Determinant Of Blood Viscosity Research Articles

Hormonal Control of Blood Viscosity.

The hemodynamic milieu differs throughout the vascular tree because of varying vascular geometry and blood velocities.Accordingly, the risk of turbulence, which is dictated by the Reynolds and Dean numbers, also varies. Relatively high blood viscosity is needed to prevent turbulence in the left ventricle and aorta, where high-velocity blood changes direction several times. Low blood viscosity is needed in the capillaries, where erythrocytes pass through vessels with a diameter smaller than their own. In addition, higher blood viscosity is necessary when the cardiac output and peak blood velocity increase as a part of a sympathetic response or anemia, which occurs following significant hemorrhage. Blood viscosity, as reflected in systemic vascular resistance and vascular wall shear stress, is sensed, respectively, by cardiomyocyte stretching in the left ventricle and mechanoreceptors for wall shear stress in the carotid sinus.By controlling blood volume and red blood cell mass, the renin-aldosterone-angiotensin system and the systemic vascular resistance response control the hematocrit, the strongest intrinsic determinant of blood viscosity. These responses provide gross control of blood viscosity. Fine-tuning of blood viscosity in transient conditions is provided by hormonal control of erythrocyte deformability. The short half-life of some of these hormones limits their activity to specific vascular beds. Hormones that modulate blood viscosity include erythropoietin, angiotensin II, brain natriuretic factor, epinephrine, prostacyclin E2, antidiuretic hormone, and nitric oxide.

Blood Viscosity in Subjects With Type 2 Diabetes Mellitus: Roles of Hyperglycemia and Elevated Plasma Fibrinogen.

The viscosity of blood is an indicator in the understanding and treatment of disease. An elevated blood viscosity has been demonstrated in patients with Type 2 Diabetes Mellitus (T2DM), which might represent a risk factor for cardiovascular complications. However, the roles of glycated hemoglobin (HbA1c) and plasma fibrinogen levels on the elevated blood viscosity in subjects with T2DM at different chronic glycemic conditions are still not clear. Here, we evaluate the relationship between the blood viscosity and HbA1c as well as plasma fibrinogen levels in patients with T2DM. The experimental data show that the mean values of the T2DM blood viscosity are higher in groups with higher HbA1c levels, but the correlation between the T2DM blood viscosity and the HbA1c level is not obvious. Instead, when we investigate the influence of plasma fibrinogen level on the blood viscosity in T2DM subjects, we find that the T2DM blood viscosity is significantly and positively correlated with the plasma fibrinogen level. Further, to probe the combined effects of multiple factors (including the HbA1c and plasma fibrinogen levels) on the altered blood viscosity in T2DM, we regroup the experimental data based on the T2DM blood viscosity values at both the low and high shear rates, and our results suggest that the influence of the elevated HbA1c level on blood viscosity is quite limited, although it is an important indicator of glycemic control in T2DM patients. Instead, the elevated blood hematocrit, the enhanced red blood cell (RBC) aggregation induced by the increased plasma fibrinogen level, and the reduced RBC deformation play key roles in the determination of blood viscosity in T2DM. Together, these experimental results are helpful in identifying the key determinants for the altered T2DM blood viscosity, which can be used in future studies of the hemorheological disturbances of T2DM patients.

Quantitative Monitoring of Dynamic Blood Flows Using Coflowing Laminar Streams in a Sensorless Approach

Determination of blood viscosity requires consistent measurement of blood flow rates, which leads to measurement errors and presents several issues when there are continuous changes in hematocrit changes. Instead of blood viscosity, a coflowing channel as a pressure sensor is adopted to quantify the dynamic flow of blood. Information on blood (i.e., hematocrit, flow rate, and viscosity) is not provided in advance. Using a discrete circuit model for the coflowing streams, the analytical expressions for four properties (i.e., pressure, shear stress, and two types of work) are then derived to quantify the flow of the test fluid. The analytical expressions are validated through numerical simulations. To demonstrate the method, the four properties are obtained using the present method by varying the flow patterns (i.e., constant flow rate or sinusoidal flow rate) as well as test fluids (i.e., glycerin solutions and blood). Thereafter, the present method is applied to quantify the dynamic flows of RBC aggregation-enhanced blood with a peristaltic pump, where any information regarding the blood is not specific. The experimental results indicate that the present method can quantify dynamic blood flow consistently, where hematocrit changes continuously over time.

Red Blood Cells and Hemoglobin in Human Atherosclerosis and Related Arterial Diseases.

As the main particulate component of the circulating blood, RBCs play major roles in physiological hemodynamics and impact all arterial wall pathologies. RBCs are the main determinant of blood viscosity, defining the frictional forces exerted by the blood on the arterial wall. This function is used in phylogeny and ontogeny of the cardiovascular (CV) system, allowing the acquisition of vasomotricity adapted to local metabolic demands, and systemic arterial pressure after birth. In pathology, RBCs collide with the arterial wall, inducing both local retention of their membranous lipids and local hemolysis, releasing heme-Fe++ with a high toxicity for arterial cells: endothelial and smooth muscle cells (SMCs) cardiomyocytes, neurons, etc. Specifically, overloading of cells by Fe++ promotes cell death. This local hemolysis is an event associated with early and advanced stages of human atherosclerosis. Similarly, the permanent renewal of mural RBC clotting is the major support of oxidation in abdominal aortic aneurysm. In parallel, calcifications promote intramural hemorrhages, and hemorrhages promote an osteoblastic phenotypic shift of arterial wall cells. Different plasma or tissue systems are able, at least in part, to limit this injury by acting at the different levels of this system.

Leg electrical resistance predicts venous blood viscosity and hematocrit.

We previously reported that whole body bioelectrical impedance analysis (BIA) measurements are correlated to some hemorheologic factors, suggesting a relationship between viscosity factors and electric properties of flowing blood not only in vitro but also in vivo. Recently we reported that with segmental BIA (analyzing the body considered as composed of 5 cylinders) predictive equations for various determinants of blood viscosity were closer than for the wole body. Another widely used BIA technique uses leg-to-leg impedance measurements so that two cylinders (the two legs) are analyzed. We investigated whether impedance measured with this technique (Tanita TBF-300) is also a predictor of blood viscosity factors. From viscometric measurements performed on venous blood drawn in recreative athletes over the range of shear rates 1 to 6000 s-1 (RHEOMETRE Anton Paar CP 50-1), we found a correlation between leg-leg resistance at 50 kHz (Rx[50 kHz]) and blood viscosity at 1000 s-1 (η1000= 0.0051 Rx[50 kHz] + 1.3265; r = 0.521 p = 0.028 yielding a prediction of η1000 (Bland Altman plot: bias 0.05 [RANGE - 0.24; 0.34]. Neither plasma viscosity nor the red cell rheology index «k» of Quemada's model are correlated with Rx[50 kHz], but hematocrit (Hct) does (Hct (%) = 0.0217 Rx[50 kHz] + 33.783; r = 0.480 p = 0.044) yielding a prediction of Hct (Bland Altman plot: bias - 0.11, [range - 1.67; 1.45]. The discrepancy between actual and predicted Hct is also correlated with resistance at 50 kHz (r = 0.575 p = 0.031) as does the discrepancy between actual and predicted Hct/viscosity ratio (r = -0.651 p = 0.006). Therefore, as other previously studied methods, leg to leg BIA predicts viscosity, suggesting that blood rheology may influence the passage of an electric current in the legs.

Seeking the optimal hematocrit: May hemorheological modelling provide a solution?

Hematocrit increases during exercise and is usually decreased after regular training. However the interpretation of these facts is ambiguous since hematocrit is both a determinant of oxygen supply and the major determinant of blood viscosity. Classically hematocrit was assumed to impair blood flow, but it has been evidenced to exert a biphasic effect on it. In order to cope with these two apparently opposite effects of hematocrit, hemorheologists have proposed the concept hematocrit/viscosity ratio (h/η). This h/η ratio is related to tissue oxygenation in vascular diseases (eg, POAD) but not in healthy subjects. h/η displays a bell-shaped curve as a function of hematocrit and the hematocrit value corresponding to the maximal h/η can be assumed to be a theoretically optimal hematocrit. We propose to analyse exercise-related alterations in hematocrit according to this theoretical approach, viscosity at high shear rate being reconstructed with Quemada's equation from actual plasma viscosity and red cell rigidity at various hematocrit levels. While theoretical and actual h/η are fairly correlated in athletes both before and after exercise, actual hematocrit is lower at rest and higher after exercise compared to the theoretical one. The main statistic correlate of these discrepancies between actual and predicted hematocrit is red cell rigidity. Submaximal exercise acutely decreases the h/η ratio (despite increasing both hematocrit and viscosity). This change is well predicted by the model and there is a strong correlation between predicted and actual h/η ratio. Endurance training tends to increase h/η and to reduce the discrepancy between predicted and actual hematocrit. Accordingly trained athletes have a higher h/η (both model-predicted and actual) than sedentary subjects, and a lower hematocrit, this lowering being rather correlated to training volume than to fitness improvement. On the whole, this approach suggests that homeostatic "viscoregulation" in athletes results in a fine tuning of h/η which seems to be a closely regulated parameter. Hematocrit alterations in this context are an adaptation involved in this regulation.

Hemorheological properties in patients with type-1 and type-2 diabetes mellitus

The hemorheologic disorders, which are potentially deleterious in a wide range of pathologies, were studied in patients with type-1 and type-2 diabetes mellitus. The significant determinants of blood viscosity, red blood cells (RBC) deformability and RBC reversible aggregation were assessed by ektacytometry and by laser backscattering technique, respectively. For both types of the disease, we observed acceleration of the first phase of RBC aggregation that contrasted with its deceleration at the second phase. The hydrodynamic stability of the aggregates, especially the smallest ones, exceeded the normal values in both cases. The influence of GP IIb/IIIa receptor inhibitor, monafram on RBC aggregation and disaggregation was the same in the cases of patients and normal subjects. The maximal shear induced RBC stretching exceeded the normal one in patients of both groups. The data reveal not only pathological but also compensatory character of hemorheological alterations in patients with type-1 and type-2 diabetes mellitus.

Correlation between blood rheological properties and red blood cell indices(MCH, MCV, MCHC) in healthy women.

Structure and mechanical properties of red blood cells are markedly influenced by pathophysiology of many diseases which in turn potentially impair microcirculatory blood flow. The physiological association between blood rheological parameters and red blood cell indices was investigated in otherwise healthy unselected mid-age women prior to elective gynaecological surgery. Red Blood Cell-deformability (RBC 1.2, 3.0; 6.0, 12.0; 30.0, 60.0) during exposure to low (RBC 1.2, 3.0), moderate (RBC 16.0, 12.0) and high shear forces (RBC 30.0, 60.0; Rheodyn; Myrenne), -aggregation (MA1; Myrenne) during low shear (E1; 4-1 S) and in stasis (E0) and plasma viscosity (Pv; KSV 1; Fresenius) were correlated with red blood cell indices (RBC-I: MCV, MCH and MCHC) and subjects' characteristics in 286 healthy women the day before undergoing gynaecologic standard surgery. Women with known pregnancy, malign-, infective-, chronic-disease or extreme BMI (<16; >40 Kg/m2) were excluded from this trial. From June 2014 to December 2014 a total of 286 healthy women (age: 46.5±17.6 y; BMI: 25.5±5.2 kg/m2) were eligible for inclusion into this prospective evaluation. Pv (mean±SD: 1.17±0.12 mPa s) and RBC aggregation (E0:12.6±6.3; E1:17.9±7.3) were not significantly correlated with RBC-I but with age and BMI. In contrast, RBC-deformability correlated significantly with MCV and MCH but significantly inversely correlated with MCHC. Deformability significantly increased with age but was unaffected by BMI of women. The correlation between RBC-I and RBC deformability was most remarkable during moderate shear force exposure. Neither haemoglobin nor haematocrit were correlated with RBC deformability or RBC-I. Cell volume and haemoglobin content had a strong impact on deformability in apparently healthy mid age women, whereas low MCHC and large MCV were associated with an increase in deformability while high MCHC and small MCV correlated with increased rigidity of RBC. BMI had no impact on deformability while age was associated with an increase in all determinants of blood viscosity. RBC aggregability was not affected by MCV, MCHC or MCH in mid-age women.

Are overall adiposity and abdominal adiposity separate or redundant determinants of blood viscosity?

In line with recent literature showing that both general adiposity and abdominal adiposity are independently associated with the risk of death, we recently reported that body mass index (BMI) and waist-to hip ratio (WHR) were independent predictors of blood viscosity, related to different determinants of viscosity (for BMI: plasma viscosity and red cell aggregation; for WHR: hematocrit). Since this report was challenged by a study showing that abdominal adiposity (as measured with waist circumference WC and not WHR) is the only independent determinant of viscosity, we re-assessed on our previous database correlations among viscosity factors, BMI, WHR and WC. Blood viscosity was correlated to BMI (r = 0.155 p = 0.004), WHR (r = 0.364; p = 0.027) and WC (r = 0.094; p = 0.05). Hematocrit was correlated to WHR (r = 0.524) but neither to BMI (r =-0.021) nor waist circumference (r = 0.053). WC was correlated with plasma viscosity (r = 0.154; p = 0.002) while WHR was not (r =-0.0102 NS). A stepwise regression analysis selected two determinants of whole blood viscosity at high shear rate: BMI (p = 0.0167) and WC (p = 0.0003) excluding WHR. Therefore, in this sample, abdominal fatness expressed by WC and whole body adiposity remain independent determinants of blood viscosity. WHR and WC have not the same meaning, WC measuring the size of abdominal fat while WHR measuring the shape of body distribution regardless the degree of fat excess. Interestingly, hematocrit is rather related to shape (even within a normal range of body size) than the extent of abdominal fatness, and is not related to whole body adiposity.

Dynamics of blood viscosity regulation during hypoxic challenges in the chicken embryo (Gallus gallus domesticus)

Hypoxia in chicken embryos increases hematocrit (Hct), blood O2 content, and blood viscosity. The latter may limit O2 transport capacity (OTC) via increased peripheral resistance. Hct increase may result from increased nucleated red blood cell concentration ([RBC]) and mean corpuscular volume (MCV) or reduced plasma volume. We hypothesized changes in Hct, hemoglobin concentration ([Hb]), [RBC] and MCV and their effects on viscosity would reduce OTC. Five experimental treatments that increase Hct were conducted on day 15 embryos: 60min water submergence with 60min recovery in air; exposure to 15% O2 with or without 5% CO2 for 24 h with 6 h recovery; or exposure to 10% O2 with or without 5% CO2 for 120 min with 120 min recovery. Control Hct, [Hb], [RBC], MCV, and viscosity were approximately 26%, 9g%, 2.0 106μL−1, 130μm3, and 1.6mPas, respectively. All manipulations increased Hct and blood viscosity without changing blood osmolality (276mmolkg−1). Increased viscosity was attributed to increased [RBC] and MCV in submerged embryos, but solely MCV in embryos experiencing 10% O2 regardless of CO2. Blood viscosity in embryos exposed to 15% O2 increased via increased MCV alone, and viscosity was constant during recovery despite increased [RBC]. Consequently, blood viscosity was governed by MCV and [RBC] during submergence, while MCV was the strongest determinant of blood viscosity in extrinsic hypoxia with or without hypercapnia. Increased Hct and blood O2 content did not compensate for the effect of increased viscosity on OTC during these challenges.

Hemoglobin, hematocrit, and changes in cerebral blood flow: the Second Manifestations of ARTerial disease-Magnetic Resonance study

Hemoglobin and hematocrit are important determinants of blood viscosity and arterial oxygen content and may therefore influence cerebral blood flow (CBF). We examined cross-sectional and prospective associations of hemoglobin and hematocrit with CBF in 569 patients with manifest arterial disease (mean age 57 ± 10 years) with available data on magnetic resonance angiography to measure parenchymal CBF. Mean (SD) parenchymal CBF at baseline was 52.3 (9.8) mL/min/100 mL and decreased with 1.5 (11.0) mL/min/100 mL after on average 3.9 years of follow-up. Linear regression analyses showed that greater hemoglobin and hematocrit values were associated with lower baseline parenchymal CBF and more decline in parenchymal CBF over time, independent of cardiovascular risk factors, use of antiplatelet drugs, anticoagulants, or diuretics, and brain measures: adjusted mean differences (95% confidence interval [CI]) in decline in parenchymal CBF between patients in the lower and upper quartiles of hemoglobin and hematocrit were −2.48 (95% CI −3.70 to −1.25) and −3.69 (95% CI −5.45 to −1.94) mL/min/100 mL. Higher hemoglobin and hematocrit were associated with lower baseline parenchymal CBF and a greater decline in parenchymal CBF over time, possibly as a result of physiological compensating mechanisms.

Blood rheology and aging.

The flow properties of blood play significant roles in tissue perfusion by contributing to hydrodynamic resistance in blood vessels. These properties are influenced by pathophysiological processes, thereby increasing the clinical relevance of blood rheology information. There is well-established clinical evidence for impaired blood fluidity in humans of advanced age, including enhanced plasma and whole blood viscosity, impaired red blood cell (RBC) deformability and enhanced RBC aggregation. Increased plasma fibrinogen concentration is a common finding in many studies owing to the pro-inflammatory condition of aged individuals; this finding of increased fibrinogen concentration explains the higher plasma viscosity and RBC aggregation in elderly subjects. Enhanced oxidant stress in advanced age is also known to contribute to altered blood fluidity, with RBC deformability being an important determinant of blood viscosity. Several studies have shown that physical activity may improve the hemorheological picture in elderly subjects, yet well-designed observational and mechanistic studies are required to determine the specific effects of regular exercise on hemorheological parameters in healthy and older individuals.

Exercise hemorheology: Classical data, recent findings and unresolved issues

The present review focuses on the past and recent knowledge in the field of exercise hemorheology and presents some unresolved issues for opening discussion. Acute exercise is associated with a rise in hematocrit which results in an increase in blood viscosity. Whereas increased blood viscosity was previously viewed as having negative consequences for cardiovascular function and aerobic performance, recent findings suggest dynamic changes in blood viscosity might be useful for vascular function during exercise by increasing nitric oxide production. Other determinants of blood viscosity are altered by exercise (e.g., decreased red blood cell deformability, increased red blood cell aggregation and plasma viscosity) and may, independent of the associated effect on blood viscosity, directly modulate aerobic capacity. However, the data published on the effects of exercise on the hemorheology are not consistent, with some studies showing decreased, unchanged, or increased red blood cell deformability/aggregation when compared with rest. These discrepancies seem to be related to the exercise protocol investigated, the population tested or the methodogy utilized for hemorheological measurements. Finally, this review focuses on the effects of exercise training (i.e. chronic physical activity) on the hemorheological profile of healthy individuals and patients with cardiovascular and metabolic disorders.

On-line blood viscosity monitoring in vivo with a central venous catheter, using electrical impedance technique

Blood viscosity is an important determinant of microvascular hemodynamics and also reflects systemic inflammation. Viscosity of blood strongly depends on the shear rate and can be characterized by a two parameter power-law model. Other major determinants of blood viscosity are hematocrit, level of inflammatory proteins and temperature. In-vitro studies have shown that these major parameters are related to the electrical impedance of blood. A special central venous catheter was developed to measure electrical impedance of blood in-vivo in the right atrium. Considering that blood viscosity plays an important role in cerebral blood flow, we investigated the feasibility to monitor blood viscosity by electrical bioimpedance in 10 patients during the first 3 days after successful resuscitation from a cardiac arrest. The blood viscosity–shear rate relationship was obtained from arterial blood samples analyzed using a standard viscosity meter. Non-linear regression analysis resulted in the following equation to estimate in-vivo blood viscosity (Viscosityimp) from plasma resistance (Rp), intracellular resistance (Ri) and blood temperature (T) as obtained from right atrium impedance measurements:Viscosityimp=(−15.574+15.576RpT)SR (−.138RpT−.290Ri). This model explains 89.2% (R2=.892) of the blood viscosity–shear rate relationship. The explained variance was similar for the non-linear regression model estimating blood viscosity from its major determinants hematocrit and the level of fibrinogen and C-reactive protein (R2=.884). Bland–Altman analysis showed a bias between the in-vitro viscosity measurement and the in-vivo impedance model of .04mPas at a shear rate of 5.5s−1 with limits of agreement between −1.69mPas and 1.78mPas. In conclusion, this study demonstrates the proof of principle to monitor blood viscosity continuously in the human right atrium by a dedicated central venous catheter equipped with an impedance measuring device. No safety problems occurred and there was good agreement with in-vitro measurements of blood viscosity.

Optimal hematocrit: a Procrustean bed for maximum oxygen transport rate?

physiological systems are characterized by multiple interdependent components that collectively subserve various processes and functions. In seeking better understanding of the performance of such complex systems, we must identify and evaluate alternative ways and operating schemes, comparing their

Estimation of Scatterer Diameter by Normalized Power Spectrum of High-Frequency Ultrasonic RF Echo for Assessment of Red Blood Cell Aggregation

Red blood cell (RBC) aggregation, as one of the determinants of blood viscosity, plays an important role in blood rheology, including the condition of blood. RBC aggregation is induced by the adhesion of RBCs when the electrostatic repulsion between RBCs weakens owing to increases in protein and saturated fatty acid levels in blood, excessive RBC aggregation leads to various circulatory diseases. This study was conducted to establish a noninvasive quantitative method for assessment of RBC aggregation. The power spectrum of ultrasonic RF echoes from nonaggregating RBCs, which shows the frequency property of scattering, exhibits Rayleigh behavior. On the other hand, ultrasonic RF echoes from aggregating RBCs contain the components of reflection, which have no frequency dependence. By dividing the measured power spectrum of echoes from RBCs in the lumen by that of echoes from a posterior wall of the vein in the dorsum manus, the attenuation property of the propagating medium and the frequency responses of transmitting and receiving transducers are removed from the former spectrum. RBC aggregation was assessed by the diameter of a scatterer, which was estimated by minimizing the square difference between the measured normalized power spectrum and the theoretical power spectrum. In this study, spherical scatterers with diameters of 5, 11, 15, and 30 µm were measured in basic experiments. The estimated scatterer diameters were close to the actual diameters. Furthermore, the transient change of the scatterer diameters were measured in an in vivo experiment with respect to a 24-year-old healthy male during the avascularization using a cuff. The estimated diameters (12–22 µm) of RBCs during avascularization were larger than the diameters (4–8 µm) at rest and after recirculation. These results show the possibility of the use of the proposed method for noninvasive assessment of RBC aggregation.

Blood rheology and body composition as determinants of exercise performance in female rugby players

Athletes involved in rugby are characterized by a very specific pattern of body composition with an unusually important muscle mass. In a preceding study about rugbymen we evidenced that they exhibit a correlation between red blood cell aggregability and the amount of body fat although it remains within a normal range, and that red cell rigidity was correlated to isometric adductor strength. We had the opportunity of studying the relationships among exercise performance, body composition and hemorheology in 19 female rugby players (age 19-26, mean: 24.47 ± 0.67 yr) practising 4 - 10 hr/wk (mean 7.15 ± 0.3) since 1-12 yr (mean 4,05 ± 0,694). VO2max was not related by its own to blood rheology, either hematocrit (r = -0.0717 p = 0.7706) or plasma viscosity (r = 0.0144; p = 0.9533), but other markers of performance exhivited a correlation with red cell rheology. Relationships between fitness and body composition were evidenced. Isometric handgrip strength was negatively correlated to red blood cell aggregability (Myrenne M, r = -0.57839; p = 0.00948 M1 r = -0.58910; p = 0.00795). Adductor isometric strength was negatively correlated to red blood cell aggregability Myrenne M (r = -0.5033; p = 0.0280) but not to M1 (r = -0.4227; p = 0.0714). Fat mass is a major determinant of the maximal oxygen consumption VO2max either measured by a field test (r = -0.766; p = 0.00013) or exercise test (r = -0.575; p = 0.00994) and was also negatively correlated to both handgrip (r = -0.4918; p = 0.0325) and RBC aggregability M (r = -0.57839; p = 0.00948 and M1 r = -0.5891; p = 0.00795). Independently of fat mass, FFM appears to be a determinant of blood viscosity (r = 0.4622; p = 0.0463) due to its correlation with RBC rigidity (r = 0.4781; p = 0.0384). Thus, trained young women exercising 4-10 hr/wk and thus exhibiting a low percentage of body fat exhibit clear relationships between body composition and hemorheology, but fat mass being low, the parameter correlated with blood rheology is in this case fat-free mass, consistent with recent findings indicating that high fat mass in women is sometimes correlated with parameters of the metabolic syndrome such as insulin resistance or inflammation. In addition, parameters quantifying fatness even within such a physiological range are in this sample negatively related with exercise performance.

Effects of Work Place Carbon Monoxide Exposure on Blood Viscosity

ABSTRACT Both blood viscosity and carbon monoxide (CO) has been associated with cardiovascular diseases (CVDs). In order to investigate the effects of chronic low-level CO exposure on the determinants of blood viscosity (hematocrit, plasma viscosity, erythrocyte deformability, and erythrocyte aggregation), 10 men exposed to CO at work for at least 6 months and 10 healthy controls were included in the study. Plasma viscosity was determined by a cone-plate viscometer, erythrocyte deformability and erythrocyte aggregation by laser-assisted optical rotational cell analyzer. Mean plasma viscosity of the group exposed to CO (1.4 ± 0.1 mPa·sn) was significantly higher than that of the controls (1.2 ± 0.06 mPa·sn) (p < .05). Plasma fibrinogen level of the CO group (275 ± 11 mg/dL) was slightly higher than that of the controls (263 ± 14 mg/dL). The rise in plasma viscosity by chronic low-level CO exposure may be the mechanism of CO-induced increase in the risk for CVDs.

A genetic variant in the gene encoding fibrinogen beta chain predicted development of hypertension in Chinese men

Fibrinogen, a major determinant of blood viscosity, is an acute phase protein associated with cardiovascular disease. We studied the association of hypertension with single nucleotide polymorphisms (SNPs) in the gene encoding the fibrinogen beta chain (FGB). Three tagging SNPs (rs1025154, rs4220 and rs1044291) were selected from the HapMap database on Han Chinese. Genotypes were determined in 1,294 unrelated subjects from the Hong Kong Cardiovascular Risk Factor Prevalence Study cohort. There were 199 hypertensive subjects at baseline. Among 1,095 subjects normotensive at baseline, 178 developed hypertension during a median follow-up period of 6.4 years. Among the three tagging SNPs, rs4220 showed significant association with hypertension at both baseline (odds ratio [OR]=1.49, p=0.004) and at follow-up (OR=1.32, p=0.013). The minor A allele of this SNP was associated with higher plasma fibrinogen level (beta=0.144, p<0.001 at baseline and beta=0.130, p<0.001 at follow-up). Among subjects normotensive at baseline, this SNP was also associated with the development of hypertension in men (OR=1.52, p=0.022), but not in women. The SNP rs4220 in FGB , which leads to the substitution of arginine by lysine at position 448, is independently associated with plasma fibrinogen level and hypertension in Hong Kong Chinese. This suggests a possible causal role of fibrinogen in hypertension development, especially in men.

Estimation of Scatterer Diameter Using Ultrasonic Backscattering Property for Assessment of Red Blood Cell Aggregation

Red blood cell (RBC) aggregation, a determinant of blood viscosity, plays an important role in blood flow rheology. RBC aggregation is induced by the adhesion of RBCs when the electrostatic repulsion between RBCs weakens owing to increases in protein and saturated fatty acid levels in blood, and excessive RBC aggregation may lead to various circulatory diseases. This study was conducted to establish a noninvasive quantitative method for the assessment of RBC aggregation. The spectrum of nonaggregating RBCs presents Rayleigh behavior, indicating that the power of a scattered wave is proportional to the fourth power of frequency. By dividing the measured power spectrum of echoes from scatterers by that from a silicone plate reflector, the frequency responses of transmitting and receiving transducers are removed from the former spectrum. This normalized power spectrum changes linearly with respect to logarithmic frequency. In non-Rayleigh scattering, on the other hand, the spectral slope decreases because a larger scatterer behaves as a reflector and echoes from a reflector do not show frequency dependence. Therefore, it is possible to assess RBC aggregation using the spectral slope value. In this study, spherical scatterers with diameters of 5, 11, 15, and 30 µm were measured in basic experiments. The spectral slope of the normalized power spectrum of echoes from the lumen of the vein in the dorsum manus of a 24-year-old healthy male was close to that from microspheres with a diameter of 15 µm, and the typical RBC diameter was smaller than this value. The frequency-dependent attenuation of ultrasound during propagation in a biomedical tissue was considered to be one reason for this. Furthermore, during avascularization, the slope gradually decreased owing to the aggregation of RBCs. These results show the possibility of using the proposed method for the noninvasive assessment of RBC aggregation.