36 research outputs found

    Comparison of 2D and 3D calculation of left ventricular torsion as circumferential-longitudinal shear angle using cardiovascular magnetic resonance tagging

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    <p>Abstract</p> <p>Purpose</p> <p>To compare left ventricular (LV) torsion represented as the circumferential-longitudinal (CL) shear angle between 2D and 3D quantification, using cardiovascular magnetic resonance (CMR).</p> <p>Methods</p> <p>CMR tagging was performed in six healthy volunteers. From this, LV torsion was calculated using a 2D and a 3D method. The cross-correlation between both methods was evaluated and comparisons were made using Bland-Altman analysis.</p> <p>Results</p> <p>The cross-correlation between the curves was <it>r</it><sup>2 </sup>= 0.97 ± 0.02. No significant time-delay was observed between the curves. Bland-Altman analysis revealed a significant positive linear relationship between the difference and the average value of both analysis methods, with the 2D results showing larger values than the 3D. The difference between both methods can be explained by the definition of the 2D method.</p> <p>Conclusion</p> <p>LV torsion represented as CL shear quantified by the 2D and 3D analysis methods are strongly related. Therefore, it is suggested to use the faster 2D method for torsion calculation.</p

    Red blood cell deformability influences platelets--vessel wall interaction in flowing blood

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    Abstract Hematocrit and red cell size are important factors for the transport of blood platelets toward subendothelium in flowing blood. We report that red cell deformability also influences platelet transport. Red cell deformability was estimated with Couette-flow viscosimetry at a shear rate of 130 s-1 and expressed as a ‘T’ factor--a dimensionless parameter relating the relative viscosity and the hematocrit derived from the relationship: T = (1 - mu -0.4 rel)/H, where mu rel is the relative viscosity and H is the hematocrit. The normal value of T was within a narrow range (0.91 +/- 0.02). Treatment of normal red cells with isoxsuprine and chlorpromazine caused decreased rigidity and decreased T. Cholesterol loading and treatment with diamide increased rigidity and increased T. In vitro perfusion experiments in an annular perfusion system with everted human umbilical arteries were performed with perfusates to which such treated red blood cells were added to investigate their influence on platelet adherence to artery subendothelium. Platelet adherence was well correlated with red cell rigidity, with increased adherence at increased rigidity and vice versa. A change in T of 0.10 corresponded to a change in platelet adherence of approximately 50%. These effects were more pronounced at a wall shear rate of 1,800 s-1 than at 300 s-1.</jats:p

    Red blood cell deformability influences platelets--vessel wall interaction in flowing blood

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    Hematocrit and red cell size are important factors for the transport of blood platelets toward subendothelium in flowing blood. We report that red cell deformability also influences platelet transport. Red cell deformability was estimated with Couette-flow viscosimetry at a shear rate of 130 s-1 and expressed as a ‘T’ factor--a dimensionless parameter relating the relative viscosity and the hematocrit derived from the relationship: T = (1 - mu -0.4 rel)/H, where mu rel is the relative viscosity and H is the hematocrit. The normal value of T was within a narrow range (0.91 +/- 0.02). Treatment of normal red cells with isoxsuprine and chlorpromazine caused decreased rigidity and decreased T. Cholesterol loading and treatment with diamide increased rigidity and increased T. In vitro perfusion experiments in an annular perfusion system with everted human umbilical arteries were performed with perfusates to which such treated red blood cells were added to investigate their influence on platelet adherence to artery subendothelium. Platelet adherence was well correlated with red cell rigidity, with increased adherence at increased rigidity and vice versa. A change in T of 0.10 corresponded to a change in platelet adherence of approximately 50%. These effects were more pronounced at a wall shear rate of 1,800 s-1 than at 300 s-1.</jats:p

    On the flow dependency of the electrical conductivity of blood

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    Experiments presented in the literature show that the electrical conductivity of flowing blood depends on flow velocity. The aim of this study is to extend the Maxwell-Fricke theory, developed for a dilute suspension of ellipsoidal particles in an electrolyte, to explain this flow dependency of the conductivity of blood for stationary laminar flow in a rigid cylindrical tube. Furthermore, these theoretical results are compared to earlier published measurement results. To develop the theory, we assumed that blood is a Newtonian fluid and that red blood cells can be represented by oblate ellipsoids. If blood flows through a cylindrical tube, shear stresses will deform and align the red blood cells with one of their long axes aligned parallel to the stream lines. The pathway of a low-frequency (<1 MHz) alternating electrical current will be altered by this orientation and deformation of the red blood cells. Consequently, the electrical conductivity in the flow direction of blood increases. The theoretically predicted flow dependency of the conductivity of blood corresponds well with experimental results. This theoretical study shows that red blood cell orientation and deformation can explain quantitatively the flow dependency of blood conductivity

    Role of plasma viscosity in platelet adhesion

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    Abstract Platelet adhesion to the vessel wall is initiated by transport of blood platelets from the bulk flow to the wall. The process of diffusion and convection of the platelets is affected by rheological conditions such as well shear rate, red blood cell (RBC) deformability, and viscosity of the medium. To study the effect of plasma viscosity on platelet adhesion, perfusion experiments with a rectangular perfusion chamber were performed. Reconstituted blood, consisting of washed platelets and washed RBCs, was circulated through this chamber for 5 minutes at a wall shear rate of 300 s-1. Different albumin concentrations were made, to obtain different medium viscosities (0.89 to 1.85 mPa.s). Platelet adhesion decreased with increasing medium viscosity up to viscosities of 0.95 mPa.s, but increased with medium viscosity above this value. Instead of human albumin solution, different plasma viscosities were obtained by dilution of Waldenstrom plasma with buffer. Plasma was depleted of fibronectin, which gave a final plasma viscosity of 2.0 mPa.s, and was dialyzed against HEPES buffer and subsequently diluted with the dialysis buffer in different fractions (0.89 to 2.00 mPa.s). Perfusions were performed over a purified von Willebrand factor coating on glass, or over an endothelial cell matrix, preincubated with von Willebrand factor. With both surfaces, platelet adhesion was dependent on the plasma viscosity in a similar way: at low plasma viscosities, adhesion was decreased with increasing plasma viscosity, while at higher plasma viscosities, adhesion increased with plasma viscosity. Adhesion values at higher plasma viscosity or at higher human albumin concentrations could be explained by effects of the medium on the rigidity of the RBCs, since platelet adhesion is known to be increased by enhanced RBC rigidity. Effects of the medium on the deformability of the RBCs were measured separately with the laser diffraction method. These experiments confirmed that presence of human albumin or plasma in the measuring suspension increased the rigidity of RBCs. To prevent influence of the medium on the RBCs in perfusion experiments, the RBCs were fixated with glutaraldehyde. Perfusion experiments with fixated RBCs in plasma over a von Willebrand factor preincubated endothelial cell matrix, showed a consequent decrease in adhesion with increasing plasma viscosity, according to the diffusion theories, whereas the increase of adhesion at high plasma viscosities was lacking. This suggests that the latter effect was entirely due to increased transport of platelets by more rigid RBCs.</jats:p

    Role of plasma viscosity in platelet adhesion

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    Platelet adhesion to the vessel wall is initiated by transport of blood platelets from the bulk flow to the wall. The process of diffusion and convection of the platelets is affected by rheological conditions such as well shear rate, red blood cell (RBC) deformability, and viscosity of the medium. To study the effect of plasma viscosity on platelet adhesion, perfusion experiments with a rectangular perfusion chamber were performed. Reconstituted blood, consisting of washed platelets and washed RBCs, was circulated through this chamber for 5 minutes at a wall shear rate of 300 s-1. Different albumin concentrations were made, to obtain different medium viscosities (0.89 to 1.85 mPa.s). Platelet adhesion decreased with increasing medium viscosity up to viscosities of 0.95 mPa.s, but increased with medium viscosity above this value. Instead of human albumin solution, different plasma viscosities were obtained by dilution of Waldenstrom plasma with buffer. Plasma was depleted of fibronectin, which gave a final plasma viscosity of 2.0 mPa.s, and was dialyzed against HEPES buffer and subsequently diluted with the dialysis buffer in different fractions (0.89 to 2.00 mPa.s). Perfusions were performed over a purified von Willebrand factor coating on glass, or over an endothelial cell matrix, preincubated with von Willebrand factor. With both surfaces, platelet adhesion was dependent on the plasma viscosity in a similar way: at low plasma viscosities, adhesion was decreased with increasing plasma viscosity, while at higher plasma viscosities, adhesion increased with plasma viscosity. Adhesion values at higher plasma viscosity or at higher human albumin concentrations could be explained by effects of the medium on the rigidity of the RBCs, since platelet adhesion is known to be increased by enhanced RBC rigidity. Effects of the medium on the deformability of the RBCs were measured separately with the laser diffraction method. These experiments confirmed that presence of human albumin or plasma in the measuring suspension increased the rigidity of RBCs. To prevent influence of the medium on the RBCs in perfusion experiments, the RBCs were fixated with glutaraldehyde. Perfusion experiments with fixated RBCs in plasma over a von Willebrand factor preincubated endothelial cell matrix, showed a consequent decrease in adhesion with increasing plasma viscosity, according to the diffusion theories, whereas the increase of adhesion at high plasma viscosities was lacking. This suggests that the latter effect was entirely due to increased transport of platelets by more rigid RBCs.</jats:p
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