Increased Plasma Viscosity Research Articles

Hyperviscosity in plasma cell dyscrasias

Plasma cell dyscrasias are characterized by a malignant clonal proliferation of plasma cells. Due to the excessive production of abnormal clonal gammaglobulins, or paraproteins, there are major hemorheologic changes in the circulation. As a result, clinical manifestations of the hyperviscosity syndrome become a major cause of morbidity and mortality. Pathogenic factors for the hyperviscosity are due both to increased plasma viscosity and to increased erythrocyte aggregation, leading to increased whole blood viscosity. These changes are dependent on the plasma concentration as well as the molecular size of the paraprotein with the threshold for onset of hyperviscosity for IgG >15 g/dl, for polymerized IgG3 >4-5 g/dl, for IgA >10-11 g/dl; for polymerized IgA >6-7 g/dl and for IgM >3 g/dl. Correspondingly, the incidence of symptomatic hyperviscosity in Waldenstrom's macroglobulinemia is 10-30%, while that in IgG myeloma is 2-6%. Clinically, the syndrome has neurologic features of headache and dizziness, visual changes, renal failure, and cardiac failure from increased plasma volume. Thrombotic complications are frequent. Paradoxically, there can be bleeding complications due to impairment of platelet function. Removal of the paraprotein by plasma exchange (plasmapheresis) can effectively reduce the hyperviscosity. Long-term control of paraprotein production can be achieved by chemotherapy. The early recognition of the symptoms of hyperviscosity, confirmed by laboratory findings of increased paraproteins and of increased blood viscosity, is essential for the proper management of this group of disorders.

Relationship between hemorheology and endothelial dysfunction in renal transplant patients receiving calcineurin inhibitors

Calcineurin inhibitors, mainly cyclosporin A (CsA), are associated with endothelial dysfunction in renal transplant recipients (RTRs). Hemorheological disturbances including decreased erythrocyte deformability (ED), increased plasma viscosity and erythrocyte aggregation (EA) have also been reported in CsA-treated RTRs. The aim of this study was to investigate the relationship between hemorheological factors and endothelial dysfunction in CsA- and tacrolimus (Tc)-treated RTRs. Thirty-one RTRs and 16 healthy subjects were recruited. The RTR group received either CsA (n = 16) or Tc (n = 15). Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. ED and EA were measured with laser-assisted optical rotational cell analyzer, and plasma viscosity by a cone-plate viscometer. FMD of the CsA group was significantly lower than that of controls (6.3% ± 5.1% vs. 11.9% ± 5.6%, p = 0.024), whereas, there was no significant difference between the Tc group (8.8% ± 5.4%) and controls. At shear stresses ranging between 0.95 and 30 Pa, EDs of the CsA group were significantly lower compared with controls. In the Tc group, the decrease in ED was significant at shear stresses ranging between 0.53 and 5.33 Pa. ED indices did not correlate with FMD in any of the groups. The degree of endothelial dysfunction and reduction in ED were more remarkable in patients on CsA therapy. Hemorheological factors were not likely to be associated with endothelial dysfunction in RTRs.

Reduction of Oxygen-Carrying Capacity Weakens the Effects of Increased Plasma Viscosity on Cardiac Performance in Anesthetized Hemodilution Model

We investigated the effects of reduced oxygen-carrying capacity on cardiac function during acute hemodilution, while the plasma viscosity was increased in anesthetized animals. Two levels of oxygen-carrying capacity were created by 1-step and 2-step hemodilution in male golden Syrian hamsters. In the 1-step hemodilution (1-HD), 40% of the animals' blood volume (BV) was exchanged with 6% dextran 70 kDa (Dx70) or dextran 2000 kDa (Dx2M). In the 2-step hemodilution (2-HD), 25% of the animals' BV was exchanged with Dx70 followed by 40% BV exchanged with Dx70 or Dx2M after 30 minutes of first hemodilution. Oxygen delivery in the 2-HD group consequently decreased by 17% and 38% compared to that in the 1-HD group hemodiluted with Dx70 and Dx2M, respectively. End-systolic pressure and maximum rate of pressure change in the 2-HD group significantly lowered compared with that in the 1-HD group for both Dx70 and Dx2M. Cardiac output in the 2-HD group hemodiluted with Dx2M was significantly higher compared with that hemodiluted with Dx70. In conclusion, increasing plasma viscosity associated with lowering oxygen-carrying capacity should be considerably balanced to maintain the cardiac performance, especially in the state of anesthesia.

Nitric Oxide Synthase Inhibition Weakens Beneficial Effects of Increased Plasma Viscosity on Cardiac Function in Hemodilution Model

This study tested the hypothesis that the inhibition of nitric oxide synthase negatively affects the beneficial effects of high viscogenic plasma expander (HVPE) on cardiac performance in a state of hemodilution. Five anesthetized hamsters were administered with N(G)‐nitro‐L‐arginine methyl ester (L‐NAME), nitric oxide synthase inhibitor, as a tested group whereas other five without L‐NAME infusion were used as a control group. Animals were performed an isovolemic hemodilution by 40% of estimated blood volume with dextran 2000 kDa, HVPE with viscosity 6.34 cP. L‐NAME administration followed by isovolemic hemodilution significantly decreased heart rate from 441±41 bpm at baseline to 355±27 bpm at 60 min after hemodilution. End‐systolic pressure increased 14% after L‐NAME infusion and maintained higher than baseline after hemodilution whereas it gradually decreased in animals without L‐NAME infusion. L‐NAME significantly decreased the maximum rate of ventricular pressure change, stroke volume and cardiac output after hemodilution compared to a control group. Systemic vascular resistance increased to 162% and 135% of baseline after L‐NAME infusion and 60 min after hemodilution which is particularly higher than a control group. These results indicate that nitric oxide induced by HVPE play a major role on cardiac function during an isovolemic hemodilution.

Blood Rheology and Platelet Function in Untreated Early-Stage Essential Hypertensives Complicated with Metabolic Syndrome

We examined whether hemorheology and platelet function are affected in essential hypertensives (EHTs) of the World Health Organization stage I when complicated with metabolic syndrome (Mets). In 156 untreated EHTs, blood viscosity and platelet surface markers were determined. Blood viscosity was significantly elevated in 54 subjects with Mets compared with 102 subjects without Mets. Hematocrit and plasma viscosity increased in the group with Mets, although red blood cell rigidity index “k” did not differ between groups. As a whole group, blood viscosity correlated positively with hematocrit and plasma viscosity. Additionally, plasma viscosity correlated positively with plasma leptin, triglyceride, homeostasis model assessment index, C-reactive protein, and plasma fibrinogen, but negatively with high-density lipoprotein cholesterol. In contrast, no differences were seen in platelet surface markers between groups. In conclusion, EHTs of the early stage complicated with Mets are characterized by increased blood viscosity due to hemoconcentration and increased plasma viscosity.

Does reactive thrombocytosis observed in iron deficiency anemia affect plasma viscosity?

Objective: The accompanying thrombocytosis is referred to as the major factor associated with thromboembolism in iron deficiency anemia (IDA). Increased viscosity may increase the risk of thrombosis. We hypothesized that increased platelet count -with reactive thrombocytosis- might also affect plasma viscosity. We planned to evaluate the influence of normal and high platelet count on plasma viscosity in IDA patients. Material and Methods: The patient population consisted of fifty-three newly diagnosed and untreated women aged between 18 and 62 years with IDA. Group 1 consisted of 33 patients, platelet levels below 400 x 109/L. Group 2 consisted of 20 patients, platelet levels above 400 x 109/L. Measurements of plasma viscosity were performed using Brookfield viscometer. Results: Mean plasma viscosity was found as 1.05 ± 0.08 mPa.s. in Group 1, and 1.03 ± 0.06 mPa.s. in Group 2. Mean plasma viscosity was not statistically different. White blood cell count was significantly higher in Group 2. Vitamin B12 levels were significantly higher in Group 2, while folic acid levels were higher in Group 1 (p=0.011 and p=0.033). Plasma viscosity was correlated with erythrocyte sedimentation rate (r=0.512 p=0.002) in Group 1 and inversely correlated with vitamin B12 (r=−0.480 p=0.032) in Group 2. Conclusion: Despite the significant difference between groups in terms of platelet count, no significant difference was detected in plasma viscosity and this finding could be explained as the following; 1-These platelets were not thrombocythemic platelets; 2-Similar to the theory about leukocytes, higher platelet counts – even non-thrombocythemic – may increase plasma viscosity; 3-Evaluating platelet count alone is not sufficient and the associating red-cell deformability should also be taken into account; and 4-Although other diseases that could affect viscosity are excluded, some definitely proven literature criteria such as fibrinogen, hyperlipidemia, and the inflammatory process should also be evaluated by laboratory and clinical measures.

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.

Plasminogen and fibrinogen plasma levels in coronary artery disease

The process of haemostasis ensures that following vascular damage blood remains confined to the circulatory system. This is not a single biological pathway, but rather a complex interplay of several distinct processes(1). Injury to the endothelium causes the transition of endothelial surface from a non-thrombogenic state to one actively promoting thrombus formation. The process starts when injury causes a breach in the endothelium with exposure of subendothelial collagen and tissue factor. Collagen activates platelets and tissue factor exposure initiates the coagulation cascade - both processes lead to thrombus formationthat is localised at the site of injury. While the end product is the generation of fibrin from fibrinogen, the composition of thrombi in the arterial and venous circulations is dissimilar. In the arterial system the thrombus predominantly comprises of platelets and fibrin whereas in the venous system fibrin together with red cells and white cells are the major components of the clot. Regardless of the site of clot, the formation of a stable fibrin network is the ultimate step in thrombus formation. The conversion of fibrinogen to fibrin is brought about by cleavage of fibrinogen. This process is undertaken by thrombin which cleaves fibrinogen into two smaller peptides, fibrinopeptide A and B. Fibrin monomers are then formed with subsequent polymerization. Finally, the clot is consolidated when factor XIII cross-links the fibrin monomers. Once the clot has formed and the fibrinolytic system begins the proteolytic removal of thrombi to ensure that vessel patency is restored. Plasminogen binds to fibrin and is activated by tissue plasminogen activator (tPA) to plasmin. Plasmin begins the dissolution of fibrin although; because of its broad specificity it causes degradation of fibrinogen as well. Just like the coagulation cascade, the fibrinolytic system is a complex interplay of activators and inhibitors to ensure optimal haemostasis. Obviously, in disease the fine balance of haemostasis is disturbed. Atherosclerosis is a multifactorial disease where vascular injury leads to lipid accumulation and deposition of platelets and fibrin. It is not surprising therefore, that disorders of different components of haemostasis can contribute to the pathogenesis of atherosclerosis. The current study compared the level of fibrinogen and plasminogen in angiographically normal subjects and those with mild/moderate, and severe coronary artery disease(2). A graded correlation was found between levels of fibrinogen and the severity of coronary artery disease. Elevated levels of plasma fibrinogen have been shown to be an independent risk factor for coronary artery disease(3,4). Whether this is a direct effect of hyperfibrinogenemia is unclear, although some evidence exists to suggest that elevated fibrinogen may affect the process of atherogenesis by fibrin deposition within developing atherosclerotic lesions(5). Because fibrinogen has also been associated with other traditional cardiovascular risk factors, an atherothrombotic effect mediated through a raised fibrinogen level would appear plausible. This would be indirectly supported by thrombotic association of dysfibrinogenemia(6), a condition which primarily produces a bleeding tendency but is well known to cause thrombotic events too. There are several mechanisms by which fibrinogen may increase cardiovascular risk. It binds specifically to activated platelets via glycoprotein IIb/IIIa, contributing to platelet aggregation. Elevated fibrinogen levels increase plasma viscosity and promote fibrin formation. Chronic inflammatory conditions are known to result in accelerated atherosclerosis. That fibrinogen is an acute-phase reactant with levels rising significantly in inflammatory states may be pathogenetically relevant. Like disorders of fibrinogen impaired fibrinolysis appears to have a role in thrombosis. Plasmin, which results from the cleavage of plasminogen by plasminogen activators (PAs), predominantly mediates the intravascular clearance of fibrin. The important role of plasminogen in fibrinolysis makes it an interesting parameter to evaluate in various diseases. It is recognized that a decreased plasminogen level may affect the fibrinolytic activity and result in thrombotic tendency(7). It is therefore, not surprising that plasminogen levels were not found to be significantly elevated in patients with coronary artery disease. It is well known that increased levels of plasminogen activator inhibitor-1 (PAI-1) are found in myocardial infarction(8). A raised PAI-1 level would inhibit fibrinolysis by inhibiting tissue plasminogen activator and this may result in thrombotic tendency. It would have been interesting to look at PAI-1 levels as well and this aspect needs to be considered in future studies. While this paper reaffirms the association of elevated fibrinogen with coronary artery disease, in view of the multifaceted nature of atherosclerosis, especially the emerging role of inflammation in its pathogenesis, information on inflammatory markers would have been valuable(9,10). Further follow-up on the three cohorts with serial measurements of different parameters would give additional insight into correlating the progression of the disease with different haemostatic and fibrinolytic parameters.

Estimation of the microcirculation state in cerebrovascular disorders using laser doppler flowmetry data and hemorheological parameters

The microcirculation state was assessed in the group of patients with ischemic stroke (n = 30) and the control group of healthy individuals (n = 27) using laser Doppler flowmetry and the wavelet analysis of the amplitude-frequency range of microvascular blood flow oscillations combined with absorption spectroscopy. The hemorheological parameters (blood and plasma viscosity, the degree of red blood cell aggregability and deformability) were assessed in both groups, as were their correlations with the microcirculation parameters. Decreased tissue perfusion (by 25%) and specific oxygen consumption (by 21%) were revealed in a cerebrovascular accident. Changes in the tone-forming regulatory mechanisms of microcirculation of vasodilating nature (decreased microvascular tone, activation of the secretory function of endothelium) may be regarded as a compensatory reaction aimed at maintaining the blood supply of organs and tissues in stroke. The blood viscosity increase in patients due to the plasma viscosity increase and increased red blood cell aggregability and their decreased deformability cause the blood flow to slow down and the wall shear stress to increase, which activates the endothelial secretory function and vasodilation of microvessels. Correlation between the rheological parameters and the passive (respiratory and cardiac) rhythm amplitudes was observed in the control group. In patients, the hemorheological parameters were correlated with the characteristics of the active factors of microvascular blood flow modulation (endothelial, neurogenic, and myogenic), which confirms the role of changed blood properties and regulatory tone-forming mechanisms in the maintenance of tissue perfusion in cerbrovascular accidents.

Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm

Heart failure (HF) represents a major and growing public health problem because of its prevalence, incidence, morbidity, mortality, and economic costs. The prevalence of HF is 2% to 3% of the general population.1 Five million Americans are affected, with >550 000 cases diagnosed each year.2 The mortality rate from severe HF remains >60% within 5 years of diagnosis, and 50% of hospitalized patients with HF require readmission within 6 months of discharge. In the US estimated costs amount to > $35 billion per year.3 Although several therapies (eg, β-blockers, angiotensin-converting enzyme [ACE] inhibitors, and cardiac resynchronization therapy) have been proven effective in improving HF outcomes, many unanswered questions about optimal treatment remain. One area of ongoing uncertainty is the appropriate role for antithrombotic therapy in patients with HF. Observational data suggest that patients with HF have an increased venous thromboembolism (VTE) risk (deep venous thromboembolism [DVT], pulmonary embolism [PE], peripheral arterial thromboembolism, and stroke).4 These epidemiological findings are supported by multiple mechanisms that can contribute to a hypercoagulable state in patients with HF. Despite this increased risk of VTE, the role of antithrombotic therapy remains unclear. In this article, we provide an overview of epidemiology, pathophysiology, clinical trial data, and therapeutic recommendations for prevention of thromboembolism in HF. We searched PubMed for articles published between 1958 and 2010 using the following search terms: epidemiology of heart failure , thromboembolism and heart failure , thrombogenesis and heart failure , anticoagulation in heart failure , antiplatelet agent and heart failure , aspirin and heart failure , bleeding risk and anticoagulation , and aspirin and angiotensin-converting enzyme inhibitors . We also studied abstracts from national and international cardiovascular meetings to identify unpublished studies using the key words anticoagulation and dilated cardiomyopathy . Data from published observational studies and secondary …

Increased plasma viscosity in young women with polycystic ovary syndrome using an oral contraceptive containing 35 μg ethinyl estradiol and 2 mg cyproterone acetate

Objectives. To investigate the influence of 6 months of treatment with an oral contraceptive (OC) containing 35 μg ethinyl estradiol and 2 mg cyproterone acetate on plasma viscosity (PV) in young women with polycystic ovary syndrome (PCOS).Design. Patients with PCOS were assessed for PV before and after 6 months of treatment with an OC containing 35 μg ethinyl estradiol and 2 mg cyproterone acetate. PV was determined by a viscometer Type 53610/I SCHOTT-Instruments, Mainz at 37°C.Settings. Subjects were recruited from the Department of Obstetrics and Gynaecology, Division of Reproductive Endocrinology at the University Hospital of Patras, Greece.Patients. The study included 66 young women with PCOS.Main outcome measures. PV.Results. In PCOS women as a whole, PV at baseline was 1.249 ± 0.049 mm2/s (n = 66). After 6 months of treatment with an OC containing 35 μg ethinyl estradiol and 2 mg cyproterone acetate, PV was increased to 1.268 ± 0.065 mm2/s (p = 0.038). The difference between PV before and after 6 months of treatment with an OC containing 35 μg ethinyl estradiol and 2 mg cyproterone acetate (Δviscosity) was 0.01864 ± 0.071452 mm2/s. ΔViscosity was related to Δfibrinogen (r = 0.270, p = 0.046), to Δhematocrit (r = 0.514, p = 0.09) and to Δtriglycerides (r = 0.292, p = 0.021).Conclusion. Young women with PCOS presented an increased PV under OC treatment with 35 μg ethinyl estradiol and 2 mg cyproterone acetate.

Mechanical behavior of the erythrocyte in microvessel stenosis

The passage of red blood cells (RBCs) through capillaries is essential for human blood microcirculation. This study used a moving mesh technology that incorporated leader-follower pairs to simulate the fluid-structure and structure-structure interactions between the RBC and a microvessel stenosis. The numerical model consisted of plasma, cytoplasm, the erythrocyte membrane, and the microvessel stenosis. Computational results showed that the rheology of the RBC is affected by the Reynolds number of the plasma flow as well as the surface-to-volume ratio of the erythrocyte. At a constant inlet flow rate, an increased plasma viscosity will improve the transit of the RBC through the microvessel stenosis. For the above reasons, we consider that the decreased hemorheology in microvessels in a pathological state may primarily be attributed to an increase in the number of white blood cells. This leads to the aggregation of RBCs and a change in the blood flow structure. The present fundamental study of hemorheology aimed at providing theoretical guidelines for clinical hemorheology.

The Effect of Chronic Cadmium Toxicity on Blood Pressure and Plasma Viscosity

Cadmium (Cd) is a heavy metal which affects many systems in humans and animals as a consequence of environmental and industrial pollution. The aim of this study was to investigate the effect of chronic Cd toxicity on blood pressure and plasma viscosity. Experimental group rats were given doses that contained 15 ppm CdCl₂ in drinking water for 8 weeks. The systolic blood pressure and heart rate were measured from rats’ tails and recorded by plethysmography every two weeks. Blood samples were drawn, Cd levels were determined by atomic absorption spectrophotometer and plasma viscosity values by viscometer. Blood Cd levels were found to be significantly higher in the experimental group compared to the control group (p < 0.001). The whole blood analysis was made by an analyzer. Polymorphonuclear leukocytes and monocytes increased (p < 0.01) and lymphocyte number (p < 0.05) decreased in the experimental group. Viscosity values were 2.21 ± 0.54 and 1.62 ± 0.31 centipoises in the experimental and control groups, respectively (p < 0.001). In the experimental group, changes in systolic blood pressure between weeks were significant (p < 0.001) and were found to be correlated with plasma viscosity (p < 0.001). In the experimental group, changes in heart rate between weeks were significant (p < 0.001). According to our findings, Cd toxicity may lead to an increase in blood pressure by increasing plasma viscosity.

Lipid and Hematological Parameters in Hyperleptinemic Healthy Arab Male Youth in Jordan

To analyze the influence ofhyperleptinemia on fasting lipid and hematological parameters in healthy Arab male youth in Jordan, this cross-sectional study was carried out in April 2009 on a sample of 120 students aged 18-24 years. Subjects were stratified by fasting leptin into two groups (control, <12.7 ng mL(-1) vs. hyperleptenimic, e_< 12.7 ng mL(-1)) and BMI (normal weight, < 25 kgm(-2) vs. overweight/obese, BMI e_< 25 kg m(-2)). Fasting serum leptin, blood glucose, lipid profile and hematological parameters values were determined by standard kit methods. Mean serum leptin concentrations were more than five times as high in hyperleptenemic subjects than in control subjects (p < 0.001). Compared with control group, significant elevations (p < 0.01) were observed in the means total cholesterol, LDL cholesterol and triglyceride levels of hyperleptenemic group whereas no significant differences was detected in HDL-cholesterol. Except the changes of WBC count, MCH and slightly MCHC, there were no differences between both groups in any other term of hematological parameters. In conclusion, changes in lipid variables and some hematological parameters may increase plasma viscosity as a step during atherosclerosis pathogenesis in male youth at risk for dyslipidemia and cardiovascular diseases. Thus, hyperleptinemia could be a useful index in identifying healthy youth male subjects but this hypothesis needs further investigation.

Effects of posture and ergometer-specific exercise modality on plasma viscosity and plasma fibrinogen: The role of plasma volume changes

The aim of the present study was ascertain the effects posture and exercise modality on the main determinants of blood rheology. Thirteen subjects performed two exercise trials, in random order, at approximately 70% VO(2) max for 45-min. One trial was performed on a motorized treadmill at an intensity corresponding to 70% VO(2) max, while the other was performed on a stationary pike at an intensity corresponding to 70% VO(2) max. In the cycling trial subjects stood for 30-min, followed by sitting for 30-min then cycled for 30-min at 70% VO(2) max. In the treadmill trial, subjects sat for 30-min followed by standing for 30-min then ran on the treadmill for 30-min at 70% VO(2) max. Variations of body postures prior to exercise were associated with opposite changes in plasma volume, plasma viscosity and plasma fibrinogen. When post exercise raw data were not adjusted for plasma volume changes, a significant increase (p < 0.05) in plasma viscosity and plasma fibrinogen was found with no difference between the cycling and running trials. However, the increase in plasma viscosity and fibrinogen were no longer apparent when the raw data post exercises were adjusted for plasma volume changes. Changing body posture from standing to sitting and vice versa were associated with opposite changes in plasma volume and mirrored the changes in plasma viscosity and fibrinogen. In addition, ergometer-specific vigorous exercises at the same relative intensity, irrespective of its modality, transiently increased plasma viscosity and plasma fibrinogen mainly due to exercise-associated haemoconcentration.

Influence of radiographic contrast media (Iodixanol und Iomeprol) on the morphology of human arterial and venous endothelial cells on extracellular matrix in vitro

After intra-arterial administration of radiographic contrast media (RCM), a disorder of the downstream microcirculation both with regard to blood flow velocity in microvessels and to tissue oxygen partial pressure was described. Possible factors contributing to this microcirculatory disorder are increase in plasma viscosity, a formation of echinocytes, a buckling and denudation of endothelial cells, and a disturbation of endothelial prostacyclin release. It is not known so far whether the reactions observed in the context of RCM applications are reactions of venous endothelial cells alone or also of arterial endothelial cells. Therefore, arterial ECs on ECM were exposed to the same RCMs under identical conditions. The decrease of cell-cell contacts with an increase of denuded subendothelial matrix areas in the functionally confluent endothelial cell layer on ECM were more pronounced after a five minute exposure of endothelial cells to Iomeprol compared to Iodixanol. Changes in arterial ECs after the incubation in culture media supplemented with RCM were very subtle in comparison to changes in venous ECs.

Plasma expander viscosity effects on red cell-free layer thickness after moderate hemodilution

The objective of the study was to investigate the effects of plasma viscosity after hemodilution on the thickness of the erythrocyte cell free layer (CFL) and on the interface between the flowing column of erythrocytes and the vascular endothelium. The erythrocyte CFL thickness was measured in the rat cremaster muscle preparation. Plasma viscosity was modified in an isovolemic hemodilution, in which the systemic hematocrit (Hctsys) was lowered to 30%. The plasma expanders (PE) of similar nature and different viscosities were generated by glutaraldehyde polymerization of human serum albumin (HSA) at various molar ratios glutaraldehyde to HSA: (i) unpolymerized HSA; (ii) PolyHSA24:1, molar ratio = 24 and (iii) PolyHSA60:1, molar ratio = 60. The HSA viscosities determined at 200 s(-1) were 1.1, 4.2 and 6.0 dyn x cm(-2), respectively. CFL thickness, vessel diameter and blood flow velocity were measured, while volumetric flow, shear rate and stress were calculated. Hemodilution with PolyHSA60:1 increased plasma viscosity and the blood showed marked shear thinning behavior. CFL thickness decreased as plasma viscosity increased after hemodilution; thus the CFL thickness with HSA and PolyHSA24:1 increased compared to baseline. Conversely, the CFL thickness of PolyHSA60:1 was not different from baseline. Blood flow increased with both PolyHSA's compared to baseline. Wall shear rate and shear stress increased for PolyHSA60:1 compared to HSA and PolyHSA24:1, respectively. In conclusion, PE viscosity determined plasma viscosity after hemodilution and affected erythrocyte column hydrodynamics, changing the velocity profile, CFL thickness, and wall shear stress. This study relates the perfusion caused by PolyHSA60:1 to hemodynamic changes induced by the rheological properties of blood diluted with PolyHSA60:1.

Microcirculation and blood rheology in patients with cerebrovascular disorders

We estimated hemorheological parameters of vein blood samples and cutaneous microvascular blood flow in patients with acute ischemic stroke and in controls. The worsened blood rheological properties were registered in patients with stroke: the enhanced whole blood viscosity was due to the substantial increase of plasma viscosity and the impairment of microrheological blood properties: elevated erythrocyte aggregability and decreased deformability compared to the healthy group. The decrease of oxygen consumption fixed by rheological methods and by laser Doppler flowmetry led us to conclude that the tissue hypoxia took place in patients with stroke. The regulatory mechanisms aimed to maintain blood supply to tissue were activated under cerebral infarction and the impact of unfavorably changed rheological blood properties was markedly enhanced. Revealed close interrelations between rheological and microcirculation parameters testified the important role of hemorheological factors in maintenance of microvascular blood flow and oxygen delivery to tissue.

Effect of changes in the intravascular volume during hemodialysis on blood viscoelasticity

Adoption of high rate of ultrafiltration (UF) during hemodialysis (HD) may affect the hemorhelogical blood profile, by changing Hematocrit (Hct) and the concentration of plasma proteins, which may in turn interfere with tissue perfusion. The aim of this work is to examine the effect of acute volume change during dialysis on the hemorheological variables. The study included 21 hemodialysis patients. Hematocrit (Hct) and percent decrease in blood volume (BV) were recorded by blood volume monitor. Blood samples were taken before and at the end of dialysis, for measuring plasma fibrinogen and haemorheological variables, which included blood viscosity, plasma viscosity, red cells elasticity and aggregation. The UF volume was 3.52±1.54 L. Hct increased from 34.2±6.1 to 42.1±7.3% (P<0.001), and blood volume (BV) decreased to 85.5±6.4% (P<0.001). Blood and plasma viscosity significantly increased from 3.28±0.69 to 5.48±0.85 mPa.s (P<0.001), and from 1.24 ± 0.16 to 1.65±0.24 mPa.s (P<0.001), respectively. Changes in plasma viscosity were correlated to changes in plasma fibrinogen (r=0.63, P<0.05), while the increase in blood viscosity was correlated to the percent reduction in blood volume (r=0.85, P<0.005). Red cells elasticity increased from 0.26±0.12 to 0.48±0.18 mPa.s (P<0.05), and the aggregation index rose from 0.86±0.31 to 1.25±0.26 (P<0.01). This combination of increased plasma viscosity and red cell aggregability may lower the velocity of erythrocyte transfer inside the tissue capillaries after HD, which may affect tissue perfusion. Moreover, increased elasticity may require more energy from the heart to disaggregate the cells, and this may induce problems in the patients with cardiac dysfunction. In conclusion, the hemorheological variables change after dialysis in the direction which may impede the flow inside the microvessels.

Hemorheological profile in primary Sjögren's syndrome: A case-control study

Rheological blood behavior in primary Sjögren's syndrome (SS) has been scarcely investigated. We evaluated the rheological profile (blood viscosity, plasma viscosity, erythrocyte deformability, erythrocyte aggregation, erythrocyte aggregation time and erythrocyte disaggregation threshold) along with fibrinogen, high-sensitive C reactive protein, plasma lipids, immunoglobulins, total proteins and erythrocyte sedimentation rate in 22 patients with primary SS (2 males, 20 females, aged 58 ± 9 years) and in 22 healthy volunteers (3 males, 19 females, aged 57 ± 5 years). Patients showed statistically higher plasma viscosity, erythrocyte sedimentation rate and G immunoglobulin (IgG) levels and lower total cholesterol than controls (p = 0.006, p = 0.023, p = 0.034, p = 0.036, respectively). Three patients with extraglandular involvement showed the highest plasma viscosity values: 1.98 cP, 1.70 cP and 1.65 cP, respectively. No differences were observed for the other rheological parameters analyzed. In a multivariate regression analysis, only fibrinogen, triglycerides and IgG were independent determinants for plasma viscosity values (beta coefficient: 0.335; p = 0.001; beta coefficient: 0.242; p = 0.019; beta coefficient: 0.660; p < 0.001, respectively). Our results indicate that patients with primary SS show increased plasma viscosity, mostly related with IgG levels without other alterations in the rheological profile. Further research with a larger sample size achieved by multicenter studies would be desirable.