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PubMed2004

Effects of replacement fluids on plasma viscosity used for therapeutic plasma exchange.

Plasmapheresis is a widely used alternative treatment for several diseases. Recently, synthetic plasma expanders have been used to reduce the cost of therapeutic plasma exchange (TPE). Hydroxyethyl starch (HES) is a polysaccharide colloid. Isohes and Varihes are plasma volume expanders containing 6% HES in 0.9% NaCl solution. In this study, we aimed to compare the effects of several replacement fluids used for TPE on plasma viscosity profile. At the same time, we evaluated the correlation between plasma viscosity and fibrinogen level. Twenty-nine patients were enrolled for this study. Patients were divided into four groups based on replacement fluids used: 3% HES + 4% albumin (group 1), FFP (group 2), 3% Varihes (450000/ 0.7)/Isohes(200000/0.5) (group 3), and 4% albumin (group 4). The choice of replacement fluids used was randomly assigned, as long as there were no contraindications for the patient. Seven samples were collected to determine plasma viscosity and fibrinogen level during TPE cycles. There was a positive exponential correlation between plasma viscosity and fibrinogen levels. At the second plasmapheresis procedure, plasma viscosity and fibrinogen levels decreased by 20% compared with first cycle. The effect of plasmapheresis solutions on hemorheology were roughly the same. Effects of replacement fluids on plasma viscosity were comparable.

Adult↗
PubMed1988

Streptokinase and reduced plasma viscosity: a second benefit.

The purpose of this pilot study on a small cohort of patients (n = 13) with acute myocardial infarction receiving systemic streptokinase (STK) thrombolytic therapy was to measure the decrease in plasma viscosity concomitant with fibrinogen depletion. The treatment group was compared with a similar control group not given thrombolytic therapy. Serial relevant blood studies were undertaken in both groups for a period of 6 d. In the treatment group, a maximum reduction in plasma viscosity of 17 +/- 9% (mean +/- S.D.) was achieved during the first 24 h. Plasma viscosity remained below baseline for the 6-d duration of the study. Conversely, in the control group, the plasma viscosity rose to a maximum of 19 +/- 14% (mean +/- S.D.) over the period of study, paralleling the rise in plasma fibrinogen as an acute-phase reactant. Correlation studies between viscosity and plasma fibrinogen were strongly positive with mean values of r of 0.74 and 0.66 in the STK-treated group and controls, respectively. We conclude that the benefit of systemic STK treatment may in part be due to reduced myocardial workload and oxygen consumption at a critical time, and improved microvascular circulation, consequent on reduced plasma viscosity.

Blood Cell Count↗
PubMed1992

The effect of early and late cord-clamping on blood viscosity and other hemorheological parameters in full-term neonates.

This study was done to compare postnatal alterations in blood viscosity (capillary viscometer) and its determinants: hematocrit, plasma viscosity (capillary viscometer), red cell aggregation (Myrenne aggregometer) and red cell deformability (rheoscope) in the first five days of postnatal life in full-term neonates with early (< 10 s) and late (3 min) cord-clamping. The fetal blood volume of the placenta ("residual placental blood volume") decreased from 52 +/- 8 ml/kg of neonatal body weight after early cord-clamping to 15 +/- 4 ml/kg after later cord-clamping. Neonatal blood volume, calculated as the difference between an assumed total feto-placental blood volume of 115 ml/kg and the measured fetal blood volume of the placenta, was 50% higher in the late cord-clamped infants than in the early cord-clamped infants. Both groups showed similar viscosity, hematocrit and other rheological parameters in cord blood. In the infants with early cord-clamping, the hematocrit decreased from 0.48 +/- 0.04 l/l at birth to 0.43 +/- 0.6 l/l after 24 h (p < 0.05). Whole blood viscosity did not change significantly with age. After late cord-clamping, the hematocrit rose from 0.50 +/- 0.04% at birth to 0.63 +/- 0.05 l/l at 2 h of age (p < 0.005) and dropped to 0.59 +/- 0.5 l/l (p < 0.05) at 24 h. Blood viscosity increased by 40% (p < 0.001) within the first 2 h, but did not change significantly during the following five days. In both groups, plasma viscosity and red cell aggregation increased significantly (p < 0.05) on day 5 due to significant increases in total plasma protein and fibrinogen concentrations (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Proteins↗
PubMed1993

Plasma viscosity in giant cell arteritis as a predictor of disease activity.

Thirty one patients with giant cell arteritis (GCA) receiving standardised prednisolone treatment were followed up for one year with analyses of plasma viscosity, erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and fibrinogen concentration. On the day of diagnosis all patients had an increased plasma viscosity and ESR, whereas the concentration of CRP was normal in three patients and fibrinogen concentration and haptoglobin values were normal in one patient. IgG levels were increased in two patients. Plasma viscosity correlated significantly with the ESR, IgG level, and fibrinogen concentration. Laboratory variables in subgroups of patients with GCA proved by biopsy were not different from the whole group of patients with GCA. The follow up showed that CRP normalised faster than the ESR, plasma viscosity, and fibrinogen concentration. Plasma viscosity and the ESR paralleled clinical findings more closely and predicted flare ups better than the other variables. Plasma viscosity had advantages over the ESR for predicting flare ups and in the clinical monitoring of treatment with glucocorticoids.

Aged↗
PubMed1990

Hypoxic viscosity and diabetic retinopathy.

Diabetic and sickle retinopathy have features in common--for example, venous dilatation, microaneurysms, and capillary closure preceding neovascularisation. Bearing in mind that haemoglobin in poorly controlled diabetes is abnormal and that extremely low oxygen tensions (known to cause sickling) exist in the healthy cat retina, we wished to explore the possibility that diabetic blood, like that of sickle cell disease, may become more viscous when deoxygenated. To do this we measured whole blood viscosity, under oxygenated and deoxygenated conditions, of 23 normal persons, 23 diabetic patients without retinopathy, and 34 diabetic patients with retinopathy. The shear rate used was 230 s-1, which is similar to that thought to prevail in the major retinal veins. The viscosity of blood from normal persons, corrected for packed cell volume, did not change significantly on deoxygenation: mean 4.54 (SD 0.38) cps, versus, 4.57 (0.39) paired t test, p = 0.66. Similarly the blood from diabetics without retinopathy showed no change: 4.42 (0.45) versus 4.42 (0.30), p = 0.98; whereas the blood from patients with retinopathy changed from 4.82 (0.48) to 4.95 (0.63), p = 0.027. The hypoxic viscosity ratio (deoxygenated divided by oxygenated viscosity) correlated with total serum cholesterol (r = 0.44, p = 0.018) but not with HbA1, serum glucose, triglycerides, or age. A disproportionate increase in venous viscosity relative to arterial viscosity would lead to increased intraluminal and transmural pressure and therefore exacerbate leakage across capillary walls.

Adult↗
PubMed1980

Relation between extent of coronary artery disease and blood viscosity.

Blood viscosity (shear rate 100/s) and its major determinants (packed cell volume, plasma fibrinogen concentration, and plasma viscosity) were measured before coronary angiography in 50 men aged 30-55 and related to the extent of coronary artery disease. Twenty-six men had extensive disease (stenosis of two or three major coronary vessels), and 24 had either stenosis of one vessel or no stenosis. The 26 men with extensive disease had significantly higher mean blood viscosity than those with mild or no disease and 25 healthy controls (p less than 0.001). The increased viscosity was due partly to a higher packed cell volume and partly to a higher fibrinogen concentration; plasma viscosity was not significantly increased. These differences could not be explained by smoking history. These results suggest an association between increased blood viscosity and extensive coronary artery disease in men, which merits further investigation.

Adult↗
PubMed1981

Blood viscosity after splenectomy.

Blood viscosity and its contributory factors--namely, plasma viscosity, fibrinogen concentration, packed cell volume, red-cell deformability, and platelet count--were measured in 20 asymptomatic patients after splenectomy and compared with those in controls. Whole-blood viscosity was significantly increased after splenectomy and was associated with increased platelet count and, more importantly, decreased red-cell deformability. Blood viscosity was measured in six patients before and after splenectomy and in each an increase in viscosity occurred that did not occur in patients who underwent laparotomy without splenectomy. these findings suggest that the inclusions and protein complexes within the red cell that are normally removed by the spleen decrease red-cell deformability and lead to an increase in blood viscosity. This may account for the observed increase in deaths from ischaemic heart disease many years after splenectomy.

Adolescent↗
PubMed1988

Automated measurement of plasma viscosity by capillary viscometer.

Plasma viscosity has several advantages over the erythrocyte sedimentation rate as a measurement of an acute phase response of more than 24 hours' duration. A new capillary viscometer (Coulter Viscometer II), which gives an automated measurement of plasma viscosity, was compared with the selected manual method (Harkness viscometer) of the International Committee for Standardization in Haematology. Automated measurement of plasma viscosity at 25 degrees C showed close correlation (r = 0.979, p less than 0.002) with the selected method for 160 specimens of plasma. Satisfactory precision both within batch and between batch (coefficients of variation of 1.7% or less) was obtained at viscosity values up to 5.7 mPa.s. There was no detectable carry over between samples and viscosity values were corrected adequately for ambient temperature for the range 15-32 degrees C. Careful daily cleaning was required to prevent accumulation of protein within the automatic sampling valve of the instrument. Automated measurement of plasma viscosity is an attractive alternative to measurement of the erythrocyte sedimentation rate.

Acute-Phase Proteins↗
PubMed2000

Viscosity and solute dependence of F-actin translocation by rabbit skeletal heavy meromyosin.

We tested the hypothesis that solvent viscosity affects translocation of rhodamine phalloidin-labeled F-actin by rabbit skeletal heavy meromyosin (HMM). When viscosity was increased using either glycerol, fructose, sucrose, or dextran (1.5, 6.0, or 15-20 kDa mol mass), there was little or no effect on the fraction of moving filaments, whereas sliding speed decreased in inverse proportion to viscosity. The results could be explained neither by an effect of osmotic pressure at high solute concentrations nor by altered solvent drag on the actin filament. Elevated viscosity inhibited HMM ATPase activity in solution, but only at much higher viscosities than were needed to reduce sliding speed. Polyethylene glycols (300, 1,000, or 3,000 mol wt) also inhibited speed via elevated viscosity but secondarily inhibited by enhancing electrostatic interactions. These results demonstrate that a diffusion-controlled process intrinsic to cross-bridge cycling can be limiting to actomyosin function.

Actins↗
PubMed2003

Cerebrovascular response to decreased hematocrit: effect of cell-free hemoglobin, plasma viscosity, and CO2.

The effect of transfusing a nonextravasating, zero-link polymer of cell-free hemoglobin on pial arteriolar diameter, cerebral blood flow (CBF), and O2 transport (CBF x arterial O2 content) was compared with that of transfusing an albumin solution at equivalent reductions in hematocrit (approximately 19%) in anesthetized cats. The influence of viscosity was assessed by coinfusion of a high-viscosity solution of polyvinylpyrrolidone (PVP), which increased plasma viscosity two- to threefold. Exchange transfusion of a 5% albumin solution resulted in pial arteriolar dilation, increased CBF, and unchanged O2 transport, whereas there were no significant changes over time in a control group. Exchange transfusion of a 12% polymeric hemoglobin solution resulted in pial arteriolar constriction and unchanged CBF and O2 transport. Coinfusion of PVP with albumin produced pial arteriolar dilation that was similar to that obtained with transfusion of albumin alone. In contrast, coinfusion of PVP with hemoglobin converted the constrictor response to a dilator response that prevented a decrease in CBF. Pial arteriolar dilation to hypercapnia was unimpaired in groups transfused with albumin or hemoglobin alone but was attenuated in the largest vessels in albumin and hemoglobin groups coinfused with PVP. Unexpectedly, hypocapnic vasoconstriction was blunted in all groups after transfusion of albumin or hemoglobin alone or with PVP. We conclude that 1) the increase in arteriolar diameter after albumin transfusion represents a compensatory response that prevents decreased O2 transport at reduced O2-carrying capacity, 2) the decrease in diameter associated with near-normal O2-carrying capacity after cell-free polymeric hemoglobin transfusion represents a compensatory mechanism that prevents increased O2 transport at reduced blood viscosity, 3) pial arterioles are capable of dilating to an increase in plasma viscosity when hemoglobin is present in the plasma, 4) decreasing hematocrit does not impair pial arteriolar dilation to hypercapnia unless plasma viscosity is increased, and 5) pial arteriolar constriction to hypocapnia is impaired at reduced hematocrit independently of O2-carrying capacity.

Albumins↗
PubMed2002

Endothelium-dependent arterial wall tone elasticity modulated by blood viscosity.

The role of blood viscosity on arterial wall elasticity before and after deendothelization (DE) was studied. Seven ovine brachiocephalic arteries were studied in vitro under physiological pulsatile flow conditions achieved by a mock circulation loop. Instantaneous pressure and diameter signals were assessed in each arterial segment. Incremental elastic modulus (E(inc)) was calculated using the slope of the pure elastic stress-strain relationship. There was no significant difference between E(inc) values before and after DE (3.11 vs. 3.16 10(7) dyn/cm(2)) at a blood viscosity of 2.00 mPa. s. Increases in blood viscosity (2.50, 3.00, 3.50, and 4.00 mPa. s) always resulted in decreases of E(inc) before DE; inversely, increases in blood viscosity resulted in increases of E(inc) after DE. These values of E(inc), for identical levels of blood viscosity, were always significantly lower (P < 0.05) before DE than those obtained after DE. Arterial wall elasticity assessed through E(inc) was strongly influenced by blood viscosity, probably due to presence or absence of endothelium relaxing factors or to direct shear smooth muscle activation when endothelial cells are removed.

Animals↗
PubMed2002

A novel approach to blood plasma viscosity measurement using fluorescent molecular rotors.

Molecular rotors, a group of fluorescent molecules with viscosity-dependent quantum yield, were tested for their suitability to act as fluorescence-based plasma viscometers. The viscosity of samples of human plasma was modified by the addition of pentastarch (molecular mass 260 kDa, 10% solution in saline) and measured with a Brookfield viscometer. Plasma viscosity was 1.6 mPa x s, and the mixtures ranged up to 4.5 mPa x s (21 degrees C). The stimulated light emission of the molecular rotors mixed in the plasma samples yielded light intensity that was nonoverlapping and of significantly different intensity for viscosity steps down to 0.3 mPa x s (n = 5, P < 0.0001). The mathematical relationship between intensity (I) and viscosity (eta) was found to be eta = (kappaI)(nu). After calibration and scaling the fluorescence based measurement had an average deviation versus the conventional viscometric measurements that was <1.8%. These results show the suitability of molecular rotors for fast, low-volume biofluid viscosity measurements achieving accuracy and precision comparable to mechanical viscometers.

Blood Viscosity↗
PubMed2004

Naturally derived commercial surfactants differ in composition of surfactant lipids and in surface viscosity.

Pulmonary surfactant biophysical properties are best described by surface tension and surface viscosity. Besides lecithin, surfactant contains a variety of minor lipids, such as plasmalogens, polyunsaturated fatty acid-containing phospholipids (PUFA-PL), and cholesterol. Plasmalogens and cholesterol improve surface properties of lipid mixtures significantly. High PUFA-PL and plasmalogen content in tracheal aspirate of preterm infants reduces the risk of developing chronic lung disease. Different preparations are available for exogenous surfactant substitution; however, little is known about lipid composition and surface viscosity. Thus lipid composition and surface properties (measured by oscillating drop surfactometer) of three commercial surfactant preparations (Alveofact, Curosurf, Survanta) were compared. Lipid composition exhibited strong differences: Survanta had the highest proportion of disaturated PL and total neutral lipids and the lowest proportion of PUFA-PL. Highest plasmalogen and PUFA-PL concentrations were found in Curosurf (3.8 +/- 0.1 vs. 26 +/- 1 mol%) compared with Alveofact (0.9 +/- 0.3 vs. 11 +/- 1) and Survanta (1.5 +/- 0.2 vs. 6 +/- 1). In Survanta samples, viscosity increased >8 x 10(-6) kg/s at surface tension of 30 mN/m. Curosurf showed only slightly increased surface viscosity below surface tensions of 25 mN/m, and viscosity did not reach 5 x 10(-6) kg/s. By adding defined PL to Survanta, we obtained a Curosurf-like lipid mixture (without plasmalogens) that exhibited biophysical properties like Curosurf. Different lipid compositions could explain some of the differences in surface viscosity. Therefore, PL pattern and minor surfactant lipids are important for biophysical activity and should be considered when designing synthetic surfactant preparations.

Animals↗
PubMed1986

Effects of blood viscosity on plasma renin activity and renal hemodynamics.

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

Animals↗
PubMed1986

Effect of covalently bound fatty acids and associated lipids on the viscosity of gastric mucus glycoprotein in cystic fibrosis.

The contribution of associated and covalently bound lipids to the viscosity of gastric mucus glycoprotein in healthy and cystic fibrosis (CF) individuals was investigated. While both preparations exhibited similar contents of protein and carbohydrate, the CF glycoprotein contained 1.3 times more associated lipids and 6 times more covalently bound fatty acids. The viscosity of CF mucus glycoprotein was about 1.8 times higher than that of normal glycoprotein. Extraction of associated lipids lead to 3-fold drop in the viscosity of CF glycoprotein and 5-fold drop in the case of normal glycoprotein. Removal of covalently bound fatty acids caused further 1.6-fold reduction in the viscosity of normal mucus glycoprotein and 6-fold in CF glycoprotein. The viscosity of the delipidated and deacylated CF mucus glycoprotein was only about 10% higher than that of the similarly treated normal glycoprotein. The results suggest that the elevated level of covalently bound and associated lipids is responsible for the increased viscosity of CF mucin.

Adolescent↗
PubMed1997

In vivo/in vitro comparison of rat abdominal aorta wall viscosity. Influence of endothelial function.

Arterial wall viscosity (AWV) is a potential source of energy dissipation in circulation. That arteries, which are known to be markedly viscous in vitro, have lower viscosity in vivo has been suggested but not demonstrated under similar pressure conditions. Endothelium, which may modulate AWV through smooth muscle tone, could contribute to the low level of viscosity in vivo. Our objectives were first to compare AWV of the rat abdominal aorta, in vivo and in vitro, with similar pulse-pressure waves, and second, to determine whether endothelial function influences AWV in vivo and in vitro. The diameter of the abdominal aorta and distending pressure were measured in vivo and in vitro with a high-resolution echotracking system and a micromanometer, respectively. AWV was calculated as the area of the pressure-volume curve hysteresis. After in vivo examination, the arterial segments were isolated in vitro and submitted to resynthesized pressure waves identical to those recorded in vivo. Deendothelialization was performed in vivo by balloon rubbing; then arteries were examined either in vivo or in vitro. AWV was markedly lower in vivo than in vitro (6.6 +/- 0.7 versus 22.7 +/- 3.7 J.m-1.10(-5), respectively; P < .001). After deendothelialization, a sustained 40% increased AWV was observed during a 15-minute follow-up (P < .01). In vitro, deendothelialized arteries have a 64% higher AWV than segments with endothelium (P < .01). Our results indicate that the physiological effective viscosity, measured in vivo in intact animals, is threefold lower than the intrinsic viscosity of the arterial wall, measured in vitro. Endothelium removal determines a sustained increase in AWV, either in vivo or in vitro. These results suggest that active mechanisms compensate for intrinsic viscosity under physiological conditions. One of these energy-saving mechanisms might be dependent on normal endothelial function.

Animals↗
PubMed1998

Plasma viscosity and the risk of coronary heart disease: results from the MONICA-Augsburg Cohort Study, 1984 to 1992.

Plasma viscosity is determined by various macromolecules, eg, fibrinogen, immunoglobulins, and lipoproteins. It may therefore reflect several aspects involved in cardiovascular diseases, including the effects of classic risk factors, hemostatic disturbances, and inflammation. We examined the association of plasma viscosity with the incidence of a first major coronary heart disease event (CHD; fatal and nonfatal myocardial infarction and cardiac death; n=50) in 933 men aged 45 to 64 years of the MONICA project of Augsburg, Germany. The incidence rate was 7.23 per 1000 person-years (95% confidence interval [CI], 5.37 to 9.53), and the subjects were followed up for 8 years. All suspected cases of an incident CHD event were classified according to the MONICA protocol. There was a positive and statistically significant unadjusted relationship between plasma viscosity and the incidence of CHD. The relative risk of CHD events associated with a 1-SD increase in plasma viscosity (0.070 mPa x s) was 1.60 (95% CI, 1.25 to 2.03). After adjustment for age, total cholesterol, high density lipoprotein cholesterol, smoking, blood pressure, and body mass index, the relative risk was reduced only moderately (1.42; 95% CI, 1.09 to 1.86). The relative risk of CHD events for men in the highest quintile of the plasma viscosity distribution in comparison with the lowest quintile was 3.31 (95% CI, 1.19 to 9.25) after adjustment for the aforementioned variables. A large proportion of events (40%) occurred among men in the highest quintile. These findings suggest that plasma viscosity may have considerable potential to identify subjects at risk for CHD events.

Blood Viscosity↗
PubMed1991

Fibrinogen, viscosity, and white blood cell count are major risk factors for ischemic heart disease. The Caerphilly and Speedwell collaborative heart disease studies.

BACKGROUND: Recent studies have suggested that hemostatic factors and white blood cell count are predictive of ischemic heart disease (IHD). The relations of fibrinogen, viscosity, and white blood cell count to the incidence of IHD in the Caerphilly and Speedwell prospective studies are described. METHODS AND RESULTS: The two studies have a common core protocol and are based on a combined cohort of 4,860 middle-aged men from the general population. The first follow-up was at a nearly constant interval of 5.1 years in Caerphilly and 3.2 years in Speedwell; 251 major IHD events had occurred. Age-adjusted relative odds of IHD for men in the top 20% of the distribution compared with the bottom 20% were 4.1 (95% confidence interval, 2.6-6.5) for fibrinogen, 4.5 (95% confidence interval, 2.8-7.4) for viscosity, and 3.2 (95% confidence interval, 2.0-4.9) for white blood cell count. Associations with IHD were similar in men who had never smoked, exsmokers, and current smokers, and the results suggest that at least part of the effect of smoking on IHD is mediated through fibrinogen, viscosity, and white blood cell count. Multivariate analysis shows that white blood cell count is an independent risk factor for IHD as is either fibrinogen or viscosity, or possibly both. Jointly, these three variables significantly improve the fit of a logistic regression model containing all the main conventional risk factors. Further, a model including age, smoking habits, fibrinogen, viscosity, and white blood cell count predicts IHD as well as one in which the three hemostatic/rheological variables are replaced by total cholesterol, diastolic pressure, and body mass index. CONCLUSION: Jointly, fibrinogen, viscosity, and white blood cell count are important risk factors for IHD.

Blood Viscosity↗