Microviscometry reveals reduced blood viscosity and altered shear rate and shear stress profiles in microvessels after hemodilution

Long, David S.; Smith, Michael L.; Pries, Axel R.; Ley, Klaus; Damiano, Edward R.

doi:10.1073/pnas.0402937101

Cited by 180 publications

(224 citation statements)

References 35 publications

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“…The effects of non-Newtonian property on the flow distribution in large arteries have been investigated and some studies show dramatic effects (Gijsen et al 1999a,b) while others report a small effect limited to a fraction of the cardiac cycle (Perktold et al 1991;Johnston et al 2004). When the shear rates are higher than 50 or 100 s 21 (Long et al 2004;Fischer et al 2007), blood can be treated as a Newtonian fluid with constant viscosity. In our simulations, we assumed that the physiological flow rates in the ICA are in the range 200-250 ml min 21 , which gives an average velocity in the range of 0.265 -0.331 m s 21 .…”

Section: Discussionmentioning

confidence: 99%

Flow instability and wall shear stress variation in intracranial aneurysms

Baek

Jayaraman

Richardson

et al. 2009

J. R. Soc. Interface.

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We investigate the flow dynamics and oscillatory behaviour of wall shear stress (WSS) vectors in intracranial aneurysms using high resolution numerical simulations. We analyse three representative patient-specific internal carotid arteries laden with aneurysms of different characteristics: (i) a wide-necked saccular aneurysm, (ii) a narrower-necked saccular aneurysm, and (iii) a case with two adjacent saccular aneurysms. Our simulations show that the pulsatile flow in aneurysms can be subject to a hydrodynamic instability during the decelerating systolic phase resulting in a high-frequency oscillation in the range of 20-50 Hz, even when the blood flow rate in the parent vessel is as low as 150 and 250 ml min 21 for cases (iii) and (i), respectively. The flow returns to its original laminar pulsatile state near the end of diastole. When the aneurysmal flow becomes unstable, both the magnitude and the directions of WSS vectors fluctuate at the aforementioned high frequencies. In particular, the WSS vectors around the flow impingement region exhibit significant spatio-temporal changes in direction as well as in magnitude.

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Section: Discussionmentioning

confidence: 99%

Flow instability and wall shear stress variation in intracranial aneurysms

Baek

Jayaraman

Richardson

et al. 2009

J. R. Soc. Interface.

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“…A least squares method is then applied to determine three unknown parameters (A a , A b , and k Blood ) in Eq. (10). The characteristic time (k Blood ) can be calculated from the three parameters.…”

Section: B Analytical Regression Formulae Based On the Linear Viscoementioning

confidence: 99%

“…9 Furthermore, the viscosity of blood is altered depending on the chemical and biological functions of red blood cells (RBCs). 10 Therefore, viscosity has been clinically used to monitor patients with cardiovascular diseases (CVDs). On the other hand, the elasticity of blood, which is influenced by cytoskeleton and integral proteins and has been neglected in steady blood flows, has an influence on pulsatile blood flows in arteries and arterioles.…”

Section: Introductionmentioning

confidence: 99%

Blood viscoelasticity measurement using steady and transient flow controls of blood in a microfluidic analogue of Wheastone-bridge channel

Kang

Lee

2013

Biomicrofluidics

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Accurate measurement of blood viscoelasticity including viscosity and elasticity is essential in estimating blood flows in arteries, arterials, and capillaries and in investigating sub-lethal damage of RBCs. Furthermore, the blood viscoelasticity could be clinically used as key indices in monitoring patients with cardiovascular diseases. In this study, we propose a new method to simultaneously measure the viscosity and elasticity of blood by simply controlling the steady and transient blood flows in a microfluidic analogue of Wheastone-bridge channel, without fully integrated sensors and labelling operations. The microfluidic device is designed to have two inlets and outlets, two side channels, and one bridge channel connecting the two side channels. Blood and PBS solution are simultaneously delivered into the microfluidic device as test fluid and reference fluid, respectively. Using a fluidic-circuit model for the microfluidic device, the analytical formula is derived by applying the linear viscoelasticity model for rheological representation of blood. First, in the steady blood flow, the relationship between the viscosity of blood and that of PBS solution (l Blood /l PBS ) is obtained by monitoring the reverse flows in the bridge channel at a specific flow-rate rate (Q PBS SS /Q Blood L ). Next, in the transient blood flow, a sudden increase in the blood flow-rate induces the transient behaviors of the blood flow in the bridge channel. Here, the elasticity (or characteristic time) of blood can be quantitatively measured by analyzing the dynamic movement of blood in the bridge channel. The regression formulais selected based on the pressure difference (DP ¼ P A À P B ) at each junction (A, B) of both side channels. The characteristic time of blood (k Blood ) is measured by analyzing the area (A Blood ) filled with blood in the bridge channel by selecting an appropriate detection window in the microscopic images captured by a high-speed camera (frame rate ¼ 200 Hz, total measurement time ¼ 7 s). The elasticity of blood (G Blood ) is identified using the relationship between the characteristic time and the viscosity of blood. For practical demonstrations, the proposed method is successfully applied to evaluate the variations in viscosity and elasticity of various blood samples: (a) various hematocrits form 20% to 50%, (b) thermal-induced treatment (50 C for 30 min), (c) flow-induced shear stress (53 6 0.5 mL/h for 120 min), and (d) normal rat versus spontaneously hypertensive rat. Based on these experimental demonstrations, the proposed method can be effectively used to monitor variations in viscosity and elasticity of bloods, even with the absence of fully integrated sensors, tedious labeling and calibrations. V C 2013 AIP Publishing LLC.

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“…To assess centerline blood flow velocities in HEV, 1-m diameter fluorescent YG microspheres (Polysciences, Warrington, PA) were injected systemically, and blood flow velocity was measured by frameto-frame displacement of the bead (three microspheres per venule). Wall shear rates (␥ w ) were estimated as 4.9 (8vb/d), where vb is the mean blood flow velocity and d is the diameter of the vessel (37,38).…”

Section: Targeted Disruption Of the Murine Golgi Gdp-fucose Transportmentioning

confidence: 99%

Golgi GDP-fucose Transporter-deficient Mice Mimic Congenital Disorder of Glycosylation IIc/Leukocyte Adhesion Deficiency II

Hellbusch

Sperandio

Frommhold

et al. 2007

Journal of Biological Chemistry

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Modification of glycoproteins by the attachment of fucose residues is widely distributed in nature. The importance of fucosylation has recently been underlined by identification of the monogenetic inherited human disease "congenital disorder of glycosylation IIc," also termed "leukocyte adhesion deficiency II." Due to defective Golgi GDP-fucose transporter (SLC35C1) activity, patients show a hypofucosylation of glycoproteins and present clinically with mental and growth retardation, persistent leukocytosis, and severe infections. To investigate effects induced by the loss of fucosylated structures in different organs, we generated a mouse model for the disease by inactivating the Golgi GDP-transporter gene (Slc35c1). Lectin binding studies revealed a tremendous reduction of fucosylated glycoconjugates in tissues and isolated cells from Slc35c1 ؊/؊ mice. Fucose treatment of cells from different organs led to partial normalization of the fucosylation state of glycoproteins, thereby indicating an alternative GDP-fucose transport mechanism. Slc35c1-deficient mice presented with severe growth retardation, elevated postnatal mortality rate, dilatation of lung alveoles, and hypocellular lymph nodes. In vitro and in vivo leukocyte adhesion and rolling assays revealed a severe impairment of P-, E-, and L-selectin ligand function. The diversity of these phenotypic aspects demonstrates the broad general impact of fucosylation in the mammalian organism.The covalent attachment of oligosaccharide moieties to newly synthesized proteins comprises one of the most frequent but also complex forms of co-and posttranslational protein modifications, which has been found in nearly all living organisms (1). Glycan structures affect the physicochemical properties and the function of proteins in a variety of biological processes, including folding, solubility, sorting, proteolytic stability, and receptor-ligand interactions. In mammalian organisms, the biosynthesis of the oligosaccharide chains requires a broad spectrum of glycosyltransferases, glycosidases, transport proteins, and 13 different monosaccharides (2-4).Due to its variability of binding types (␣-1,2-, ␣-1,3-, ␣-1,4-, and ␣-1,6-fucosylation have been described), the monosaccharide fucose plays an important role in the microheterogeneity of oligosaccharide structures (5). Fucose residues are predominantly linked to peripheral parts of N-, O-, and lipid-linked oligosaccharides, thereby building cap structures, which have been observed in many surface-localized and secreted proteins,

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Microviscometry reveals reduced blood viscosity and altered shear rate and shear stress profiles in microvessels after hemodilution

Cited by 180 publications

References 35 publications

Flow instability and wall shear stress variation in intracranial aneurysms

Flow instability and wall shear stress variation in intracranial aneurysms

Blood viscoelasticity measurement using steady and transient flow controls of blood in a microfluidic analogue of Wheastone-bridge channel

Golgi GDP-fucose Transporter-deficient Mice Mimic Congenital Disorder of Glycosylation IIc/Leukocyte Adhesion Deficiency II

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