缺氧性肝损伤机制及其凝血因子水平变化的研究进展

王珍; 张培莉; 杨发满

doi:10.16766/j.cnki.issn.1674-4152.002154

缺氧性肝损伤机制及其凝血因子水平变化的研究进展

doi: 10.16766/j.cnki.issn.1674-4152.002154

1.
青海大学研究生院临床医学系，青海西宁 810000
2.
青海大学附属医院全科医学科，青海西宁 810000

基金项目:

青海省卫生计生委重点科研项目 2018-wjzd-12

详细信息

通讯作者:
张培莉, E-mail: zplxn@sina.com

中图分类号: R575
计量
- 文章访问数: 267
- HTML全文浏览量: 57
- PDF下载量: 15
- 被引次数: 0
出版历程
- 收稿日期: 2020-08-31
- 网络出版日期: 2022-02-15

Research progress on the mechanism of hypoxic liver injury and the changes of coagulation factor levels

1.
Department of Clinical Medicine, Graduate School of Qinghai University, Xining, Qinghai 810000, China

摘要

摘要: 肝脏是机体合成凝血因子的主要器官，常氧的环境下肝功能受损后会影响凝血因子合成，导致出血等疾病发生。在周围环境缺氧(高海拔)、基础疾病(心源性、肺源性、血液系统疾病)存在以及加重均会导致肝脏组织缺氧。先前学者对“缺氧性肝病”的定义是由于肝脏供血不足(前负荷衰竭)或严重淤血(后负荷衰竭)引起肝细胞缺血缺氧甚至坏死, 即肝脏的供氧量不能满足其需氧量时, 导致肝脏中央区细胞的坏死。在肝源性疾病来看，目前部分研究认为非酒精性脂肪肝病、酒精性肝损伤、肝纤维化、肝硬化、缺血-再灌注性肝损伤等肝脏疾病均存在肝脏组织缺氧。这些疾病的共同特征首先表现在肝脏本身疾病，其次是由于代谢供需不平衡而导致的肝脏组织缺氧。机体在慢性缺氧下会出现凝血因子水平变化，如高海拔地区居民长期生活在低氧环境下，机体代偿性出现血细胞计数变化，如红细胞及血红蛋白水平升高，导致血液黏稠、血液黏滞，高凝状态下血栓或者微血栓形成，出现凝血酶原时间、部分活化凝血酶原时间的延长以及继发性部分凝血因子表达水平的异常。在临床工作中对肝病患者凝血功能的测定尤为重要，上述这些肝源疾病是否会对凝血因子表达水平产生影响？本文对各种肝源性疾病出现肝脏组织缺氧性肝损伤的发生机制以及相关缺氧性肝损伤后凝血因子变化的水平进行描述。
- 缺氧 /
- 肝损伤 /
- 机制 /
- 凝血因子
Abstract: The liver is the main organ that synthesises blood coagulation factors. Damage to liver function in a normoxic environment will affect the synthesis of blood coagulation factors and cause bleeding and other diseases. Hypoxic environment (high altitude) and the presence and aggravation of underlying diseases (cardiogenic, pulmonary and blood system diseases) can cause hypoxia in liver tissue. Hypoxic liver disease is defined as the lack of blood supply to the liver (preload failure) or severe congestion (afterload failure), which causes ischemia, hypoxia and even necrosis of hepatocytes in the central area of the liver. In terms of liver-derived diseases, non-alcoholic fatty liver disease, alcoholic liver injury, liver fibrosis, cirrhosis, ischemia-reperfusion liver injury and other liver diseases all have liver tissue hypoxia. The common feature of these diseases is first manifested in the liver itself, and liver tissue hypoxia is caused by the imbalance of metabolic supply and demand. The body will experience changes in the level of coagulation factors under chronic hypoxia. For example, if residents in high-altitude areas live in a low-oxygen environment for a long time, the body will have compensatory changes in blood cell counts, such as increased levels of red blood cells and hemoglobin, resulting in thick and sticky blood; stagnation, thrombosis or microthrombus formation in a hypercoagulable state; prolongation of prothrombin time and partially activated prothrombin time; and abnormal expression of secondary partial coagulation factors. Thus, the blood coagulation function of patients with liver disease and whether liver-derived diseases will affect the expression of coagulation factors need to be determined. This article describes the mechanism of hypoxic liver injury in various liver-derived diseases and the changes in blood coagulation factors after hypoxic liver injury.
- Hypoxia /
- Liver injury /
- Mechanism /
- Coagulation factors

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参考文献(31)

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