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At least 127 records · Page 7Linked to original sources
PubMed2006

Erythrocyte deformability, plasma viscosity and oxidative status in patients with severe obstructive sleep apnea syndrome.

BACKGROUND AND PURPOSE: In patients with severe obstructive sleep apnea syndrome (OSAS), diurnal changes of plasma viscosity and erythrocyte deformability were measured to elucidate the possible mechanism of cardiovascular diseases in OSAS patients. PATIENTS AND METHODS: Plasma viscosity and erythrocyte deformability was determined in 11 OSAS patients and 11 healthy subjects matched by sex and age. Plasma viscosity was measured by a cone-plate viscometer, and erythrocyte deformability was determined by filtration technique. Whole blood counts were performed and oxidative status of the patients' plasma and erythrocytes were evaluated. RESULTS: OSAS patients had higher plasma viscosity than controls, both in the morning (1.74+/-0.3 vs. 1.36+/-0.2 mPas, P<0.002) and evening (1.55+/-0.2 vs. 1.27+/-0.1 mPas, P<0.002), and morning plasma viscosity was significantly higher than the evening level (P<0.05). Morning plasma viscosity of patients was inversely correlated with their mean nocturnal SaO(2). Morning plasma malonyldialdehyde level was significantly higher in the patients than in the controls (69.7+/-30.5 vs. 45.5+/-11.0 nmol/l, P<0.005). Erythrocyte deformability of the patients was slightly lower. CONCLUSIONS: We have observed that plasma viscosity is high both in the morning and in the evening in severe OSAS patients. This elevation may predispose OSAS patients to myocardial infarction and stroke by increasing blood viscosity. Low nocturnal mean SaO(2) may be responsible for the high plasma viscosity in these patients.

Adult↗
PubMed2001

Blood viscosity and blood pressure: role of temperature and hyperglycemia.

We planned a study to research the relations among blood pressure (BP), viscosity, and temperature in healthy subjects and among BP, viscosity, and glucose in diabetics. With simple random sampling method, 53 healthy and 29 diabetes mellitus (DM) type II subjects were selected. Parameters were determined with capillary viscometer and glucometer at 22 degrees C, 36.5 degrees C, and 39.5 degrees C in healthy subjects, and at 22 degrees C on diabetic patients during OGTT with 75 g of glucose. Statistical evaluations of the data were made with regression analysis, Student t test, Spearman's correlation, and analysis of variance. When temperature decreased from 36.5 degrees C to 22 degrees C, blood viscosity increased 26.13%. This increase resulted in a 20.72% decrease in blood flow rate. According to the Hagen-Poiseuille equation, the required BP increase for compensation of the resulting tissue ischemia was 20.72%. Also, a 34.73% decrease in erythrocyte deformability and 18.71% increase in plasma viscosity were seen. When temperature increased from 36.5 degrees to 39.5 degrees C, blood viscosity decreased 10.38%. This caused 11.15% decrease in blood flow rate, and 11.15% decrease in BP, according to the equation. Erythrocyte deformability increase of 9.92% and plasma viscosity decrease of 4.99% arose from the temperature rise. There is a correlation between total data for temperatures and viscosities (r = -0.84, P < .001). When the mean value of blood glucose increased from 100 to 400 mg/dL, viscosity increased 25% (r= 0.59, P = .002). In this state, blood flow rate decrease was 20% and BP increase for physiological compensation was 25%. Consequently, temperature, glucose and viscosity levels of blood are important factors for BP.

Adult↗
PubMed2001

Studies on rye (Secale cereale L.) lines exhibiting a range of extract viscosities. 2. Rheological and baking characteristics of rye and rye/wheat blends and feeding value for chicks of wholemeals and breads.

Five rye lines exhibiting a wide range of extract viscosities were evaluated for the rheological and baking properties of their flours, individually and in blends with hard red spring wheat flour. Commercial cultivars of rye and triticale were included in the study as controls. Extract viscosities of rye flours were higher than those of corresponding wholemeals, indicating shifting of water-extractable arabinoxylan into flour during roller milling. Falling numbers of the rye flours correlated positively with their extract viscosities in the presence (r = 0.73, p < 0.05) or absence (r = 0.65, p < 0.05) of an enzyme inhibitor. Farinograms revealed the weakness of rye and triticale flours compared to wheat flour. Extract viscosities of rye flours were negatively correlated (r = -0.65, p < 0.05) with mixing tolerance index and positively correlated (r = 0.64, p < 0.05) with dough stability, suggesting a positive impact of extract viscosity on dough strength. Extract viscosity was negatively correlated (r = -0.74, p < 0.05) with loaf volume and specific volume (r = -0.73, p < 0.05) and positively correlated (r = 0.73, p < 0.05) with loaf weight of rye/wheat bread. Overall, the results indicated that 30% of flour from high or low extract viscosity rye could be incorporated into rye/wheat breads without seriously compromising bread quality. Inclusion of rye, particularly high extract viscosity rye, in chick diets seriously impeded growth performance and feed efficiency. Part of the arabinoxylan survived bread-making and exerted an effect on chicks, although substantially lower digesta viscosities were observed in chicks fed rye bread diets than in those fed rye wholemeals.

Animal Feed↗
PubMed1982

Plasma and blood viscosities, and aggregation of red cells in racehorses.

Nineteen racehorses have been studied for haemorheologic factors as earlier studies showed a definite correlation between physical fitness and these factors in humans. Results included individual values for all viscosity factors, and the arithmetic means, the latter showing 4.70 +/- 0.49 cP for blood viscosity measured at a shear rate of 180 s-1; 1.100 +/- 0.048 cP for plasma viscosity; 1.045 +/- 0.063 for the rigidity of red cells defined by term 'Tk'; 42.2 +/- 4.1% haematocrit; 290 +/- 39 mg per 100 ml for fibrinogen level; and 278 +/- 75 mm h-1 for aggregation of red cells at 37 degrees C (corrected for plasma viscosity and at constant haematocrit of 30%). Data for subgroups have also been obtained. Linear regressions of apparent blood viscosity against log shear rate were found to be specific to individual racehorses, and differed significantly between some racehorses. Data for blood viscosity, plasma viscosity and haematocrit were near the values reported for human athletes, but rigidity of red cells and aggregation of red cells was found to be much higher in horses. No correlation was found between aggregation of red cells and fibrinogen level. In blood samples from some horses, the erythrocyte sedimentation rates increased with decrease of temperature, while in other samples they increased with increase of temperature. It appears that it is possible to characterise individual horses by blood viscosity factors and viscosity functions.

Animals↗
PubMed1999

Effects of dietary viscosity and energy density on total daily energy consumption by young Peruvian children.

BACKGROUND: Results of prior studies of the effect of viscosity reduction of high-energy-density, starch-containing diets on young children's energy intakes are inconsistent, possibly because of differences in the characteristics of the unmodified diets with which the low-viscosity diets were compared. OBJECTIVE: Our objective was to determine the effects of dietary viscosity and energy density on total daily energy consumption by young, non-breast-fed children. DESIGN: We measured the amount of food consumed and the duration of meals during 3 substudies, in each of which 3 study diets were offered for 4 consecutive days each in random sequence: high energy density, high viscosity (HD-HV); high energy density, low viscosity (HD-LV); and low energy density, low viscosity (LD-LV). The viscosity and energy density of the unmodified starch-containing HD-HV diet were varied across substudies to determine whether the effect of amylase liquefaction was related to the initial characteristics of the HD-HV diet. The viscosity of the HV diets ranged from 79000 to 568000 mPa s; energy density of the HD diets ranged from approximately 4.18 to 4.93 kJ (1.00-1.18 kcal)/g. Viscosity of the LV diets was approximately 3000 mPa s and the energy density of the LD diets was approximately 2.47 kJ (0.6 kcal)/g. RESULTS: In each substudy, children consumed more of the LD-LV diet (g kg body wt(-)(1) d(-)(1)) than of the other diets and more of the HD-LV diet than of the HD-HV diet (P < 0.001). Energy consumption from the HD-LV diet was greater than from the other diets (P < 0.001), but the energy intakes from the latter diets were not significantly different. CONCLUSION: Amylase liquefaction of HD-HV porridges resulted in increased energy consumption by young children.

Anthropometry↗
PubMed1991

The estimation of whole blood viscosity by a porous bed method.

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.

Anticoagulants↗
PubMed1991

Association between plasma viscosity and blood pressure. Results from the MONICA-project Augsburg.

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.

Adult↗
PubMed1987

Plasma viscosity and haematocrit in the course of acute myocardial infarction.

Plasma viscosity and haematocrit were determined in 44 patients with acute myocardial infarction on the 1st, 2nd, 3rd and 10th day of hospitalization. The highest haematocrit value for the entire group was found on the 1st day of acute myocardial infarction--43.3 SD +/- 4.6% declining progressively to 38.8 SD +/- 3.5% on the 10th day (P less than 0.001). Plasma viscosity for the entire group was normal on the first day of acute myocardial infarction (1.44 SD +/- 0.10 cp) and started to increase on the second day (1.51 SD +/- 0.16 cp, P less than 0.001). A relationship was found between reinfarction or death (17 patients) occurring during hospitalization and changes in haematocrit and plasma viscosity. In this group plasma viscosity rose to 1.63 SD +/- 0.19 cp on the second day of acute myocardial infarction (P less than 0.001 vs plasma viscosity value on the first day). This elevation persisted on the third day. Haematocrit values in this group were 47.9 SD +/- 3.6% on the first day of acute myocardial infarction declining progressively and significantly afterwards. In the remaining patients both plasma viscosity and haematocrit were normal and did not change. No correlation of plasma viscosity and haematocrit were found when tested for other clinical complications, sex, age, maximal creatine phosphokinase values and coronary risk factors. We suggest that variations in haematocrit and plasma viscosity during acute myocardial infarction exist in a group of patients in whom reinfarction or death occurs. The changes in haematocrit and plasma viscosity precede the complications by 4-8 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2000

Influence of blood viscosity on blood flow in the forebrain but not hindbrain after carotid occlusion in rats.

That cerebral blood flow remains unchanged at an increased blood viscosity, as long as the vascular supply is not compromised, was tested. To induce a reduced blood supply of some parts of the brain and to keep the supply unchanged in others both carotid arteries were occluded in anesthetized, ventilated rats. By this procedure, blood supply to the rostral brain, but not to the brainstem and cerebellum, was compromised. Blood viscosity was increased by intravenous infusion of 20% polyvinylpyrrolidone (high viscosity group) or decreased by infusion of 5% albumin (low viscosity group). Cerebral blood flow was measured by the [14C]iodoantipyrine method in 50 complete coronal sections of the rostral brain and 22 complete coronal sections of the brainstem and cerebellum in each rat. In the high viscosity group, mean cerebral blood flow of the rostral brain was significantly lower (46 +/- 7 mL/100 g(-1) x min(-1)) than in the low viscosity group (82 +/- 18 mL/100 g(-1) x min(-1)). No differences could be observed in brainstem and cerebellum between both groups (162 +/- 29 mL/100 g(-1) x min(-1) vs. 156 +/- 18 mL/100 g(-1) x min(-1)). Local analysis of cerebral blood flow in different brain structures of the coronal sections showed the same identical results; i.e., in 29 of the 31 brain structures analyzed in rostral brain, local cerebral blood flow was lower in the high viscosity group, whereas no differences could be observed in the 11 brain structures analyzed in the brainstem and cerebellum. It is concluded that under normal conditions cerebral blood flow can be maintained at an increased blood viscosity by a compensatory vasodilation. When the capacity for vasodilation is exhausted by occlusion of supplying arteries, an increased blood viscosity results in a decrease of cerebral blood flow.

Animals↗
PubMed1998

Increase in blood viscosity in the sprinting horse: can it account for the high pulmonary arterial pressure?

Blood was taken from 49 Thoroughbred horses before and after racing at the track to determine if frusemide modified the apparent viscosity of the blood and to determine the effects of changes in shear rate and packed cell volume (PCV), associated with strenuous exercise, on apparent and relative viscosities. Small increases in apparent viscosity of the blood (at a specified PCV and shear rate) occurred in horses given frusemide compared to those receiving no frusemide; however, no differences were seen in relative viscosity. Although 2 groups of horses, those receiving frusemide before racing and those not receiving this drug were studied, the results suggest no influence of frusemide on any red blood cell variable that might modify apparent blood viscosity. Apparent viscosity of the blood was slightly (but significantly) higher after racing than before racing at any given PCV and shear rate, but relative viscosity was lower in the post race than in the prerace blood sample. The most important contributing factor to the increase in apparent viscosity in blood during racing is the increase in PCV, because the blood becomes nearly shear rate independent at shear rates likely to exist in the cardiovascular system during exercise. With an increase in PCV from 40 to 65% at shear rates above 225/s, apparent viscosity approximately doubled. However, this increase alone cannot account for the elevated pulmonary vascular pressure in the running horse, and additional factors, especially those causing the high left atrial pressure, must be considered. The cause of the elevated pressure may be multifactorial in nature.

Animals↗
PubMed2005

Precision assessment of biofluid viscosity measurements using molecular rotors.

Blood viscosity changes with many pathologic conditions, but its importance has not been fully investigated because the current methods of measurement are poorly suited for clinical applications. The use of viscosity-sensitive fluorescent molecular rotors to determine fluid viscosity in a nonmechanical manner has been investigated recently, but it is unknown how the precision of the fluorescence-based method compares to established mechanical viscometry. Human blood plasma viscosity was modulated with high-viscosity plasma expanders, dextran, pentastarch, and hetastarch. The samples were divided into a calibration and a test set. The relationship between fluorescence emission and viscosity was established using the calibration set. Viscosity of the test set was determined by fluorescence and by cone-and-plate viscometer, and the precision of both methods compared. Molecular rotor fluorescence intensity showed a power law relationship with solution viscosity. Mechanical measurements deviated from the theoretical viscosity value by less than 7.6%, while fluorescence-based measurements deviated by less than 6%. The average coefficient of variation was 6.9% (mechanical measurement) and 3.4% to 3.8% (fluorescence-based measurement, depending on the molecular rotor used). Fluorescence-based viscometry exhibits comparable precision to mechanical viscometry. Fluorescence viscometry does not apply shear and is therefore more practical for biofluids which have apparent non-Newtonian properties. In addition, fluorescence instrumentation makes very fast serial measurements possible, thus promising new areas of application in laboratory and clinical settings.

Blood Chemical Analysis↗
PubMed1992

Blood viscosity in tube flow: dependence on diameter and hematocrit.

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.

Animals↗
PubMed2002

Bulk shear viscosities of endogenous and exogenous lung surfactants.

Bulk shear viscosities were measured with a cone and plate microviscometer as a function of concentration, shear rate, and temperature for lavaged calf lung surfactant (LS), Exosurf, Infasurf, Survanta, and synthetic lipid mixtures dispersed in normal saline. Viscosity increased with phospholipid concentration for all surfactants, but its magnitude and shear dependence varied widely among the different preparations. Saline dispersions of Exosurf and synthetic phospholipids had low viscosities of only a few centipoise (cp) and exhibited minimal shear dependence. LS, Infasurf, Survanta, and lipid mixtures containing palmitic acid and tripalmitin had larger non-Newtonian viscosities that increased as shear rate decreased. At 35 mg of phospholipid/ml and 37 degrees C, viscosity values were 52.3 cp (Survanta), 31.1 cp (LS), and 25 cp (Infasurf) at a shear rate of 77 s(-1) and 16.9 cp (Survanta), 10.1 cp (LS), and 6.6 cp (Infasurf) at 770 s(-1). At 25 mg of phospholipid/ml and 37 degrees C, viscosity values at 77 s(-1) were 28.8 cp (Survanta), 4.7 cp (LS), and 12.5 cp (Infasurf). At fixed shear rate, viscosity was substantially decreased at 23 degrees C compared with 37 degrees C for LS and Infasurf but was increased for Survanta. Calcium (5 mM) greatly reduced the viscosity of both Survanta and Infasurf at 37 degrees C. Studies on synthetic mixtures indicated that phospholipid/apoprotein interactions were important in the rheology of lung-derived surfactants and that palmitic acid and tripalmitin contributed to the increased viscosity of Survanta. The viscous behavior of clinical exogenous surfactants potentially influences their delivery and distribution in lungs and varies significantly with composition, concentration, temperature, ionic environment, and physical formulation.

Animals↗
PubMed1989

Effects of temperature and composition on the viscosity of respiratory gases.

The steady-state sensitivity of resistance pneumotachographs is proportional to viscosity. Dynamic characteristics of pneumotachographs, pressure transducers, and mass spectrometers are also viscosity dependent. We derive linear equations to approximate the viscosities of O2, N2, CO2, H2O, He, N2O, and Ar for temperatures between 20 and 40 degrees C by using published viscosity data and a nonlinear extrapolation equation. We verify the accuracy of the extrapolation equation by comparison with published data. Our linear equations for pure gas viscosities yield standard errors less than 0.35 microP. We also compare a nonlinear equation for calculating the viscosities of mixtures of gases with published measured viscosities of dry air, humid air, and He-O2 and N2-CO2 mixtures. The maximum difference between published and calculated values is 1.3% for 10% CO2 in N2. All other differences are less than 0.38%. For saturated humid air at 35 degrees C, a linear concentration-weighted combination of viscosities differs from our nonlinear equation by 4.9, 2.1, and 1.7% at barometric pressures of 32, 83, and 100 kPa, respectively. By use of our method, the viscosity of normal respiratory gases can be calculated to within 1% of measured values.

Argon↗
PubMed1998

Hormone replacement therapy improves cardiovascular risk by lowering plasma viscosity in postmenopausal women.

Hormone replacement therapy may protect against cardiovascular disease through several mechanisms that have variable actions on the major determinants of plasma viscosity. Plasma viscosity is an important predictor of incident and recurrent cardiovascular events and mortality in coronary heart disease patients. The effect of estrogen alone or in combination with progestin on plasma viscosity is not known. Using a randomized, double-blind design, we examined the impact of the following daily hormone regimens on plasma viscosity in 23 women: (1) 1 mg estradiol and 2.5 mg medroxyprogesterone (n=7); (2) 1 mg estradiol alone (n=8); and (3) placebo (n=8). Plasma viscosity, fibrinogen, and standard lipoprotein levels were determined at baseline and after 12 weeks of intervention. Plasma viscosity was measured at 37 degreesC with a coaxial microviscometer. Fibrinogen was measured by the Clauss method. Significant changes in plasma viscosity (mPa.s) levels occurred among treatment groups (P<0.01) after the intervention. Plasma viscosity was significantly reduced with estrogen replacement therapy (P<0.01). These data demonstrate that estrogen replacement therapy lowers plasma viscosity. This study suggests an additional mechanism for the cardiovascular protection conferred to postmenopausal women on estrogen replacement therapy.

Aged↗
PubMedDate not supplied

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 +/- 6 ml/100g/min, in the left 38 +/- 6 (p less than 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p less than 0.01 and p less than 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right (p less than 0.001 and p less than 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism.

Animals↗
PubMed1974

Disturbance of serum viscosity in diabetes mellitus.

The serum viscosity of diabetic patients has been found to be increased. The elevation averaged 8% above healthy subjects and 6% above nondiabetic patients. The serum viscosity elevation was greater when diabetic sequelae associated with microangiopathy were present. No relation of serum viscosity to age, sex, obesity, duration of disease, or type of treatment was demonstrated. Serum total protein and glucose levels were found to be correlated with serum viscosity, and increases in their serum concentrations were observed in diabetes. Analysis demonstrated that their elevation did not explain either the viscosity increase or the difference in viscosity between diabetics with and without sequelae.Intrinsic viscosity, abbreviated [eta], is a concentration-independent solute property related to molecular shape. [eta] was found to be 7% higher in diabetic than in normal serum. The [eta] difference accounted for at least half of the serum viscosity elevation. The rest of the increase was due to increased serum protein level and increased nonprotein solids, presumably glucose and lipid. Associated with increased [eta] was a decline in albumin: globulin ratio and elevation of the acute phase reactant proteins, alpha(1)-acid glycoprotein, alpha(1)-antitrypsin, haptoglobin, and ceruloplasmin. Studies comparing diabetic and normal serum fractionated by using 21.5% sodium sulfate showed that changes in [eta] were attributable to changes in serum protein composition rather than an inherent qualitative disturbance of protein present in one of the fractions. Since serum viscosity is elevated in early diabetes, it may be a part of the metabolic disturbance of diabetes and could play a role in the development of diabetic microangiopathy.

Adult↗
PubMed1993

Increased plasma viscosity as a reason for inappropriate erythropoietin formation.

The aim of this study was to examine whether altered plasma viscosity could contribute to the inappropriately low production rate of erythropoietin (EPO) observed in patients suffering from hypergammaglobulinemias associated with multiple myeloma or Waldenström's disease. We found that the EPO formation in response to anemia in these patients was inversely related to plasma viscosity. A similar inverse relationship between plasma viscosity and EPO production was seen in rats in which EPO formation had been stimulated by exchange transfusion and the plasma viscosity of which was thereby altered by using exchange solutions of different composition to alter plasma viscosity and thus whole blood viscosity independently from hematocrit. Raising the gammaglobulin concentration to approximately 40 mg/ml plasma in the rats almost totally blunted the rise in serum EPO levels despite a fall of the hematocrit to 20%. Determination of renal EPO mRNA levels by RNase protection revealed that the reductions in serum EPO levels at higher plasma viscosities were paralleled by reductions in renal EPO mRNA levels. Taken together, our findings suggest that plasma viscosity may be a significant inhibitory modulator of anemia-induced EPO formation. The increased plasma viscosity in patients with hypergammaglobulinemias may therefore contribute to the inappropriate EPO production, which is a major reason for the anemia developing in these patients.

Adult↗