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• W2913536427 abstract "Recent advances in cell culture and microfabrication technologies have enabled the development of perfusable endothelialized channels in vitro. To date, these techniques have primarily been applied to tissue engineering research. However, this set-up provides the unique opportunity to simulate blood product transfusion in a cost-effective, robust and reproducible manner – incorporating blood, endothelial and flow components in one unit. This Perspective describes the value of vascular models in transfusion research and discusses key decision points in the design process.What happens to blood after transfusion?On transfusion, blood products interact with blood cells and plasma components to alter platelet activation, leukocyte function and red blood cell (RBC) oxygen-carrying capacity. The pro-/anti-inflammatory balance hinges on whether neutrophil or macrophage responses dominate after blood product transfusion.1–3 These responses are dependent on the activation state of recipient neutrophils and macrophages which, in turn, is influenced by cytokines in the local microenvironment. RBCs and platelets modify immune system function by activating complement, releasing cytokines and participating in receptor-ligand interactions.4Blood products and recipient blood are encased by endothelium in blood vessels, one of the largest organs in the body with a surface area of 350-1000 m2.5 The endothelium conveys blood to tissues, provides a surface that prevents improper clotting and cellular activation, acts as a selective barrier to macromolecule extravasation and regulates microvascular blood flow.6 Activated endothelium participates in inflammation by releasing chemotactic molecules (e.g., interleukin-8 and monocyte chemoattractant protein-1), generating reactive oxygen species and expressing adhesion molecules (CD62, CD106, CD54, CD31) to attract leukocytes and facilitate leukocyte transmigration.7,8 Furthermore, activated endothelium also enhances thrombosis by elaborating procoagulant surface molecules (von Willebrand factor, tissue factor) and microparticles.8 Endothelial dysfunction has been implicated in transfusion-related acute lung injury, sepsis and multiple organ dysfunction.8,9The mixture of blood product and recipient blood is constantly mixed and propelled by the cardiac cycle – maximizing cellular interactions and minimizing inappropriate endothelial adhesion.10 After leaving the heart, blood flows through arteries to reach capillaries in the tissues and then veins before returning to the heart. The three types of blood vessels differ in structure, diameter, flow patterns and shear stress.10 In arteries and veins, RBCs and leukocytes flow in the center of the flow stream and platelets are distributed to the periphery of the stream.11 RBCs exhibit a parabolic velocity profile with shear-dependent rotation which continuously mixes the blood components. The configuration of cells in the flow stream can be modified by RBC plasticity, shear rate and fluid viscosity.12,13 In the microvasculature, cells travel in single file with uniform distribution of platelets, RBCs and leukocytes in the flow stream.Additionally, blood flow exerts shear stress on endothelium thereby altering endothelial gene expression, apoptosis, migration, permeability and alignment.6,14 Endothelial cells cultured under flow conditions demonstrate enhanced barrier function in conjunction with minimal adhesion molecule activation.15,16 Physiological shear stress is protective against inappropriate endothelial cytokine release compared to low shear stress.9 Additionally, flow patterns (e.g. continuous versus pulsatile) influence endothelial adhesion protein expression, structure and alignment.6 Lastly, shear stress modifies endothelial interactions with blood cells. For example, monocytes perfused over endothelium activated by tumor necrosis factor-α expressed more tissue factor and CD11b compared to monocytes co-incubated with activated endothelium under static conditions.9It follows that intravascular transfusion events are affected by blood product-recipient blood interactions and blood mixture-endothelium interactions under flow conditions. Simulation of the post-transfusion intravascular mileau in vitro requires recipient whole blood, blood product, endothelium and perfusate flow. To date, the majority of models used to test transfusion effects have involved static models in which blood products are co-incubated with specific cells such as neutrophils,1,17–21 macrophages,3 platelets22 or endothelial cells23 to examine interactions between two cell types. While blood co-incubation experiments enable the investigation of multiple cellular interactions,2,24 they do not recapitulate the frequency and type of cellular interactions that occur under endogenous flow conditions. In vivo models are the “gold standard” for capturing the sum of intravascular interactions that occur after transfusion of stored, packed RBCs. However, such models are limited by increased variability (requiring larger sample sizes), reduced capacity to isolate parameters and longer set-up times. Endothelialized in vitro flow models circumvent these limitations by using cell culture methods, packed RBCs and fresh whole blood, which are easier to acquire with fewer associated ethical considerations, shorter model development time and lower cost." @default.
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• W2913536427 date "2019-02-14" @default.
• W2913536427 modified "2023-10-16" @default.
• W2913536427 title "Endothelialized flow models for blood transfusion research" @default.
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• W2913536427 doi "https://doi.org/10.3324/haematol.2018.205203" @default.
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