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体内剪切应力决定终末期肾病患者循环内皮微粒水平。

In vivo shear stress determines circulating levels of endothelial microparticles in end-stage renal disease.

作者信息

Boulanger Chantal M, Amabile Nicolas, Guérin Alain P, Pannier Bruno, Leroyer Aurélie S, Mallat Clément Nguyen Ziad, Tedgui Alain, London Gérard M

机构信息

INSERM Cardiovascular Research Center, Hôpital Lariboisière, Paris, France.

出版信息

Hypertension. 2007 Apr;49(4):902-8. doi: 10.1161/01.HYP.0000259667.22309.df. Epub 2007 Feb 19.

DOI:10.1161/01.HYP.0000259667.22309.df
PMID:17309952
Abstract

Shear stress is a major determinant of endothelial apoptosis, but its role in the in vivo release of shed membrane microparticles by endothelial cells remains unknown. Thus, we sought to evaluate the possible relationship between circulating endothelial microparticle levels and laminar shear stress in end-stage renal disease patients with high cardiovascular risk, whose levels of endothelial microparticles are elevated. In 34 hemodialyzed patients, we analyzed the relationships between brachial artery and aortic shear stress and circulating microparticles levels. Only endothelial microparticles were inversely correlated with laminar shear stress values (P<0.0001) or its components shear rate and whole blood viscosity, independent of age or arterial blood pressure. Changes in hematocrit resulting from hemodialysis-induced hemoconcentration or erythropoietin anemia improvement induced a significant increase in whole blood viscosity and shear stress and were associated with a significant decrease in endothelial microparticles with a significant and inverse correlation with changes in hematocrit/hemoglobin or laminar shear stress. These results demonstrate that, in end-stage renal disease patients, laminar shear stress is an important determinant of plasma levels of endothelial microparticles. Anemia as an important determinant of whole blood viscosity and shear stress, contributes to endothelial apoptosis, and could play an indirect role in the pathogenesis of accelerated arteriosclerosis in this high-risk population.

摘要

剪切应力是内皮细胞凋亡的主要决定因素,但其在内皮细胞释放脱落膜微粒的体内过程中的作用尚不清楚。因此,我们试图评估心血管风险高且内皮微粒水平升高的终末期肾病患者循环内皮微粒水平与层流剪切应力之间的可能关系。在34例接受血液透析的患者中,我们分析了肱动脉和主动脉剪切应力与循环微粒水平之间的关系。仅内皮微粒与层流剪切应力值(P<0.0001)或其组成部分剪切速率和全血粘度呈负相关,且不受年龄或动脉血压的影响。血液透析引起的血液浓缩或促红细胞生成素改善贫血导致的血细胞比容变化,会使全血粘度和剪切应力显著增加,并与内皮微粒显著减少相关,且与血细胞比容/血红蛋白或层流剪切应力的变化呈显著负相关。这些结果表明,在终末期肾病患者中,层流剪切应力是血浆内皮微粒水平的重要决定因素。贫血作为全血粘度和剪切应力的重要决定因素,会导致内皮细胞凋亡,并可能在这一高危人群加速动脉粥样硬化的发病机制中起间接作用。

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