Blood Rheology after Hemorrhage and Endotoxin

Chien, Shu; Usami, Shunichi; Dellenback, J.; Magazinovic, V

doi:10.1007/978-1-4684-3228-2_9

Cited by 5 publications

(2 citation statements)

References 26 publications

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“…Acquisition of the viscosity of blood by bulk viscometry has emphasized the importance of shear rate, hematocrit, and red cell aggregation and deformability as it pertains to flow in large blood vessels [11] . With the use of tube, Couette, and cone‐plate viscometers, under the assumption that blood is a homogeneous fluid with an intrinsic viscosity, in vitro studies have revealed that blood viscosity falls about 75% as shear rates (dotγ) rise from on the order of 0.1 to 1000 sec −1 .…”

Section: The In Vitro Frameworkmentioning

confidence: 99%

Microvascular Rheology and Hemodynamics

2005

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The goal of elucidating the biophysical and physiological basis of pressure-flow relations in the microcirculation has been a recurring theme since the first observations of capillary blood flow in living tissues. At the birth of the Microcirculatory Society, seminal observations on the heterogeneous distribution of blood cells in the microvasculature and the rheological properties of blood in small bore tubes raised many questions on the viscous properties of blood flow in the microcirculation that captured the attention of the Society's membership. It is now recognized that blood viscosity in small bore tubes may fall dramatically as shear rates are increased, and increase (dramatically with elevations in hematocrit. These relationships are strongly affected by blood cell deformability and concentration, red cell aggregation, and white cell interactions with the red cells anti endothelium. Increasing strength of red cell aggregation may result in sequestration of clumps of red cells with either reductions or increases in microvascular hematocrit dependent upon network topography. During red cell aggregation, resistance to flow may thus decrease with hematocrit reduction or increase due to redistribution of red cells. Blood cell adhesion to the microvessel wall may initiate flow reductions, as, for example, in the case of red cell adhesion to the endothelium in sickle cell disease, or leukocyte adhesion in inflammation. The endothelial glycocalyx has been shown to result from a balance of the biosynthesis of new glycans, and the enzymatic or shear-dependent alterations in its composition. Flow-dependent reductions in the endothelial surface layer may thus affect the resistance to flow and/or the adhesion of red cells and/or leukocytes to the endothelium. Thus, future studies aimed at the molecular rheology of the endothelial surface layer may provide new insights into determinants of the resistance to flow.

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Section: The In Vitro Frameworkmentioning

confidence: 99%

Microvascular Rheology and Hemodynamics

2005

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“…77 Experimental measurements using different methods have shown that in human the magnitudes of shear stress range from 1 to 6 dyn/cm 2 in the venous system and from 10 to 70 dyn/cm 2 in the arterial vessels. 25,77,90 In vitro assays using cultured vascular ECs demonstrate that ECs can respond to fluid shear stress at the levels lower than 0.2 dyn/cm 2 through various mechanotransduction pathways. 94 In vivo observations indicate that shear stress can play critical roles in modulating vascular homeostasis and remodeling.…”

Section: Fluid Shear Stress and Endothelial Dysfunctionmentioning

confidence: 99%

Epigenetic Regulation of Vascular Endothelial Biology/Pathobiology and Response to Fluid Shear Stress

2011

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Vascular endothelial cells (ECs) are constantly exposed to hemodynamic forces, including blood flowinduced shear stress, which modulates EC gene expression and function and hence vascular biology/pathobiology in health and disease. Epigenetics refers to chromatin-based mechanisms, including DNA methylation, histone modifications, and RNA-based machinery, which regulate gene expression without changes in the underlying DNA sequences. The role of epigenetic mechanisms in regulating EC gene expression and function under static condition and in response to shear stress has recently emerged. This review provides an introduction to epigenetic concepts for vascular bioengineers and biologists. Using endothelial nitric oxide synthase, angiogenesis, and atherogenesis as examples, this review presents a conceptual framework for understanding how epigenetic factors, including histone deacetylases and microRNAs, are involved in the control of EC gene expression and function and hence vascular disease development, and summarizes the current knowledge on the role of epigenetic pathways in regulating EC responses to shear stress. Such information can contribute to our understanding of how mechanical environment of ECs impacts their genome to modify disease susceptibility and help to generate new approaches for therapeutic interventions.

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