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遗传性膜缺陷患者中人工心脏瓣膜对红细胞的机械负荷

Prosthetic heart valves' mechanical loading of red blood cells in patients with hereditary membrane defects.

作者信息

Grigioni Mauro, Caprari Patrizia, Tarzia Anna, D'Avenio Giuseppe

机构信息

Department of Technology and Health, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.

出版信息

J Biomech. 2005 Aug;38(8):1557-65. doi: 10.1016/j.jbiomech.2004.11.020. Epub 2005 Jan 19.

DOI:10.1016/j.jbiomech.2004.11.020
PMID:15958211
Abstract

Implantable cardiovascular devices such as prosthetic heart valves (PHVs) are widely applied clinical tools. Upon implantation, the patient can suffer from anemia as a result of red cell destruction and hemolysis can be more relevant whenever the patient is also affected by red cell disorders in which erythrocytes are more susceptible to mechanical stress such as hereditary spherocytosis (HS) and hereditary elliptocytosis (HE). Considering the typical morphological alterations observed in HS and HE, a study of the influence of cell geometry on the distribution of the shear stress on red cells in biological fluids was carried out. A numerical simulation of the loading caused by Reynolds shear stresses on a prolate spheroid was performed, with the ellipticity of the particle as the independent parameter. The average shear stress on a particle in the blood stream was found to depend on the particle's geometry, besides the stress field produced by the prosthetic device. The relevance of an increasing particle ellipticity on the global load is discussed. The model was applied to erythrocytes from implanted patients with HE or HS, enabling to explain the occurrence of moderate or severe anemia, respectively. The clinical data support the relevance of the proposed global parameter as erythrocyte trauma predictor with regard to the fluid dynamics of artificial organs.

摘要

诸如人工心脏瓣膜(PHV)之类的可植入心血管装置是广泛应用的临床工具。植入后,患者可能会因红细胞破坏而患贫血,当患者同时患有红细胞疾病(如遗传性球形红细胞增多症(HS)和遗传性椭圆形红细胞增多症(HE)),其中红细胞更容易受到机械应力影响时,溶血可能更为严重。考虑到在HS和HE中观察到的典型形态学改变,开展了一项关于细胞几何形状对生物流体中红细胞上剪应力分布影响的研究。以颗粒椭圆率作为独立参数,对长椭球体上雷诺剪应力引起的载荷进行了数值模拟。发现血流中颗粒上的平均剪应力除了取决于人工装置产生的应力场外,还取决于颗粒的几何形状。讨论了颗粒椭圆率增加对整体载荷的影响。该模型应用于植入了HE或HS的患者的红细胞上,分别能够解释中度或重度贫血的发生。临床数据支持所提出的全局参数作为人工器官流体动力学方面红细胞创伤预测指标具有相关性。

相似文献

1
Prosthetic heart valves' mechanical loading of red blood cells in patients with hereditary membrane defects.遗传性膜缺陷患者中人工心脏瓣膜对红细胞的机械负荷
J Biomech. 2005 Aug;38(8):1557-65. doi: 10.1016/j.jbiomech.2004.11.020. Epub 2005 Jan 19.
2
Comment on "Prosthetic heart valves' mechanical loading of red blood cells in patients with hereditary membrane defects" by Grigioni et al., Journal of Biomechanics 38, 1557-1565.
J Biomech. 2006;39(13):2542; author reply 2542-4. doi: 10.1016/j.jbiomech.2006.06.008. Epub 2006 Aug 17.
3
Abnormalities in the membrane material properties of hereditary spherocytes.遗传性球形红细胞膜材料特性异常。
J Biomech Eng. 1980 Aug;102(3):240. doi: 10.1115/1.3149580.
4
Update on the clinical spectrum and genetics of red blood cell membrane disorders.红细胞膜疾病的临床谱与遗传学进展
Curr Hematol Rep. 2004 Mar;3(2):85-91.
5
Fragility of abnormal erythrocytes evaluated by response to shear stress.通过对剪切应力的反应评估异常红细胞的脆弱性。
J Lab Clin Med. 1975 Jan;85(1):67-74.
6
Disorders of red cell membrane.红细胞膜疾病
Br J Haematol. 2008 May;141(3):367-75. doi: 10.1111/j.1365-2141.2008.07091.x. Epub 2008 Mar 12.
7
Physiologically important secondary modifications of red cell membrane in hereditary spherocytosis-evidence for in vivo oxidation and lipid rafts protein variations.遗传性球形红细胞增多症中红细胞膜的生理重要性继发性修饰——体内氧化及脂筏蛋白变异的证据
Blood Cells Mol Dis. 2007 May-Jun;38(3):210-20. doi: 10.1016/j.bcmd.2006.10.163. Epub 2007 Jan 5.
8
Red cell membrane damage.红细胞膜损伤
J Heart Valve Dis. 1998 Jul;7(4):387-95.
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Hereditary red cell membrane defects: diagnostic and clinical aspects.遗传性红细胞膜缺陷:诊断与临床方面
Blood Transfus. 2011 Jul;9(3):274-7. doi: 10.2450/2011.0086-10. Epub 2011 Jan 13.
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Models of flow-induced loading on blood cells in laminar and turbulent flow, with application to cardiovascular device flow.层流和湍流中血流诱导对血细胞加载的模型及其在心血管装置血流中的应用。
Ann Biomed Eng. 2007 Aug;35(8):1347-56. doi: 10.1007/s10439-007-9308-8. Epub 2007 Apr 13.

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