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肝硬化时肝血管系统适应血液循环恶化状况的机制

Mechanisms of adaptation of the hepatic vasculature to the deteriorating conditions of blood circulation in liver cirrhosis.

作者信息

Garbuzenko Dmitry Victorovich, Arefyev Nikolay Olegovich, Belov Dmitry Vladimirovich

机构信息

Dmitry Victorovich Garbuzenko, Nikolay Olegovich Arefyev, Department of Faculty Surgery, South Ural State Medical University, 454092 Chelyabinsk, Russia.

出版信息

World J Hepatol. 2016 Jun 8;8(16):665-72. doi: 10.4254/wjh.v8.i16.665.

DOI:10.4254/wjh.v8.i16.665
PMID:27326313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4909428/
Abstract

PubMed, EMBASE, Orphanet, MIDLINE, Google Scholar and Cochrane Library were searched for articles published between 1983 and 2015. Relevant articles were selected by using the following terms: "Liver cirrhosis", "Endothelial dysfunction", "Sinusoidal remodeling", "Intrahepatic angiogenesis" and "Pathogenesis of portal hypertension". Then the reference lists of identified articles were searched for other relevant publications as well. Besides gross hepatic structural disorders related to diffuse fibrosis and formation of regenerative nodules, the complex morphofunctional rearrangement of the hepatic microvascular bed and intrahepatic angiogenesis also play important roles in hemodynamic disturbances in liver cirrhosis. It is characterized by endothelial dysfunction and impaired paracrine interaction between activated stellate hepatocytes and sinusoidal endotheliocytes, sinusoidal remodeling and capillarization, as well as development of the collateral microcirculation. In spite of the fact that complex morphofunctional rearrangement of the hepatic microvascular bed and intrahepatic angiogenesis in liver cirrhosis are the compensatory-adaptive reaction to the deteriorating conditions of blood circulation, they contribute to progression of disease and development of serious complications, in particular, related to portal hypertension.

摘要

我们检索了PubMed、EMBASE、Orphanet、MIDLINE、谷歌学术和考克兰图书馆,查找1983年至2015年间发表的文章。通过使用以下检索词选择相关文章:“肝硬化”、“内皮功能障碍”、“窦状隙重塑”、“肝内血管生成”和“门静脉高压的发病机制”。然后,我们还在已识别文章的参考文献列表中查找其他相关出版物。除了与弥漫性纤维化和再生结节形成相关的肝脏大体结构紊乱外,肝微血管床的复杂形态功能重排和肝内血管生成在肝硬化的血流动力学紊乱中也起重要作用。其特征为内皮功能障碍以及活化的星状肝细胞与窦状内皮细胞之间旁分泌相互作用受损、窦状隙重塑和毛细血管化,以及侧支微循环的发展。尽管肝硬化时肝微血管床的复杂形态功能重排和肝内血管生成是对血液循环恶化状况的代偿适应性反应,但它们会促进疾病进展和严重并发症的发生,尤其是与门静脉高压相关的并发症。

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本文引用的文献

1
Recent advancement of molecular mechanisms of liver fibrosis.肝纤维化分子机制的最新进展
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2
Angiogenesis and liver fibrosis.血管生成与肝纤维化
World J Hepatol. 2015 Mar 27;7(3):377-91. doi: 10.4254/wjh.v7.i3.377.
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Molecular pathophysiology of portal hypertension.门静脉高压症的分子病理生理学。
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Origins and functions of liver myofibroblasts.肝肌成纤维细胞的起源与功能
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