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中华危重症医学杂志(电子版) ›› 2022, Vol. 15 ›› Issue (04) : 337 -342. doi: 10.3877/cma.j.issn.1674-6880.2022.04.016

综述

脓毒症中内皮细胞高通透性的机制研究进展
常泽楠1, 温仕宏2, 张义楠2, 赖汉津1, 詹雅清2, 刘紫锰1,()   
  1. 1. 510030 广州,中山大学附属第一医院重症医学科
    2. 510030 广州,中山大学附属第一医院麻醉科
  • 收稿日期:2021-11-29 出版日期:2022-08-31
  • 通信作者: 刘紫锰
  • Received:2021-11-29 Published:2022-08-31
引用本文:

常泽楠, 温仕宏, 张义楠, 赖汉津, 詹雅清, 刘紫锰. 脓毒症中内皮细胞高通透性的机制研究进展[J]. 中华危重症医学杂志(电子版), 2022, 15(04): 337-342.

脓毒症常由感染引起宿主免疫和过度炎症反应,是非心源性危重症患者死亡的主要原因之一[1]。正常情况下,循环的微血管内皮细胞结合紧密并与基膜形成半通透性屏障,仅限于水和电解质外渗;脓毒症时,强烈的炎症刺激导致血管内皮屏障功能受损,对溶质分子的选择性丧失、渗透性增加并导致血管大分子渗漏,从而形成组织水肿和器官损伤。脓毒症早期,病原体引起的过度炎症反应常伴有严重的微血管功能障碍,从而导致多器官功能不全甚至循环衰竭。因此,微血管内皮细胞损伤和微循环障碍是引发脓毒症中多器官功能障碍的重要环节,改善血管的内皮屏障功能和微血管的渗漏对控制病情进展及降低脓毒症的病死率具有重要意义。

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