significant using an excitation wavelength pair of 361/389 nm, whereas at 350/380 nm [Ca2+] was underestimated by 34% in the higher viscosity solution. Thus, provided potential pitfalls are taken into account, a simple change in imaging protocol can avoid the viscosity artifact without recourse to correction factors. This approach may be employed either routinely, or else merely to test whether apparent [Ca2+]i differences observed at more conventional wavelengths arise from the viscosity artifact.
Relative variations of fluidity in bilayers and membranes are currently evaluated by numerous physical methods, but comparison between different systems remain difficult because the effects of order (anisotropy) and fluidity are involved in the diffusion coefficients for correlation times, or frictional coefficients) given by experiment. The present report represents an attempt to generalize the use of isotropic liquids as viscosity standards for disordered lipidic systems. It advances a simple check to verify the quasi-isotropic behaviour of probe environments and avoids the introduction of estimated values of the molecular dimensions in Perrin-Einstein relations. The equivalent viscosities obtained with 1,6-diphenyl hexatriene and with 2-pentyl-2'-butyl-4,4'-dimethyl oxazolidinoxyl are strikingly similar in egg lecithin vesicles above 0 degrees C, while in dipalmitoylphosphatidylcholine dispersions above their transition temperature, a discrepancy of about 30% seems to remain, even at high temperatures.
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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.
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.
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)
Erythrocyte shape changes are known to occur in vivo and can readily be induced in vitro. We have analysed the influence of increasing stomatocytosis produced by 0-0.64 mmol l-1 chlorpromazine and increasing echinocytosis induced with 0-120 mmol l-1 salicylate or 0-8 mmol l-1 2,4-dinitrophenol on suspension viscosities. The morphological index of each sample was determined and related to the suspension viscosity. It was found that the viscosity was increased by echinocytosis in dextran-free solutions, where no aggregation occurred. The viscosity could be normalized by retransforming echinocytes into discocytes. Under conditions with erythrocyte aggregation (suspension with 4 g dl-1 dextran 70, low shear rate: 0.1 s-1) a small degree of echinocytosis produced the highest viscosity, whereas at higher degrees of echinocytosis the ability to aggregate was reduced and the viscosity was similar to that of discocytes or stomatocytes. Erythrocytes incubated in hypotonic medium (constant cell number/volume) had a higher viscosity than cells in iso- or hypertonic medium. Severely hypotonic medium led to sphering of erythrocytes which reduced the ability of these cells to aggregate and hence decreased the viscosity of suspensions with dextran at low shear rate. The results indicate that discocytes have the lowest viscosity and thus the best oxygen transport efficiency and that iso- to hypertonicity provides a lower viscosity and better oxygen transport efficiency than hypotonicity. These results may contribute to the understanding of blood flow in health and disease.
Hematocrit (Hct) and whole blood viscosity was studied at a mean age of ten hours in 100 neonates. Group A (n = 25), were term normal newborns, Group B (n = 25) were preterms, Group C (n = 20) were term small for gestation (SGA) and Group D (n = 30) had perinatal hypoxia. Blood viscosity was estimated in all cases at shear rates 94.5, 51.2, 20.4 and 8.1 and intergroup variability in viscosity compared at shear rate 51.2. The mean hematocrit (Hct) (59.4%) and viscosity (8.2 cps) was higher in Group A as compared to other groups, but the difference was not significant (p greater than 0.05). The upper limit of viscosity in Group C (11.9 cps) was higher than in all other groups but this difference was also not significant (p greater than 0.05). With decrease in shear rates a reciprocal increase in viscosity was noted in all four groups. Seventeen neonates (17%) had polycythemia of which eight (47.5%) were SGA. Twelve per cent preterms were polycythemic. Only 3% of neonates had hyperviscosity. The mean Hct and viscosity of the 17 cases with polycythemia was 70.9 and 9.21 cps, respectively, which was significantly higher than mean Hct and viscosity of Group A (p less than 0.05). Partial exchange transfusions were done in five neonates with Hct greater than 75%, of which only one had hyperviscosity. Post-exchange viscosity was not estimated. Whereas, three neonates with polycythemia were symptomatic, none of these had hyperviscosity. A linear correlation between Hct and viscosity was observed (r = 0.67).
Patients with Waldenström macroglobulinemia were studied for the presence or absence of the hyperviscosity syndrome, the relative serum viscosity value, and the calculated whole blood viscosity to identify a level at which symptoms occurred. The majority of symptomatic patients had whole blood viscosity values above 8.0 centipoises. There was a direct correlation between whole blood viscosity and relative serum viscosity, r = 0.75. One patient with central nervous system abnormalities was identified as having a high whole blood viscosity but a low serum viscosity. It was concluded that the vast majority of patients with the hyperviscosity syndrome will be identified by measuring the relative serum viscosity. In patients with central nervous system findings and a low serum viscosity, the whole blood viscosity should be determined either by direct measurement or by calculation.
Detailed viscosity measurements have been made of barium sulfate mixtures over a wide range of viscosities for use in radiography of the esophagus, stomach, and duodenum. A new methodology was developed for more accurate estimation of viscosity in non-Newtonian fluids in conventional cylinder-type viscometers. As base cases, the variation of viscosity with shear rate was measured for standard commercial mixes of e.z.hd (250% w/v) and a diluted mixture of liquid e.z.paque (40% w/v). These suspensions are strongly shear thinning at low shear rates. Above about 3s-1 the viscosity is nearly constant, but relatively low. To increase the viscosity of the barium sulfate mixture, Knott's strawberry syrup was mixed to different proportions with e.z.hd powder. In this way viscosity was systematically increased to values 130,000 times that of water. For these mixtures the variation of viscosity with temperature, and the change in mixture density with powder-syrup ratio are documented. From least-square fits through the data, simple mathematical formulas are derived for approximate calculation of viscosity as a function of mixture ratio and temperature. These empirical formulas should be useful in the design of "test kits" for systematic study for pharyngeal and esophageal motility, and clinical analysis of motility disorders as they relate to bolus consistency.
A significant impediment in determining the relative contribution of whole blood viscosity to the pathogenesis of cardiovascular and cerebrovascular disease has been the lack of an uncomplicated method to measure whole blood viscosity. To address this problem, a simplified porous bed viscometer has been developed to measure whole blood viscosity. Whole blood is passed through a porous bed of branching channels with a mean pore diameter of 69.6 +/- 20.2 microns and an estimated mean shear rate of 19.6 seconds-1. The effects of sample collection, sample storage, and temperature are described. The mean whole blood viscosity of 242 healthy persons was 22.7 +/- 5.3 seconds, which, when corrected to centipoise using Darcy's equation, corresponds to an apparent viscosity of 5.7 +/- 1.3 cp. There was a significant difference in the whole blood viscosity of normal men and women related to their different packed cell volumes. Platelets and granulocytes influenced whole blood viscosity in proportion to their contribution to the total packed cell volume. Fibrinogen levels did not significantly influence measured whole blood viscosity, which is consistent with the disaggregating conditions and the mean shear rate of the instrument. The porous bed viscometer is a convenient means to measure whole blood viscosity and it should be useful as a screening test for clinical and epidemiologic studies.
The relationship between determinants of blood viscosity and blood pressure (BP) variables was studied in a large sample of a population aged 25 to 64 years. Plasma viscosity, hemoglobin, and total serum protein were examined. Systolic and diastolic BP and the prevalence of hypertension showed a crude positive association with plasma viscosity levels in both sexes. Age, body mass index, and total serum protein appeared to have a confounding effect on this relationship, whereas hemoglobin, smoking behavior, and alcohol consumption did not. A crude positive association was also found between total serum protein levels and the prevalence of hypertension in men and women; however, since total serum protein was treated as a covariable, no further analyses were carried out. In contrast to findings reported in the literature, hemoglobin levels were not correlated with BP variables in either sex. After adjusting for all confounders, a significant main effect of plasma viscosity still was found. However, the magnitude of the effect was not as large as for body mass index, a well-established risk variable for hypertension. These results indicate that BP is positively associated with plasma viscosity. Whether increased plasma viscosity in hypertension constitutes a primary or a secondary phenomenon remains to be answered. Since plasma viscosity is significantly associated with hypertension but any BP variable, increased levels of plasma proteins (particularly fibrinogen as the main determinant of plasma viscosity) may represent the cause for elevated plasma viscosity. This might contribute to persistently increased resistance to blood flow on the microcirculatory level in arterial hypertension.
Since the original publications by Martini et al. (Dtsch. Arch. Klin. Med. 169: 212-222, 1930) and Fahraeus and Lindqvist (Am. J. Physiol. 96: 562-568, 1931), it has been known that the relative apparent viscosity of blood in tube flow depends on tube diameter. Quantitative descriptions of this effect and of the dependence of blood viscosity on hematocrit in the different diameter tubes are required for the development of hydrodynamic models of blood flow through the microcirculation. The present study provides a comprehensive data base for the description of relative apparent blood viscosity as a function of tube diameter and hematocrit. Data available from the literature are compiled, and new experimental data obtained in a capillary viscometer are presented. The combined data base comprises measurements at high shear rates (u > or = 50 s-1) in tubes with diameters ranging from 3.3 to 1,978 microns at hematocrits of up to 0.9. If corrected for differences in suspending medium viscosity and temperature, the data show remarkable agreement. Empirical fitting equations predicting relative apparent blood viscosity from tube diameter and hematocrit are presented. A pronounced change in the hematocrit dependence of relative viscosity is observed in a range of tube diameters in which viscosity is minimal. While a linear hematocrit-viscosity relationship is found in tubes of < or = 6 microns, an overproportional increase of viscosity with hematocrit prevails in tubes of > or = 9 microns. This is interpreted to reflect the hematocrit-dependent transition from single- to multifile arrangement of cells in flow.
Blood viscosity is an important determinant of blood flow resistance. Because a substantial part of flow resistance arises in small arteries and arterioles with diameters of 100 microns and less, rheologic properties of blood from preterm infants (24 to 36 wk of gestation), full-term neonates, and adults were measured in glass tubes with diameters of 50, 100, and 500 microns for a wide range of adjusted feed hematocrits (0.15-0.70). At each of the feed hematocrits, blood viscosity decreased when going from a 500-microns tube to a 50-microns tube. The viscosity reduction increased with increasing hematocrit. Moreover, the viscosity reduction was more pronounced in the neonates than in the adults. At a hematocrit of 0.70, the viscosity reduction averaged 56% in preterm infants, 50% in full-term neonates, and 39% in adults (p less than 0.005). However, the viscosity reductions at a hematocrit of 0.30 were only 35, 29, and 19%, respectively (p less than 0.05). In all four groups, blood viscosity increased exponentially with increasing hematocrit. The steepness of the hematocrit-viscosity curves decreased with decreasing tube diameter and with decreasing maturity of the infants. Erythrocyte transport efficiency (hematocrit/blood viscosity) was calculated to estimate the optimal hematocrit (i.e. hematocrit with maximum erythrocyte transport). In 500-microns tubes, the optimal hematocrit was about 0.40 in all of the groups. In 100-microns tubes, the optimal hematocrit was 0.44 +/- 0.05 in the adults and 0.52 +/- 0.04 in the neonates (p less than 0.05). In 50-microns tubes, the optimal hematocrit was 0.51 +/- 0.04 in adults and 0.60 +/- 0.05 in the neonates.(ABSTRACT TRUNCATED AT 250 WORDS)
The viscosity of 130 human seminal plasma samples was studied with a rotational viscometer instead of by the traditional subjective rating method. The average seminal viscosity one hour after ejaculation was 9.35 +/- 0.99 centipoise (cps), which was statistically identical to that in the third hour (8.63 +/- 0.77 cps). Seminal viscosity showed a significant negative correlation with the percentage of motile sperm (p < 0.05); however, no significant correlation between seminal viscosity and sperm concentration could be found (r = -0.15, p = 0.098). The seminal viscosity of the oligoasthenospermic group was significantly higher than that of the normospermic group (p < 0.01); there was also a trend towards higher viscosity in the semen of asthenospermia and oligospermia when compared with the normospermic group. It is concluded that seminal viscosity may be higher in cases of poor-quality semen; however, sperm motility and concentration are not the sole determinants of viscosity. Determining the seminal viscosity with this rapid, objective and quantitative method is valuable in identifying and treating the subgroup of infertile men with viscid semen.
The changes of whole blood viscosity and plasma viscosity were studied in 15 normal non-pregnant women, and 120 normal pregnant women ranging from 8 to 39 weeks of gestation. The values of whole blood viscosity during normal pregnancy were significantly lower from 20 to 31 weeks of gestation than those in the other periods of gestation, and there was a positive correlation between whole blood viscosity and hematocrit. Plasma viscosity, however, did not change significantly during pregnancy. There was no correlation between whole blood viscosity and plasma viscosity, and there was also no correlation between plasma viscosity and plasma fibrinogen concentration. These findings suggest that decreases in whole blood viscosity, resulting from the change of packed-cell volume, may strongly contribute hemorheologically to the decrease in peripheral resistance during the second trimester.