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PubMed1996

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↗
PubMed2004

White blood cell and platelet counts could affect whole blood viscosity.

BACKGROUND: Blood viscosity is correlated with cerebral blood flow and cardiac output, and increased viscosity may increase the risk of thrombosis or thromboembolic events. The relationship between hematocrit and viscosity is well-known, however, the relationships between white blood cell (WBC) or platelet count and viscosity were not fully studied. The aim of the present study was to determine the influences of platelet count and WBC count on blood viscosity. METHODS: One-hundred and 13 subjects with different hemoglobin, WBC and platelet count were enrolled into the study. The variables measured included serum fibrinogen, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), complete blood counts including hemoglobin, hematocrit, platelet count, red blood cell (RBC) count, WBC count, whole blood and plasma viscosity. The relationships of these variables with whole blood or plasma viscosity were analyzed. RESULTS: Serum fibrinogen, cholesterol, triglyceride, HDL and LDL did not correlate with whole blood viscosity. Not only hematocrit, hemoglobin and RBC, but also WBC and platelet count, could affect whole blood viscosity. On the other hand, none of the variables could affect plasma viscosity. CONCLUSIONS: All the blood cell components, but not the plasma proteins detected above, could affect whole blood viscosity. When patients are with high leukocytosis and thrombocytosis, impaired blood viscosity should also be considered to obtain appropriate clinical management.

Adult↗
PubMed2000

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↗
PubMed1981

Direct relationship between blood pressure and blood viscosity in normal and hypertensive subjects. Role of fibrinogen and concentration.

Blood pressure and components of blood viscosity were measured in 49 normal subjects and in 49 untreated patients with essential hypertension. Blood viscosity values measured at six different shear rates were significantly correlated with blood pressure (r = 0.432 to 0.505, p less than 0.001). Blood viscosity was higher in hypertensive patients. This was due to both higher plasma viscosity (1.29 +/- 0.08 standard deviation versus 1.24 +/- 0.05 centipoise (cPs), p less than 0.001) and increased hematocrit values (44.4 +/- 4 percent versus 41.5 +/- 3 percent, p less than 0.005). When blood viscosity was evaluated in subgroups of normal and hypertensive subjects with matched hematocrit values, it remained higher in the hypertensive patients, and the relationship between blood pressure and viscosity was still significant. Regardless of the hematocrit value, fibrinogen levels were elevated in hypertensive patients (p less than 0.006) and, in association with the increased globulin concentration, fibrinogen was largely responsible for the increased plasma viscosity in hypertensive patients. Since the viscosity of defibrinated blood was similar in normal and hypertensive subjects with matched hematocrit values, the elevated fibrinogen level also affected whole blood viscosity. Defibrinated blood viscosity and arterial pressures were not correlated. These studies demonstrate a direct correlation between blood pressure and blood viscosity among normotensive and hypertensive subjects. This relationship is, in part, due to the rheologic effects of an elevated fibrinogen level and to an increased hematocrit value. The basis for hyperfibrinogenemia in hypertensive patients is unclear.

Adult↗
PubMed2004

The viscosity of fibrinogen subfractions and of EDTA denatured fibrinogen do not differ from that of native fibrinogen.

INTRODUCTION: Fibrinogen is a major determinant of plasma viscosity. The increased risk of atherothrombotic disease associated with a high fibrinogen concentration may partly be attributed to its effect on viscosity. Since the ratio between the three main fibrinogen subfractions high molecular weight (HMW)-, low molecular weight (LMW)-, and very low molecular weight (LMW')-fibrinogen is altered during acute phase conditions, and an increased HMW/LMW-fibrinogen ratio is associated with increased thromboembolic risk, we have examined how these subfractions affect viscosity. The viscosity of plasma is usually determined in ethylenediaminetetra-acetic acid (EDTA) plasma at 37 degrees C. Under such conditions the clotting properties of fibrinogen is affected due to denaturation. Denaturation of plasma proteins may affect their viscosity. Therefore, we have also investigated the effects of EDTA on the viscosity of fibrinogen. MATERIALS AND METHODS: Purified fibrinogen was obtained by beta-alanine precipitation of plasma from healthy donors. Separation of the fibrinogen fractions was performed by gradual precipitation of purified fibrinogen by ammonium sulphate. The viscosity was determined using a Haake Microvisco 2 viscometer. RESULTS: There was no statistically significant difference between the viscosity of native fibrinogen and the three fibrinogen subfractions. A substantial prolongation of the thrombin clotting time was observed in the fibrinogen solution containing EDTA at 37 degrees C compared to 20 degrees C. However, the viscosity of EDTA anticoagulated purified fibrinogen and plasma samples did not differ from that of heparin anticoagulated samples. CONCLUSION: The viscosity of the main fibrinogen subfractions HMW-, LMW- and LMW-fibrinogen did not differ from that of native fibrinogen, and the use of EDTA as anticoagulant did not significantly affect the viscosity of fibrinogen at 37 degrees C.

Citric Acid↗
PubMed1998

Treatment of severe hypertriglyceridemia lowers plasma viscosity.

Elevated plasma viscosity is a predictor of atherosclerotic vascular disease and is a potential mechanism by which hypertriglyceridemia increases cardiovascular risk. Previous studies of plasma viscosity reduction in hypertriglyceridemic patients used medications that lowered both triglyceride and fibrinogen levels. Because fibrinogen is a major determinant of viscosity, it is unclear whether triglyceride reduction alone is sufficient to reduce plasma viscosity. The purpose of this study was to determine whether triglyceride-lowering therapy reduces plasma viscosity. This was a prospective study of 24 adult patients with severe hypertriglyceridemia (> or = 5.67 mmol/l). Fasting lipid, total serum protein, fibrinogen, plasma viscosity and serum viscosity levels were measured before and after therapy with 1200 mg/d of gemfibrozil. Triglyceride levels decreased by 70% (P < 0.001). Mean plasma and serum viscosity levels decreased by 0.082 mPa/s (P = 0.003) and 0.086 mPa/s (P = 0.013), respectively. Fibrinogen levels did not change significantly. Triglyceride-lowering therapy reduced plasma and serum viscosity without changes in fibrinogen levels. Since serum samples are deplete of fibrinogen, the serum viscosity reduction observed is corroborative evidence for an independent effect of triglyceride-lowering therapy on plasma viscosity. This observation provides a physiological rationale for triglyceride-lowering therapy in patients at risk for atherosclerotic vascular disease, the chylomicronemia syndrome and pancreatitis.

Adult↗
PubMed2005

Food viscosity influences caloric intake compensation and body weight in rats.

OBJECTIVE: To determine the effects of food viscosity on the ability of rats to compensate for calories in a dietary supplement. RESEARCH METHODS AND PROCEDURES: In a series of four experiments, rats consumed dietary supplements equated for caloric and nutritive content but differing in viscosity. Experiments 1 to 3 examined the ability of the rats to compensate for the calories consumed in low- compared with high-viscosity premeals by reducing intake of a subsequent test meal. Caloric compensation was assessed with a wide range of premeal viscosity levels and with two different non-nutritive thickening agents. Experiment 4 assessed the effects of consuming daily a low-viscosity compared with an equicaloric high-viscosity dietary supplement on longer term body weight gain. RESULTS: Consuming a lower viscosity premeal was followed by significantly more caloric intake (i.e., less caloric compensation) compared with consuming premeals with higher viscosity levels. This effect was not specific to one thickening agent. Furthermore, rats given a low-viscosity supplement daily gained significantly more weight over a 10-week period compared with rats given a high-viscosity supplement. DISCUSSION: The results of these experiments suggest that food viscosity may be an important determinant of short-term caloric intake and longer term body weight gain.

Animals↗
PubMed2001

Elevated blood viscosity in systemic lupus erythematosus.

OBJECTIVES: It has been proposed that elevated blood viscosity contributes to atherothrombotic and thromboembolic processes. We evaluated whether there is increased blood viscosity in systemic lupus erythematosus (SLE) that might contribute to cardiovascular complications and reduced tissue perfusion. METHODS: Blood viscosity profiles were evaluated in SLE patients to determine whether rheologic disturbances contribute to the cardiovascular risk profile. Blood viscosity profiles were evaluated in 27 patients with SLE and 46 age- and gender-matched controls. Blood viscosity was measured at 37 degrees C and shear rates of 1 s(-1) and 100 s(-1), then corrected to the average hematocrit of the SLE patients. RESULTS: Corrected blood viscosity values were higher in SLE patients than in controls at 100 s(-1) (P =.002). Positive correlations were found between the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index for SLE, which quantifies damage to 12 organ systems and fibrinogen (rho =.39; P =.042) and plasma viscosity (rho =.38; P =.049). CONCLUSIONS: Our data indicate that blood viscosity values at a standard hematocrit are elevated in SLE patients. Further investigations are needed to evaluate whether the increased blood viscosity values in SLE patients contribute to cardiovascular complications and tissue ischemia. CLINICAL RELEVANCE: Because blood viscosity values correlate with the clinical severity of SLE, blood viscosity may contribute to the cardiovascular complications and reduced tissue perfusion in SLE patients. Semin Arthritis Rheum 31:52-57.

Adult↗
PubMed1994

Chemosensory similarities among oils: does viscosity play a role?

It is widely thought that viscosity plays an important role in the perception of fats. Rats were conditioned to avoid oil suspensions by treating them with lithium chloride after they had ingested the oil suspension. Control rats received the same lithium chloride injection after they drank vehicle. Three, chemically different, oils were examined, triglyceride oil, silicone oil and mineral oil. Rats trained to avoid a 4% aqueous suspension of one of these oils, reliably avoided suspensions containing any of the other oils, although the rats could discriminate between the oils. The viscosity of the oil suspension was slightly greater than the viscosity of the vehicle alone. However, rats trained to avoid an oil suspension, did not avoid a fluid having a viscosity similar to that of the oil suspension. In order to assess the possibility that rats could sense the viscosity of the oil separately from that of the vehicle, rats were tested for their aversion to oils having viscosities much higher and much lower than that of the oil they were trained to avoid. Rats trained to avoid triolein having a viscosity of 67 cp, reliably avoided silicone oils having viscosities of 5 and 203 cp. However, rats trained to avoid oil did not avoid an oil-free fluid having a viscosity of 22-29 cp. A final experiment examined whether the use of viscous or non-viscous vehicles influenced the conditioned aversion. No significant effect of vehicle viscosity appeared. Thus, chemically-diverse oils are perceived, by rats, to have some perceptible attribute in common. It is proposed that this common physical attribute is boundary lubrication rather than viscosity.

Animals↗
PubMed1993

The relationship between blood viscosity and blood pressure in a random sample of the population aged 55 to 74 years.

Blood viscosity is elevated in hypertensive subjects, but the association of viscosity with arterial blood pressure in the general population, and the influence of social, lifestyle and disease characteristics on this association, are not established. In the Edinburgh Artery Study, 1592 men and women aged 55-74 years selected randomly from the general population attended a university clinic. A fasting blood sample was taken for the measurement of blood viscosity and its major determinants (haematocrit, plasma viscosity and fibrinogen). Systolic pressure was related univariately to blood viscosity (P < 0.001), plasma viscosity (P < 0.001) and plasma fibrinogen (P < 0.01), but the association with fibrinogen did not persist after adjusting for body mass index. Diastolic pressure was related univariately to blood viscosity (P < 0.001) and plasma viscosity (P < 0.001) and haematocrit (P < 0.001) but not to fibrinogen. The only difference between the sexes was that the association between blood viscosity and systolic pressure was confined to males. Blood viscosity was associated equally with systolic and diastolic pressures in males, and remained independently related on multivariate analysis adjusting for age, sex, body mass index, social class, smoking, alcohol intake, exercise, angina, HDL and non-HDL cholesterol, diabetes mellitus, plasma viscosity, fibrinogen, and haematocrit.

Aged↗
PubMed2000

Hematocrit, volume expander, temperature, and shear rate effects on blood viscosity.

UNLABELLED: Our goal was to determine and predict the effects of temperature, shear rate, hematocrit, and different volume expanders on blood viscosity in conditions mimicking deep hypothermia for cardiac operations. Blood was obtained from six healthy adults. Dilutions were prepared to hematocrits of 35%, 30%, 22.5%, and 15% using plasma, 0.9% NaCl, 5% human albumin, and 6% hydroxyethyl starch. Viscosity was measured over a range of shear rates (4.5-450 s(-1)) and temperature (0 degrees -37 degrees C). A parametric expression for predicting blood viscosity based on the study variables was developed, and its agreement with measured values tested. Viscosity was higher at low shear rates and low temperatures, especially at temperatures less than 15 degrees C (P: < 0.016 for all conditions in comparison with 37 degrees C). Decreasing hematocrit, especially to less than 22.5%, decreased viscosity. Hemodilution with albumin or 0.9% NaCl decreased blood viscosity more than hemodilution with plasma or 6% hydroxyethyl starch (P: < 0.01 for all cases). The derived mathematical model for viscosity as a function of temperature, hematocrit, shear rate, and diluent predicted viscosity values that correlated well with the measured values in experimental samples (r(2) > 0.92, P: < 0.001). IMPLICATIONS: A theoretical model for blood viscosity predicted independent effects of temperature, shear rate, and hemodilution on viscosity over a wide range of physiologic conditions, including thermal extremes of deep hypothermia in an experimental setting. Moderate hemodilution to a hematocrit of 22% decreased blood viscosity by 30%-50% at a blood temperature of 15 degrees C, suggesting the potential to improve microcirculatory perfusion during deep hypothermia.

Adult↗
PubMed1998

Whole-blood viscosity and the insulin-resistance syndrome.

BACKGROUND: In a previous study we found that elevated blood viscosity was linked to the insulin resistance syndrome, and we proposed that high blood viscosity may increase insulin resistance. That study was based on calculated viscosity. OBJECTIVE: To determine whether directly measured whole-blood viscosity was related to the insulin-resistance syndrome in the same way as calculated viscosity had been found to be. METHODS: Healthy young men were examined with the hyperinsulinemic isoglycemic glucose clamp technique, and we related insulin sensitivity (glucose disposal rate) to other metabolic parameters and to blood viscosity. We established a technique for direct measurement of whole-blood viscosity. RESULTS: There were statistically significant negative correlations between glucose disposal rate and whole-blood viscosity at low and high shear rates (r = -0.41, P = 0.007 for both, n = 42). Whole-blood viscosity was correlated positively (n = 15) to serum triglyceride (r = 0.54, P = 0.04) and total cholesterol (r = 0.52, P = 0.05), and negatively with high-density lipoprotein cholesterol (r = -0.53, P = 0.04) concentrations. Insulin sensitivity index was correlated positively to high-density lipoprotein cholesterol (r = 0.54, P = 0.04) and negatively to serum triglyceride (r = -0.69, P = 0.005) and to total cholesterol (r = -0.81, P = 0.0003) concentrations. CONCLUSIONS: The present results demonstrate for the first time that there is a negative relationship between directly measured whole-blood viscosity and insulin sensitivity as a part of the insulin-resistance syndrome. Whole-blood viscosity contributes to the total peripheral resistance, and these results support the hypothesis that insulin resistance has a hemodynamic basis.

Adult↗
PubMed2001

Effect of meal viscosity and nutrients on satiety, intragastric dilution, and emptying assessed by MRI.

The relationship between the intragastric distribution, dilution, and emptying of meals and satiety was studied using noninvasive magnetic resonance imaging techniques in 12 healthy subjects with four polysaccharide test meals of varying viscosity and nutrient content as follows: 1) low-viscosity nonnutrient, 2) low-viscosity nutrient, 3) high-viscosity nonnutrient, and 4) high-viscosity nutrient. Increasing the nutrient content of the high-viscosity meal delayed gastric emptying from 46 +/- 9 to 76 +/- 6 min (P < 0.004), whereas increasing viscosity had a smaller effect. The volume of secretions within the stomach 60 min after ingestion was higher for the high-viscosity nutrient meal (P < 0.04). A simple model to calculate the total volume of secretion added to the test meal is presented. Color-coded dilution map images showed the heterogeneous process of progressive gastric dilution of high-viscosity meals, whereas low-viscosity meals were uniformly diluted. Fullness was found to be linearly related to total gastric volumes for the nutrient meals (R(2) = 0.98) and logarithmically related for the nonnutrient meals (R(2) = 0.96). Fullness was higher for high- compared with low-viscosity meals (P < 0.02), and with the nutrient meals this was associated with greater antral volumes (P < 0.05).

Adult↗
PubMed1998

Blood viscosity and elevated carotid intima-media thickness in men and women: the Edinburgh Artery Study.

BACKGROUND: Several hemostatic and rheological factors have been associated with incident cardiovascular events. However, there have been no reports on the relationship of rheological factors with early atherosclerosis and very few on hemostatic factors. We therefore studied the relationship between these factors and carotid intima-media thickness (IMT). METHODS AND RESULTS: The Edinburgh Artery Study measured fibrinogen, tissue plasminogen activator (tPA), fibrin D-dimer, von Willebrand factor (vWF), blood and plasma viscosities, and hematocrit as part of its baseline examination during 1988-1989. At the 5-year follow-up, valid measurements of IMT had been recorded in 1106 men and women 60 to 80 years old. In men, blood viscosity (P< or =.001) and its major determinants, plasma viscosity, fibrinogen (both P< or =.01), and hematocrit (P< or =.05), were all linearly related to IMT. Furthermore, blood viscosity, fibrinogen (both P< or =.01), and plasma viscosity (P< or =.05) remained significantly associated on multivariate analysis. Correcting blood viscosity to a standard hematocrit of 45% had little effect on its association. In men, there was a significantly increased risk of having an IMT above versus below the upper quartile of its distribution (1.05 mm) for SD increases in blood viscosity (P< or =.01), fibrinogen, corrected blood viscosity, and plasma viscosity (all P< or =.05). With the exception of plasma viscosity, these risks were unaffected by adjustment for other common cardiovascular risk factors. No significant associations were found between any of the hemorheological factors and IMT in women or for tPA, fibrin D-dimer, or vWF in either sex. CONCLUSIONS: These findings suggest that in men, blood viscosity and its major determinants are associated not only with incident cardiovascular events but also with the early stages of atherosclerosis. This may be one explanation for the link between rheological factors and events.

Age Factors↗
PubMed2001

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

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

Adult↗
PubMed1975

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

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

Blood Viscosity↗
PubMed2003

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

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

Adult↗
PubMedDate not supplied

Whole blood viscosity in beta thalassemia minor.

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

Blood Viscosity↗