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Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow

We investigate numerically the microscale blood flow in which red blood cells (RBCs) are partially infected by Plasmodium falciparum, the malaria parasite. The infected RBCs are modeled as more rigid cells with less deformability than healthy ones. Our study illustrates that, in a 10 μm microvessel...

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Autores principales: Wang, Tong, Xing, Zhongwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5937607/
https://www.ncbi.nlm.nih.gov/pubmed/29850568
http://dx.doi.org/10.1155/2018/8065252
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author Wang, Tong
Xing, Zhongwen
author_facet Wang, Tong
Xing, Zhongwen
author_sort Wang, Tong
collection PubMed
description We investigate numerically the microscale blood flow in which red blood cells (RBCs) are partially infected by Plasmodium falciparum, the malaria parasite. The infected RBCs are modeled as more rigid cells with less deformability than healthy ones. Our study illustrates that, in a 10 μm microvessel in low-hematocrit conditions (18% and 27%), the Plasmodium falciparum-infected red blood cells (Pf-IRBCs) and healthy ones first form a train of cells. Because of the slow moving of the Pf-IRBCs, the local hematocrit (H(ct)) near the Pf-IRBCs is then increased, to approximately 40% or even higher values. This increase of the local hematocrit is temporary and is kept for a longer length of time because of the long RBC train formed in 27%-H(ct) condition. Similar hematocrit elevation at the downstream region with 45%-H(ct) in the same 10 μm microvessel is also observed with the cells randomly located. In 20 μm microvessels with 45%-H(ct), the Pf-IRBCs slow down the velocity of the healthy red blood cells (HRBCs) around them and then locally elevate the volume fraction and result in the accumulation of the RBCs at the center of the vessels, thus leaving a thicker cell free layer (CFL) near the vessel wall than normal. Variation of wall shear stress (WSS) is caused by the fluctuation of local H(ct) and the distance between the wall and the RBCs. Moreover, in high-hematocrit condition (45%), malaria-infected cells have a tendency to migrate to the edge of the aggregates which is due to the uninterrupted hydrodynamic interaction between the HRBCs and Pf-IRBC. Our results suggest that the existence of Pf-IRBCs is a nonnegligible factor for the fluctuation of hematocrit and WSS and also contributes to the increase of CFL of pathological blood flow in microvessels. The numerical approach presented has the potential to be utilized to RBC disorders and other hematologic diseases.
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spelling pubmed-59376072018-05-30 Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow Wang, Tong Xing, Zhongwen Biomed Res Int Research Article We investigate numerically the microscale blood flow in which red blood cells (RBCs) are partially infected by Plasmodium falciparum, the malaria parasite. The infected RBCs are modeled as more rigid cells with less deformability than healthy ones. Our study illustrates that, in a 10 μm microvessel in low-hematocrit conditions (18% and 27%), the Plasmodium falciparum-infected red blood cells (Pf-IRBCs) and healthy ones first form a train of cells. Because of the slow moving of the Pf-IRBCs, the local hematocrit (H(ct)) near the Pf-IRBCs is then increased, to approximately 40% or even higher values. This increase of the local hematocrit is temporary and is kept for a longer length of time because of the long RBC train formed in 27%-H(ct) condition. Similar hematocrit elevation at the downstream region with 45%-H(ct) in the same 10 μm microvessel is also observed with the cells randomly located. In 20 μm microvessels with 45%-H(ct), the Pf-IRBCs slow down the velocity of the healthy red blood cells (HRBCs) around them and then locally elevate the volume fraction and result in the accumulation of the RBCs at the center of the vessels, thus leaving a thicker cell free layer (CFL) near the vessel wall than normal. Variation of wall shear stress (WSS) is caused by the fluctuation of local H(ct) and the distance between the wall and the RBCs. Moreover, in high-hematocrit condition (45%), malaria-infected cells have a tendency to migrate to the edge of the aggregates which is due to the uninterrupted hydrodynamic interaction between the HRBCs and Pf-IRBC. Our results suggest that the existence of Pf-IRBCs is a nonnegligible factor for the fluctuation of hematocrit and WSS and also contributes to the increase of CFL of pathological blood flow in microvessels. The numerical approach presented has the potential to be utilized to RBC disorders and other hematologic diseases. Hindawi 2018-04-23 /pmc/articles/PMC5937607/ /pubmed/29850568 http://dx.doi.org/10.1155/2018/8065252 Text en Copyright © 2018 Tong Wang and Zhongwen Xing. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Wang, Tong
Xing, Zhongwen
Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title_full Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title_fullStr Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title_full_unstemmed Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title_short Local Hematocrit Fluctuation Induced by Malaria-Infected Red Blood Cells and Its Effect on Microflow
title_sort local hematocrit fluctuation induced by malaria-infected red blood cells and its effect on microflow
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5937607/
https://www.ncbi.nlm.nih.gov/pubmed/29850568
http://dx.doi.org/10.1155/2018/8065252
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