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肝硬化肝脏肝内微循环的改变。

Alteration of intrahepatic microcirculation in cirrhotic livers.

作者信息

Yang Ying-Ying, Lin Han-Chieh

机构信息

Division of Clinical Training, Department of Medical Education, Taipei Veterans General Hospital, Taipei, Taiwan, ROC.

Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC.

出版信息

J Chin Med Assoc. 2015 Aug;78(8):430-7. doi: 10.1016/j.jcma.2015.05.005.

DOI:10.1016/j.jcma.2015.05.005
PMID:26074366
Abstract

From a hemodynamic point of view, hepatic vascular resistance and portal inflow determine the level of portal pressure. Factors that determine hepatic vascular resistance include both structural and dynamic components. Among the structural components are histological characteristics such as steatosis, fibrosis, regeneration nodules, and neo-angiogenesis. Dynamic structures include cells with contractile properties such as hepatocytes, hepatic stellate cells, sinusoidal endothelial cells, and Kupffer cells. The contributions of the interactions between four cells in cirrhotic livers resulted in hepatic endothelial dysfunction, hepatic microcirculatory dysfunction, hepatic venous dysregulation, hepatic fibrogenesis, and subsequently increased intrahepatic resistance and portal hypertension in cirrhosis. The pathogenic mechanisms that trigger the associated abnormalities in hepatic microcirculations include persistent endotoxemia, increased hepatic oxidative stress, activated endocannabinoids substances, pathogenic sinusoidal remodeling, and hypoperfusion in cirrhotic livers. Cumulative data suggested that various therapeutic strategies targeting hepatic microcirculation provided effective improvement of the systemic abnormalities of cirrhosis. Accordingly, the mechanistic and therapeutic approaches focusing on the disarrangement of hepatic microcirculation will be introduced in this article.

摘要

从血流动力学角度来看,肝血管阻力和门静脉血流决定门静脉压力水平。决定肝血管阻力的因素包括结构和动态成分。结构成分包括组织学特征,如脂肪变性、纤维化、再生结节和新生血管形成。动态结构包括具有收缩特性的细胞,如肝细胞、肝星状细胞、窦状内皮细胞和库普弗细胞。肝硬化肝脏中这四种细胞之间相互作用的结果导致肝内皮功能障碍、肝微循环功能障碍、肝静脉调节异常、肝纤维化,随后肝硬化时肝内阻力增加和门静脉高压。引发肝微循环相关异常的致病机制包括持续性内毒素血症、肝氧化应激增加、内源性大麻素物质激活、致病性窦状重塑以及肝硬化肝脏中的灌注不足。累积数据表明,针对肝微循环的各种治疗策略有效改善了肝硬化的全身异常。因此,本文将介绍关注肝微循环紊乱的机制和治疗方法。

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