Literature DB >> 16202011

Plasma dependent reduction in red blood cell aggregation after dextran sulfate low-density lipoprotein apheresis--implications for rheological studies.

Vered Schechner1, Ronen Ben-Ami, Tiberiu Hershcovici, Shaul Yedgar, Ytzhak Beigel, Itzhak Shapira, Shlomo Berliner, Gershon Barsthein.   

Abstract

Red blood cell (RBC) aggregation is increased in familial hypercholesterolemia, and is reduced significantly after low density lipoprotein (LDL) apheresis. The purpose of the present study was to clarify whether this reduction depends on changes in plasma composition, RBC membrane properties, or both. RBC aggregation was determined in a computerized cell flow-properties analyzer, before and after LDL apheresis. We compared RBC aggregation in autologous plasma with aggregation in a plasma-free standard solution (0.5% of dextran 500 kDa) to define the separate contributions of plasma and cellular properties to the observed RBC aggregation. RBC aggregation in autologous plasma was reduced by 35.5% after LDL apheresis (P=0.01) but was not significantly affected when measured in dextran 500. This suggests that LDL apheresis attenuated RBC aggregation by altering plasma composition rather than RBC membrane properties. These results are relevant to the understanding of hemorheological changes which follow therapeutic apheresis in hypercholesterolemic patients.

Entities:  

Mesh:

Substances:

Year:  2005        PMID: 16202011     DOI: 10.1111/j.1744-9987.2005.00317.x

Source DB:  PubMed          Journal:  Ther Apher Dial        ISSN: 1744-9979            Impact factor:   1.762


  1 in total

1.  Longxuetongluo Capsule Improves Erythrocyte Function against Lipid Peroxidation and Abnormal Hemorheological Parameters in High Fat Diet-Induced ApoE-/- Mice.

Authors:  Jiao Zheng; Binglin Liu; Qixing Lun; Weijuan Yao; Yunfang Zhao; Wei Xiao; Wenzhe Huang; Yonghua Wang; Jun Li; Pengfei Tu
Journal:  Oxid Med Cell Longev       Date:  2015-11-16       Impact factor: 6.543

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.