Variance, factors of influence and clinical relevance of plasma viscosity]

The problem of measuring plasma viscosity has been solved through the use of capillary and falling-ball viscosimeters which have a determination variance of less than 1%. On account of the influence of overeating, forced thirst, psychological and physical stress plasma viscosity should be determined in the morning; the patient should be fasting and well hydrated. Plasma viscosity is influenced by diseases with alterated plasma protein composition. An elevated viscosity also significantly increases the risk of developing an arterial occlusion. Since the physician can both decrease and increase plasma viscosity, it should be determined parallel to therapy. Accordingly, plasma viscosity is one of the most important rheological parameters.     

Cardiac mechanoenergetic cost of elevated plasma viscosity after moderate hemodilution

The purpose of this study was to investigate how plasma viscosity affects cardiac and vascular function during moderate hemodilution. Twelve anesthetized hamsters were hemodiluted by 40% of blood volume with two different viscosity plasma expanders. Experimental groups were based on the plasma expander viscosity, namely: high viscosity plasma expander (HVPE, 6.3 mPa?·?s) and low viscosity plasma expander (LVPE, 2.2 mPa?·?s). Left ventricular (LV) function was intracardiacally measured with a high temporal resolution miniaturized conductance catheter and concurrent pressure-volume results were used to calculate different LV indices. Independently of the plasma expander, hemodilution decreased hematocrit to 28% in both groups. LVPE hemodilution reduced whole blood viscosity by 40% without changing plasma viscosity, while HVPE hemodilution reduced whole blood viscosity by 23% and almost doubled plasma viscosity relative to baseline. High viscosity plasma expander hemodilution significantly increased cardiac output, stroke volume and stroke work compared to baseline, whereas LVPE hemodilution did not. Furthermore, an increase in plasma viscosity during moderate hemodilution produced a higher energy transfer per unit volume of ejected blood. Systemic vascular resistance decreased after hemodilution in both groups. Counter-intuitively, HVPE hemodilution showed lower vascular resistance and vascular hindrance than LVPE hemodilution. This result suggests that geometrical changes in the circulatory system are induced by the increase in plasma viscosity. In conclusion, an increase in plasma viscosity after moderate hemodilution directly influenced cardiac and vascular function by maintaining hydraulic power and reducing systemic vascular resistance through vasodilation.     

Non-Newtonian rheology of leukemic blood and plasma: are n and k parameters of power law model diagnostic?

When discussing the rheological properties of normal and leukemic blood it must be considered that blood is a suspension of cells in aqueous solution which is also known as plasma. Whole blood viscosity and plasma viscosity were determined by Rheometer LS30 which allows measuring whole blood and plasma viscosity in the middle and low shear rate ranges. The measurements of the viscosity showed that whole blood and plasma behave as non-Newtonian power law fluid. The values of n (non-Newtonian index) and k (consistency index) of power law fluid were calculated for both leukemic blood and plasma samples. The importance of this phenomenon for the micro-circulation is discussed.     

High viscosity plasma expanders: Volume restitution fluids for lowering the transfusion trigger

Hemorheological studies lead to the axiom that high plasma viscosity is detrimental and that it is beneficial to lower blood viscosity, a precept embodied in the practice of hemodilution, where improved perfusion is attributed to the lowering of blood viscosity. Hemodilution is limited by the transfusion trigger, hemoglobin content of blood of about 7-8 g/dl, which indicates when further volume replacements must restore oxygen carrying capacity with red blood cells (RBC). However, oxygen consumption and delivery are not compromised upon passing this landmark. The reduced blood viscosity does not transmit adequate pressure to the capillaries, causing functional capillary density (FCD) to decrease, jeopardizing organ function through the inadequate extraction of products of metabolism from the tissue by the capillaries. Studies in hemorrhagic shock show that survival is primarily determined by the maintenance of FCD and secondarily by tissue oxygenation. FCD is maintained as hematocrit is reduced beyond the transfusion trigger by increasing plasma viscosity, which transmits systemic pressure to the capillaries and induces vasodilatation through the increased shear stress dependent release of vasodilators. Consequently the transfusion trigger is also a "viscosity trigger" indicating when blood and plasma viscosity are too low. In this condition increasing plasma viscosity is beneficial and extends the transfusion trigger reducing the use of blood transfusions.     

Detection of red cell aggregation by low shear rate viscometry in whole blood with elevated plasma viscosity

The viscosity of whole blood measured at low shear rates is determined partly by shear resistance of the red cell aggregates present, stronger aggregation increasing the viscosity in the absence of other changes. Effects of cell deformability can confound interpretation and comparison in terms of aggregation, however, particularly when the plasma viscosity is high. We illustrate the problem with a comparison of hematocrit-adjusted blood from type 1 diabetes patients and controls in which it is found the apparent and relative viscosities at a true shear rate of 0.20 s-1 are lower in the patient samples than age matched controls, in spite of reports that aggregation is increased in such populations. Because the plasma viscosities of the patients were higher on average than controls, we performed a series of experiments to examine the effect of plasma protein concentration and viscosity on normal blood viscosity. Dilution or concentration by ultrafiltration of autologous plasma and viscosity measurements at low shear on constant hematocrit red cell suspensions showed (a) suspension viscosity at 0.25 and 3 s-1 increased monotonically with plasma protein concentration and viscosity but (b) the relative viscosity increased, in concert with the microscopic aggregation grade, up to a viscosity of approximately 1.25 mPa-s but above this the value the relative viscosity no longer increased as the degree of aggregation increased in concentrated plasmas. It is suggested that in order to reduce cell deformation effects in hyperviscous pathological plasmas, patient and control plasmas should be systematically diluted before hematocrit is adjusted and rheological measurements are made. True shear rates should be calculated. Comparison of relative viscosities at low true shear rates appears to allow the effects of red cell aggregation to be distinguished by variable shear rate viscometry in clinical blood samples.     

Relation between blood plasma viscosity and presence of vascular and neurological complications in diabetic Africans

The relation between changes in plasma and serum viscosity and the presence of diabetic vascular and neurological complications was investigated in 50 diabetic Africans. Diabetics with complications had significantly elevated plasma and serum viscosity compared with those of both diabetics without complications and healthy non-diabetics. Hypertension also contributed to the elevation of plasma and serum viscosity in diabetics with complications. Plasma and serum viscosity of diabetics significantly correlated with the number of vascular and neurological complications. Diabetics with cerebrovascular disease had the highest plasma and serum viscosity due to the presence of many complications. The results of this study suggest that changes in plasma and serum viscosity may be associated with abnormalities of vascular and neurological function present in diabetic Africans.     

Effect of plasma exchange on blood viscosity and cerebral blood flow.

The effects of plasma exchange using a low viscosity plasma substitute on blood viscosity and cerebral blood flow were investigated in eight subjects with normal cerebral vasculature. Plasma exchange resulted in significant reductions in plasma viscosity, whole blood viscosity, globulin and fibrinogen concentration without affecting packed cell volume. The reduction in whole blood viscosity was more pronounced at low shear rates suggesting an additional effect on red cell aggregation. Despite the fall in viscosity there was no significant change in cerebral blood flow. The results support the metabolic theory of autoregulation. Although changes in blood viscosity appear not to alter the level of cerebral blood flow under these circumstances, plasma exchange could still be of benefit in the management of acute cerebrovascular disease.     

Evaluation of various hemorheologic parameters in diabetes mellitus

It has been speculated that changes in intrinsic blood flow properties may contribute to the evolution of vascular complications in diabetes mellitus. To verify this hypothesis we measured hematocrit, fibrinogen, plasma and blood viscosity in 30 diabetic patients and in 25 healthy volunteers. Diabetics showed blood and plasma viscosity and fibrinogenemia higher than healthy subjects, although only plasma viscosity and fibrinogenemia were statistically significant (p less than 0.001). Moreover the diabetic patients with the highest HbAlc values had a significant increase in plasma viscosity compared with the patients with lower HbAlc values (p less than 0.001), despite a similar fibrinogenemia. This study confirms the presence of hemorheological changes in diabetes mellitus and shows a correlation between plasma viscosity and metabolic control.     

No change of whole blood of plasma viscosity in cardiac patients after subcutaneous calcium heparin.

Whole blood viscosity, plasma viscosity and haematocrit were studied in a group of cardiac patients before and during subcutaneous heparin treatment. No significant change was noted in any of the parameters investigated. Relative viscosity (whole blood viscosity/plasma viscosity ratio) was also unaffected. These data indicate that heparin has no effect on the rheology of blood in vitro.     

Risk factors evaluation in some cardiovascular diseases

Cardiovascular risk factors are associated with limitations of blood fluidity. Rheological behaviour of blood in transient flow may result from the internal organization, which in turn depends upon many parameters, which may be considered as possible elements of a profiling algorithm for diagnostic and prognostic values in various pathophysiological states. This study was designed to investigate haemorheological parameters in patients being treated for hypertension, coronary heart disease and myocardial infarct. On the basis of plasma viscosity, whole blood viscosity, haematocrit, red cell aggregation and red cell deformation, the risk was evaluated. In cases of hypertension there was a significant rise in plasma viscosity, whole blood viscosity, red cell aggregation and a fall in red cell deformability. In cases of coronary disease, plasma viscosity and red cell aggregation was increased, while in patients with myocardial infarcts, where the degree of severity is greater it was found that there was a significant rise in both plasma and whole blood viscosity. Haematocrit values were unaffected in all three groups.     

The effects of experimental hypo- and hyperthyroidism on blood viscosity and other blood parameters in the rat

Three groups of male Sprague Dawley rats received methimazole without or with Na-thyroxine in drinking water (3 and 0.33 mg T4/l, respectively) to induce characteristic alterations of their thyroid status (hypothyroid, hyperthyroid, euthyroid). A fourth group served as an untreated control without any additive to the drinking water. With respect to the different thyroid status, the following changes in the blood parameters were found: increasing plasma-T3-levels caused a reduction in plasma viscosity, in total plasma protein and in alpha 1-globulin, but an increase in hematocrit, whole blood viscosity, the number of erythrocytes and leukocytes, alpha 2-globulin and beta-globulin. It was concluded that the increase in the plasma viscosity in the hypothyroid status is mainly due to an alteration of the plasma protein pattern, and that the increase in whole blood viscosity in the hyperthyroid rat is a consequence of increased hematocrit.     

Influence of resonant charge exchange on the viscosity of partially ionized plasma in a magnetic field

The influence of resonant charge exchange for ion-atom interaction on the viscosity of partially ionized plasma embedded in the magnetic field is investigated. The general system of equations used to derive the viscosity coefficients for an arbitrary plasma component in the 21-moment approximation of Grad’s method is presented. The expressions for the coefficients of total and partial viscosities of a multicomponent partially ionized plasma in the magnetic field are obtained. As an example, the coefficients of the parallel and transverse viscosities for the ionic and neutral components of the partially ionized hydrogen plasma are calculated. It is shown that the account for resonant charge exchange can lead to a substantial change of the parallel and transverse viscosity of the plasma components in the region of low degrees of ionization on the order of 0.1.     

Blood viscosity parameter correlation with types of leukemia.

We investigated the hemorheological, hematological and biochemical parameters in 30 cases of acute lymphocytic leukemia (ALL), 21 cases of acute myelogenous leukemia (AML) and 30 cases of chronic myelogenous leukemia (CML). The parameters studied include whole blood viscosity, plasma viscosity, erythrocyte sedimentation rate (ESR), red cell filterability, hematocrit, platelet count and aggregation, fibrinogen, hemoglobin, leucocyte count, bleeding time and lactate dehydrogenase activity (LDH). In the cases of ALL we observed significant decrease in whole blood viscosity, hemoglobin, hematocrit and platelet count but an increase in plasma viscosity, fibrinogen, bleeding time and LDH activity. In the cases of AML, we observed increase in whole blood viscosity, plasma viscosity, ESR, fibrinogen, leucocyte count, bleeding time and LDH activity but decrease in the hemoglobin, hematocrit and platelet count. In the cases of CML, we observed an increase of whole blood viscosity, plasma viscosity, ESR, fibrinogen elevation but decreases in bleeding time. In all cases, red cell filterability was unaffected.     

Plasma viscosity and cerebral blood flow

We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on "baseline" CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H(2) clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 +/- 10.2 ml. 100 g(-1). min(-1) (+/-SD). In control animals, changing plasma viscosity to 1. 0 or 3.0 cP resulted in CBF of 55.9 +/- 8.6 and 42.5 +/- 12.7 ml. 100 g(-1). min(-1), respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1. 0 cP, CBF varied from 98 to 115 ml. 100 g(-1). min(-1). When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml. 100 g(-1). min(-1) and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.     

Distribution of body fluid and change of blood viscosity in broilers (Gallus domesticus) under high temperature exposure

This study was to observe the distribution of body fluid by measuring blood volume, extracellular and intracellular fluid volumes and total body water under heat exposure, in order to clarify the mechanism of decrease in whole blood viscosity of the heat-exposed broilers. Whole blood viscosity, haematocrit, plasma protein concentration, plasma osmolality and extracellular fluid volume decreased during high temperature exposure, while plasma and blood volumes increased. No significant changes were found in both intracellular fluid volume and total body water between thermoneutral and high temperature exposure. These results indicate the decreased whole blood viscosity is induced by a plasma volume expansion, in which water may come from the interstitial space and alimentary tract, under heat exposure.     

Blood Viscosity in Healthy Subjects and Patients with Coronary Heart Disease

Viscosity of whole blood and plasma was measured in 258 apparently healthy subjects of both sexes from 5 to 60 years of age, and in 86 patients with unequivocal evidence of chronic coronary heart disease. Children and young healthy females had the lowest viscosity readings. Healthy young and middle-aged males had significantly higher blood viscosity than females. Patients with coronary heart disease had significantly higher blood viscosity values than healthy groups of the same sex. It is suggested that the higher viscosity of whole blood and of plasma is a contributory factor in development of clinical manifestations of coronary heart disease and possibly of the basic vascular lesion itself.     

Variability of plasma viscosity in monoclonal IgM gammopathies.

Hyperviscosity syndromes can caused by both plasmatic and cellular factors. We have studied 20 patients affected by IgM gammopathy of different origin and 12 healthy subjects matched for sex and age, in order to evaluate the relation between paraprotein levels and plasma viscosity. We have observed a significant plasma viscosity increase only in 14 patients with monoclonal IgMk gammopathy. In the same patients was also evident an hyperviscosity syndrome. In the other 6 patients, with monoclonal IgM or polyclonal gammopathy and without clinical symptoms, plasma viscosity was only slightly increased. We have also observed a significant correlation between IgM and light chains (kappa, lambda) serum level and increased plasma viscosity. These results suggest that one can't consider all IgM gammopathies as cause of hyperviscosity syndrome.     

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.     

The effects of chronic long-term intermittent hypobaric hypoxia on blood rheology parameters

The effect of chronic long-term intermittent hypobaric hypoxia (CLTIHH) on blood rheology is not completely investigated. We designed this study to determine the effect of CLTIHH on blood rheology parameters. Present study was performed in 16 male Spraque-Dawley rats that divided into CLTIHH and Control groups. To obtain CLTIHH, rats were placed in a hypobaric chamber (430 mmHg; 5 hours/day, 5 days/week, 5 weeks). The control rats stayed in the same environment as the CLTIHH rats but they breathed room air. In the blood samples aspirated from the heart, hematocrit, whole blood viscosity, plasma viscosity, plasma fibrinogen concentration, erythrocyte rigidity index and oxygen delivery index were determined. The whole blood viscosity, plasma viscosity, hematocrit and fibrinogen concentration values in the CLTIHH group were found to be higher than those of the control group. However, no significant difference was found in erythrocyte rigidity index and oxygen delivery index between the groups. Our results suggested that CLTIHH elevated whole blood viscosity by increasing plasma viscosity, fibrinogen concentration and hematocrit value without effecting the erythrocyte deformability. Hence, CLTIHH that may occur in intermittent high altitude exposure and some severe obstructive sleep apnea (OSA) patients may be responsible for hemorheologic changes in those subjects.