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微循环功能障碍的病理生理学与脓毒性休克的发病机制。

Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock.

机构信息

Department of Intensive Care; Erasme University Hospital; Université Libre de Bruxelles (ULB); Bruxelles, Belgium.

出版信息

Virulence. 2014 Jan 1;5(1):73-9. doi: 10.4161/viru.26482. Epub 2013 Sep 25.

DOI:10.4161/viru.26482
PMID:24067428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3916386/
Abstract

Multiple experimental and human trials have shown that microcirculatory alterations are frequent in sepsis. In this review, we discuss the various mechanisms that are potentially involved in their development and the implications of these alterations. Endothelial dysfunction, impaired inter-cell communication, altered glycocalyx, adhesion and rolling of white blood cells and platelets, and altered red blood cell deformability are the main mechanisms involved in the development of these alterations. Microcirculatory alterations increase the diffusion distance for oxygen and, due to the heterogeneity of microcirculatory perfusion in sepsis, may promote development of areas of tissue hypoxia in close vicinity to well-oxygenated zones. The severity of microvascular alterations is associated with organ dysfunction and mortality. At this stage, therapies to specifically target the microcirculation are still being investigated.

摘要

多项实验和人体试验表明,脓毒症患者常伴有微循环改变。在这篇综述中,我们讨论了可能涉及微循环改变发展的各种机制及其影响。内皮功能障碍、细胞间通讯受损、糖萼改变、白细胞和血小板黏附和滚动,以及红细胞变形能力改变是这些改变发展的主要机制。微循环改变增加了氧气的扩散距离,并且由于脓毒症中微循环灌注的异质性,可能会导致在靠近氧合区的地方形成组织缺氧区。微血管改变的严重程度与器官功能障碍和死亡率相关。在现阶段,仍在研究专门针对微循环的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7531/3916386/c54137b6db9f/viru-5-73-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7531/3916386/7775f3da8536/viru-5-73-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7531/3916386/c54137b6db9f/viru-5-73-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7531/3916386/7775f3da8536/viru-5-73-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7531/3916386/c54137b6db9f/viru-5-73-g2.jpg

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